To see the other types of publications on this topic, follow the link: Lung congesti.
Journal articles on the topic 'Lung congesti'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Lung congesti.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Lloyd, T. C. "Breathing response to lung congestion with and without left heart distension." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 131–36. http://dx.doi.org/10.1152/jappl.1988.65.1.131.
Full textAbstract:
This study compared the effect of lung congestion with and without left heart (LH) distension on breathing frequency (fr) and discriminated among responses mediated by myelinated and nonmyelinated vagal afferents. Cardiopulmonary bypass perfusion of anesthetized dogs was used to isolate reflexes. The following three groups were prepared: 1) lung vessels pressurized by pumping into the main pulmonary artery (MPA); 2) lungs and fibrillating LH pressurized by pumping into MPA while draining from LH; 3) lungs congested by occluding several pulmonary veins while holding cardiac output constant. Congestion of lungs alone in groups 1 and 3 depressed fr. Congestion of lungs and distension of LH (group 2) caused transient depression of fr but a steady-state excitation. Cooling cervical vagi to 8 degrees C prevented depression of fr by congestion in all groups. In groups 1 and 2, in which MPA pressure was higher than in group 3, congestion during vagal cooling stimulated breathing. I conclude that lung congestion may stimulate fr via C-fiber afferents, but this may be overcome by a depressor effect via myelinated afferents. Simultaneous LH distension may reflexly stimulate breathing and overcome the lung depressor reflex.
2
Skorodumova, E. G., V. A. Kostenko, E. A. Skorodumova, and A. V. Siverinа. "Assessment of interstitial edema in patients with intermediate function of the left ventricle after resolving of acute decompensation of heart failure." Translational Medicine 5, no. 3 (October 1, 2018): 23–27. http://dx.doi.org/10.18705/2311-4495-2018-5-3-23-27.
Full textAbstract:
Background.According to the recommendations of the European Society of Cardiology, ultrasound examination of the lung can be used to assess congestive changes, however, this method has so far a low recommendation class IIb and a level of evidence C, which can be regarded as a consequence of its insufficient knowledge.The aim of the research.To study ultrasound characteristics of the lung tissue in patients with intermediate left ventricular function after resolving of acute decompensation of heart failure.Materials and methods. The ultrasound profile of the lung tissue was studied in 71 patients after resolution of acute heart failure decompensation under intermediate left ventricular function. The average age of patients studied was 65.2 ± 3.6 years. 64.3% of them were males ,25.7%-females. Using the ultrasonic method, B-lines were studied, the distance between them being 3 mm and 7 mm in a semi-quantitative manner, according to the method of E. Picano in 2016. The results were statistically processedResults.In persons after the acute decompensation of the heart failure residual congestion persisted with interstitial component dominated in both lungs. Appearance of interstitial lung edema to be considered as prognostic factor of re-hospitalizations rate increasing.Conclusion.Interstitial congestion in the pulmonary parenchyma considered as a factor in the deterioration of the clinical course of heart failure sign of its acute decompensation. In this connection, it is interesting to identify interstitial pulmonary edema at the early stage to prevent real clinical presentation of acute decompensation of the heart failure.
3
Minnear, F. L., C. Kite, L. A. Hill, and H. van der Zee. "Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits." Journal of Applied Physiology 63, no. 1 (July 1, 1987): 335–41. http://dx.doi.org/10.1152/jappl.1987.63.1.335.
Full textAbstract:
The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6–10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
4
P., Praveen M., Lokesh Shanmugam, and P. Arun Prasath. "A review of role of lung ultrasound and clinical congestion score in acute left ventricular failure." International Journal of Advances in Medicine 7, no. 4 (March 21, 2020): 720. http://dx.doi.org/10.18203/2349-3933.ijam20201130.
Full textAbstract:
Congestive cardiac failure (CCF) is a worldwide phenomenon and affects millions of people years and is accompanied with high mortality. The present review is undertaken to evaluate the usefulness of Lung Ultrasound Scan in diagnosis and to identify its role as a marker of clinical outcome in patients with Acute LVF. A review of literature was done to find the role of lung ultrasound and clinical congestion score in acute left ventricular failure from search engines such as PubMed, google scholar. Major exclusion criteria were the studies that included patients with Right Ventricular Failure, renal insufficiency, other respiratory causes of breathlessness like pneumonia, pulmonary embolism, pneumothorax and pleural effusion. This review concluded that lung ultrasonography is as a rapid, non-invasive, bedside tool for the diagnosis and risk assessment of pulmonary congestion in Acute LVF.
5
Arystan, A. Z., Y. T. Khamzina, V. V. Benberin, D. V. Fettser, and Y. N. Belenkov. "Lung Ultrasound: new Opportunities for a Cardiologist." Kardiologiia 60, no. 1 (February 6, 2020): 81–92. http://dx.doi.org/10.18087/cardio.2020.1.n617.
Full textAbstract:
This review focused on ultrasound examination of lungs, a useful complement to transthoracic echocardiography (EchoCG), which is superior to chest X-ray in the diagnostic value. The lung acoustic window always remains open and allows obtaining high-quality images in most cases. For a cardiologist, the major points of the method application are determination of pleural effusion and lung congestion. This method has a number of advantages: it is time-saving; cost-effective; portable and accessible; can be used in a real-time mode; not associated with radiation; reproducible; and highly informative. The ultrasound finding of wet lungs would indicate threatening, acute cardiac decompensation long before appearance of clinical, auscultative, and radiological signs of lung congestion. Modern EchoCG should include examination of the heart and lungs as a part of a single, integrative ultrasound examination.
6
Miah, MS, M. Asaduzzaman, A. Siddika, N. Popy, MA Sufian, and MM Hossain. "Detection of Toxic Effects of Clostridial Crude Toxin in Experimental Rats." Progressive Agriculture 21, no. 1-2 (November 1, 2013): 65–72. http://dx.doi.org/10.3329/pa.v21i1-2.16753.
Full textAbstract:
The present study was conducted for the detection of toxic effects of clostridial crude toxin in experimental rats. The crude toxin of Clostridium perfringens was prepared and the rats were injected intraperitoneally (IP) 0.5 ml, 1.0 ml and 2.0 ml of crude toxin. The rats were observed for 24 hrs. The crude toxin inoculated rats showed the dose dependent clinical signs; depression, rough hair coat, respiratory distress, diarrhea and rapid heart beats, whereas PBS inoculated rats did not show any clinical sings. Necropsy changes were variable however, highly dilated and distended whole intestine with blood stained semifluid contents and gas along with congestion in all the affected rats were found dose dependently. Liver, lung and kidney were congested, hemorrhagic and swollen. More or less hydrothorax was seen during the postmortem of all affected rats. The peritoneal fat was frequently congested in all affected rats. Histopathological changes in intestine (0.5 ml inoculated rats) involved congestion, slightly swollen goblet cells and hemorrhages. The most severe lesions comprised of profuse hemorrhages in the mucosa and submucosa with complete necrosis, desquamation and intense leukocytic infiltration in 2 ml inoculated rats. Affected liver (1 ml inoculated rats) exhibited engorgement of central veins, sinusoidal spaces with blood and fatty change. The hepatocytes revealed swelling, granulation and vacuolation of cell cytoplasm, extensive hemorrhage and congestion were seen in 2 ml toxin inoculated rats. Congestion and sometimes extravasation were observed in the subepicardial region of heart. The myocardium revealed mild degenerative changes in the form of granularity of myocardial fiber. In lungs there was congestion, hemorrhage and leukocytes infiltration in the interstitial spaces around the bronchioles in both 1 and 2 ml toxin inoculated rats. Affected kidneys of different doses of crude toxin showed hemorrhage, congestion and inflammatory cells dose dependently. From the above findings, it may be concluded that clostridial crude toxin induced clinical signs, gross and histopathological lesions dose dependently in experimental rats.DOI: http://dx.doi.org/10.3329/pa.v21i1-2.16753 Progress. Agric. 21(1 & 2): 65 - 72, 2010
7
Tonu, NS, MA Sufian, S. Sarker, MM Kamal, MH Rahman, and MM Hossain. "PATHOLOGICALSTUDY ON COLIBACILLOSIS IN CHICKENS AND DETECTION OF ESCHERICHIA COLI BY PCR." Bangladesh Journal of Veterinary Medicine 9, no. 1 (July 12, 2012): 17–25. http://dx.doi.org/10.3329/bjvm.v9i1.11205.
Full textAbstract:
The aim of the present study was to detect the pathogenic Escherichia coli (E. coli) through pathological study of the colibacillosis affected birds. These isolated E. coli were further confirmed by PCR using specific primer. For this purpose, a total of 20 swabs (10 from lung and 10 from intestine of 10 dead birds) were collected in sterile nutrient broth. The histopathological samples were collected in 10% buffered neutral formalin. The used methods were histopathology, isolation and identification of E. coli by conventional methods and as well as by PCR method. A total of 10 isolates of E. coli from 20 swabs of lung and intestine was characterized by conventional routine methods of bacteriology. Gross pathological lesions of all lungs in the present investigation were congested and consolidated. Duodenum showed congestion and hemorrhages with excess mucus in the luminal surface of it. Microscopically, all the lungs showed severe congestion, infiltration of heterophils, macrophages and lymphocytes in the wall of bronchus as well as in the peribronchial alveoli. E. coli infected all the duodenum showed severe infiltration of leukocytes mainly heterophils, lymphocytes and macrophages in the submucosa of the duodenal wall. In this study, DNA of 8 isolates out of 10 isolated E. coli organisms was amplified by PCR using ECO-f and ECO-r primer targeting 16S ribosomal DNA and found 585 bp amplicon which is specific for E. coli with enteroinvasive type confirmed by histopathological lesions in duodenum. Further investigation should be focused on serotyping and detection of genes of E. coli which are responsible for pathogenicity of the organism.DOI = http://dx.doi.org/10.3329/bjvm.v9i1.11205Bangl. J. Vet. Med. (2011). 9(1): 17-25
8
Li, Hong, Yi-Dan Li, Wei-Wei Zhu, Ling-Yun Kong, Xiao-Guang Ye, Qi-Zhe Cai, Lan-Lan Sun, and Xiu-Zhang Lu. "A Simplified Ultrasound Comet Tail Grading Scoring to Assess Pulmonary Congestion in Patients with Heart Failure." BioMed Research International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/8474839.
Full textAbstract:
Ultrasound lung comets (ULCs) are a nonionizing bedside approach to assess extravascular lung water. We evaluated a protocol for grading ULC score to estimate pulmonary congestion in heart failure patients and investigated clinical and echocardiographic correlates of the ULC score. Ninety-three patients with congestive heart failure, admitted to the emergency department, underwent pulmonary ultrasound and echocardiography. A ULC score was obtained by summing the ULC scores of 7 zones of anterolateral chest scans. The results of ULC score were compared with echocardiographic results, the New York Heart Association (NYHA) functional classification, radiologic score, and N-terminal pro-b-type natriuretic peptide (NT-proBNP). Positive linear correlations were found between the 7-zone ULC score and the following: E/e′, systolic pulmonary artery pressure, severity of mitral regurgitation, left ventricular global longitudinal strain, NYHA functional classification, radiologic score, and NT-proBNP. However, there was no significant correlation between ULC score and left ventricular ejection fraction, left ventricle diameter, left ventricular volume, or left atrial volume. A multivariate analysis identified the E/e′, systolic pulmonary artery pressure, and radiologic score as the only independent variables associated with ULC score increase. The simplified 7-zone ULC score is a rapid and noninvasive method to assess lung congestion. Diastolic rather than systolic performance may be the most important determinant of the degree of lung congestion in patients with heart failure.
9
Rashid, MM, MJ Ferdoush, M. Dipti, P. Roy, MM Rahman, MI Hossain, and MM Hossain. "Bacteriological and pathological investigation of goat lungs in Mymensingh and determination of antibiotic sensitivity." Bangladesh Journal of Veterinary Medicine 11, no. 2 (June 13, 2014): 159–66. http://dx.doi.org/10.3329/bjvm.v11i2.19142.
Full textAbstract:
The foremost important goal of the present study was to investigate the bacteriological and pathological conditions in lungs of goats slaughtered in four different slaughter houses/places of Mymensingh Sadar, Mymensingh and in addition to it, antibiotic sensitivity test of commonly used antibiotics in Veterinary practices were performed on isolated bacteria. A total of 75 lungs of slaughtered goats were examined individually and out of which 20 affected lungs were collected for histopathology and bacterial isolation respectively from Mymensingh Sadar, Mymensingh in Bangladesh, during the period from January to May 2013.The lung lesions was grossly recorded 40% in goats (30 out of 75 lungs examined). Grossly, the lung lesions were categorized into (a) hemorrhages 35% (b) congestion 25% (c) hemorrhage and congestion 15% (d) emphysematous lung 15% and (e) hepatization in lung10%. In histopathology, lung lesions were categorized into (a) bronchopneumonia 30%, (b) pneumonia 25% (c) hemorrhagic pneumonia 20% (d) emphysema 15%, (e) purulent pneumonia 10%. Pasteurella sp. (15%) was isolated from the lung lesions of hemorrhagic pneumonia, E. coli. (25%) from bronchopneumonia and Staphylococcus sp. (40%) from purulent pneumonia, focal pneumonia and emphysema, and mixed infection (Staphylococcus sp. and E. coli) 20%. Finally antibiotics sensitivity test was performed on isolated bacteria to which ciprofloxacin was more powerful than others (penicillin, amoxicillin, streptomycin, nalidixic acid and kanamycin) tested and the second one was oxytetracyclin.DOI: http://dx.doi.org/10.3329/bjvm.v11i2.19142Bangl. J. Vet. Med. (2013).11(2): 159-166
10
Samkange, Alaster, Borden Mushonga, Douglas Mudimba, Bernard A. Chiwome, Mark Jago, Erick Kandiwa, Alec S. Bishi, and Umberto Molini. "African Swine Fever Outbreak at a Farm in Central Namibia." Case Reports in Veterinary Medicine 2019 (October 29, 2019): 1–6. http://dx.doi.org/10.1155/2019/3619593.
Full textAbstract:
An outbreak of African swine fever (ASF) occurred at a farm in central Namibia in March 2018. Fourteen pigs died out of a herd of 59 animals over a period of 16 days between the first and sixteenth of March 2018. The clinical signs observed included sternal recumbency, fever, weakness, pain and reluctance to move, hyperemia of the skin and anorexia, followed by death. Necropsy findings included large amounts of unclotted blood in the pleural and peritoneal cavities, diffuse carcass congestion, splenomegaly, consolidation of both lungs, hemorrhagic and frothy airways and trachea, hepatomegaly and congestion, congestion of the gastric mucosa, enlarged and congested kidneys, ecchymotic epicardial, and endocardial hemorrhages, and very enlarged and congested urinary bladder. All the remaining pigs were euthanized, burned, and buried under state veterinary supervision. The authors concluded that the outbreak resulted from indirect transmission of the ASF virus due to lapses in biosecurity measures.
11
P., Praveen M., Lokesh Shanmugam, and P. Arun Prasath. "Evaluation of lung ultrasound with clinical congestion score in diagnosis and clinical outcome of patients with acute left ventricular failure prospective study." International Journal of Advances in Medicine 7, no. 5 (April 23, 2020): 764. http://dx.doi.org/10.18203/2349-3933.ijam20201559.
Full textAbstract:
Background: Congestive cardiac failure (CCF) is often a worldwide phenomenon and usually affects millions of people years and is accompanied with high mortality. The present study is undertaken to evaluate the usefulness of Lung Ultrasound Scan in diagnosis and to identify its role as a marker of clinical outcome in patients with Acute LVF.Methods: A prospective analytical study was undertaken among the patients diagnosed as acute left ventricular failure who were admitted in tertiary care hospital. About 45 patients were enrolled by convenient sampling. The severity of acute LVF will be assessed using Clinical Congestion Score (CCS) and Lung Ultrasound Scan (LUS) based degree of congestion within 6 hours of admission, day 01 of admission and 24 hours before discharge.Results: The mean clinical congestion score was 5.36 at the time of admission. The Kerley B line at the time of admission was 15.93. The mean Kerley B line was 20.41 in the patients with clinical congestion score of more than 3.The mean Kerley B score after 24 hours of discharge was 19.69 and 5.69 during discharge among the patients with severe LV dysfunction. The mean Kerley B line score was higher at the time of admission which was statistically significant at the time of admission and within 24 hours after admission in patients with readmission.Conclusions: The mean clinical congestion scores and Kerley B lines were higher during the admission which rapidly decreased before discharge. There was a positive correlation between the Clinical congestion scores and Kerley B lines.
12
Lloyd, T. C. "Effects of lung congestion and oleic acid injury on the Hering-Breuer reflex." Journal of Applied Physiology 64, no. 2 (February 1, 1988): 832–36. http://dx.doi.org/10.1152/jappl.1988.64.2.832.
Full textAbstract:
Breathing and the Hering-Breuer (HB) reflex may be stimulated by congestion and by acute lung injury, but there is disagreement about the effects of both stimuli. This study evaluated these effects using greater stimulus isolation and control of secondary interactions than have previously been employed. Pressurization of lung vessels and left heart and oleic acid injury were individually imposed on anesthetized open-chest dogs perfused with an external pump and gas exchanger. Lungs were inflated in steps before and during those stimuli. The HB reflex was evaluated from graphs of breathing frequency (fr) vs. airway pressure. Congestion itself had no significant sustained effect on fr, but it slightly depressed the HB reflex. Oleic acid tachypnea that was depressed to pretreatment fr by inflation, implying enhancement of the HB response. Capsaicin and oleic acid had similar effects. Vagal cooling to 8 degrees C slightly depressed the effects of oleic acid and capsaicin, had no effect on the sustained fr response to congestion, and reversed the inhibitory effect of inflation. A stimulation of breathing or an enhancement of the HB reflex by congestion was not confirmed, but oleic acid increased fr and the HB reflex.
13
Le, Nguyen Phuong Khanh, Shankaramurthy Channabasappa, Mokarram Hossain, Lixin Liu, and Baljit Singh. "Leukocyte-specific protein 1 regulates neutrophil recruitment in acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 9 (November 1, 2015): L995—L1008. http://dx.doi.org/10.1152/ajplung.00068.2014.
Full textAbstract:
The mechanisms of excessive migration of activated neutrophils into inflamed lungs, credited with tissue damage, are not fully understood. We explored the hitherto unknown expression of leukocyte-specific protein 1 (LSP1) in human and mouse lungs and neutrophils and examined its role in neutrophil migration in acute lung inflammation. Autopsied septic human lungs showed increased LSP1 labeling in epithelium, endothelium, and leukocytes, including in their nuclei compared with normal lungs. We induced acute lung inflammation through intranasal administration of E. coli lipopolysaccharide (LPS) (80 μg) in LSP1-deficient ( Lsp1−/−) and wild-type (WT) 129/SvJ mice. Immunocytochemistry and Western blots showed increased expression of LSP1 and phosphorylated LSP1 in lungs of LPS-treated WT mice. Histology showed more congestion, inflammation, and Gr-1+neutrophils in lung of WT mice than Lsp1−/−mice. LPS-treated WT mice had significantly more neutrophils in bronchoalveolar lavage (BAL) and myeloperoxidase levels in lungs compared with Lsp1−/−mice. However, there were no differences in lung tissue and BAL concentrations of keratinocyte-derived chemokine, monocyte chemoattractant protein-1, macrophage inflammatory protein-1α and -1β, vascular permeability, and phosphorylated p38 MAPK between LPS-treated WT and Lsp1−/−mice, whereas TNF-α concentration was higher in BAL fluid from LPS-treated WT. Immunoelectron microscopy showed increased LSP1 in the nuclei of LPS-treated neutrophils. We also found increased levels of phosphorylated LSP1 associated with plasma membrane, nucleus, and cytosol at various times after LPS treatment of murine bone marrow-derived neutrophils, suggesting its role in modulation of neutrophil cytoskeleton and the membrane. These data collectively show increased expression of LSP1 in inflamed mouse and human lungs and its role in neutrophil recruitment and lung inflammation.
14
Senturk, Aysegul, Aysegul Karalezli, Ayse Nur Soyturk, and H. Canan Hasanoglu. "A Rare Cause of Crazy-Paving and Mediastinal Lymphadenopathy: Congestive Heart Failure." Journal of Clinical Imaging Science 3 (July 29, 2013): 30. http://dx.doi.org/10.4103/2156-7514.115762.
Full textAbstract:
Crazy-paving sign is a pattern seen on multislice computed tomography images of the lungs. It is characterized by a reticular pattern superimposed on ground-glass opacity. It was first described in the late 1980s in patients with pulmonary alveolar proteinosis, but has now been described in some other diseases of the lung. Enlarged mediastinal lymph nodes can be seen in infectious and specific inflammatory diseases and malignancies. The present report describes a case of a 44-year-old man in whom congestive heart failure presented with a crazy-paving appearance and enlarged lymph nodes of the lungs on the chest computed tomography scan.
15
Hsia, C. C. W., E. Y. Wu, E. Wagner, and E. R. Weibel. "Preventing mediastinal shift after pneumonectomy impairs regenerative alveolar tissue growth." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 5 (November 1, 2001): L1279—L1287. http://dx.doi.org/10.1152/ajplung.2001.281.5.l1279.
Full textAbstract:
To examine the effects of mechanical lung strain on regenerative growth of alveolar septal tissue after pneumonectomy (PNX), we replaced the right lungs of adult dogs with a custom-shaped inflatable silicone prosthesis. The prosthesis was either inflated (Inf) to maintain the mediastinum at the midline or deflated to allow mediastinal shift. The animals were euthanized ∼15 mo later, and the lungs were fixed at a constant distending pressure. With the Inf prostheses, lung expansion, alveolar septal tissue volumes, surface areas, and diffusing capacity of the tissue-plasma barrier were significantly lower than with the deflated prostheses; the expected post-PNX tissue responses were impaired by 30–60%. Capillary blood volume was significantly higher with Inf prostheses, consistent with microvascular congestion. Measurements in the Inf group remained consistently and significantly higher than those expected for a normal left lung, indicating persistence of partial compensation. In one dog, delayed deflation of the prosthesis 9–10 mo after PNX led to vigorous lung expansion and septal tissue growth, particularly of type II epithelial cells. We conclude that mechanical lung strain is a major signal for regenerative lung growth; however, other signals are also implicated, accounting for a significant fraction of the compensatory response to PNX.
16
Khan, MR, MG Haider, KJ Alam, MG Hossain, SMZH Chowdhury, and MM Hossain. "PATHOLOGICAL INVESTIGATION OF PESTE DES PETITS RUMINANTS (PPR) IN GOATS." Bangladesh Journal of Veterinary Medicine 3, no. 2 (July 23, 2012): 134–38. http://dx.doi.org/10.3329/bjvm.v3i2.11380.
Full textAbstract:
In pathological investigation of peste des petits ruminants (PPR), a total of 11 Black Bengal goats of both sexes about 6-12 months old were included. Six goats out of 11 were suspected to be of natural infection with PPR and 5 goats used for experimentation. Four experimental goats out of 5 were inoculated with PPR virus isolated from natural outbreak and one was used as uninoculated control. The diagnosis of PPR virus infection both in natural outbreak and experimental cases were based on clinical signs, gross pathology, histopathology and ELISA test for confirmation of the PPR virus. Clinical signs included anorexia, depression, fever (106 ± 1°F), oculonasal discharges, diarrhoea with soiled hind quarter, sunken eyes, coughing, respiratory distress and prostration and/or death in natural cases. In experimental infection the goats showed the 5 phases of PPR virus infection cycle which included varying incubation period, prodromal phase, pneumonic phase, diarrhoeic phase and prostration and/or death. Average duration of incubation period was 4 days, prodromal phase 3 days, the pneumonic phase and diarrhoeic phase started at day 5 and 7 of inoculation, respectively and continued till death. Necropsy of both natural and experimental goats revealed stomatitis, congested and/or consolidated pneumonic lungs, generalized enlargement of lymphnodes accompanied with necrosis and congestion of some lymphnodes, atrophied congested spleen and haemorrhagic gastroenteritis. Congestion of the urinary bladder, uterus and vagina in experimental goats and intestinal intussusception in dead goats of natural infection were also found. Histopathological study of both natural and experimental cases revealed congestion and edema of lungs in some cases but in other cases there were network of fibrin infiltrated with neutrophils, formation of syncytia, gaint cell and presence of pink color bacterial colony. There was infiltration of neutrophils and mononuclear cells within the alveoli, bronchioles, alveolar wall and interstitium of lungs. Lymphoid organs showed necrosis and depletion of lymphoid cell; congestion, morionuclear and neutrophilic infiltration in the lamina propria and submucosa of the abomasum, intestine, uterus and urinary bladder; loss of intestinal villi; congestion of cortical blood vessels and glomeruli of kidneys were recorded. Samples of both natural and experimental cases were confirmed as PPR by ELISA test. In this investigation, it was observed that clinical signs, gross and microscopic findings were more severe in experimental PPR infected cases than that of natural cases.
17
Atthapaisalsarudee, Suree, Pantpis Sakornpant, Supreecha Tanamai, Surapoj Saengchote, Vichao Kojaranjit, Pattanasak Lertpradit, Sant Chaiyodsilp, and Wiwat Warinsirikul. "Medium-Term Result of Domino Heart-Lung Transplantation." Asian Cardiovascular and Thoracic Annals 5, no. 4 (December 1997): 241–43. http://dx.doi.org/10.1177/021849239700500413.
Full textAbstract:
We report the medium-term result of the first domino heart-lung transplantation successfully performed in South East Asia. In January 1990, a 45-year-old female who was in severe respiratory distress and required continuous oxygen therapy for end-stage pulmonary fibrosis received the heart and lungs from a 21-year-old male with brain death due to head injury. The recipient's heart was transplanted to a 31-year-old male who was in severe congestive cardiac failure from cardiomyopathy. The heart-lung donor had blood group O and the other patients had blood group A. Both recipients are in good health 7 years after the surgery.
18
Moeller, Robert B., Beate Crossley, Arlena Pipkin, Yanqiu Li, and Udeni B. R. Balasuriya. "Systemic equid alphaherpesvirus 9 in a Grant’s zebra." Journal of Veterinary Diagnostic Investigation 30, no. 4 (April 12, 2018): 580–83. http://dx.doi.org/10.1177/1040638718767722.
Full textAbstract:
A 2-y-old female Grant’s zebra ( Equus quagga [ burchellii] boehmi) was presented with a clinical history of depression, anorexia, and weakness of 1-wk duration. Postmortem examination identified ulcers on the tongue and palate; a large abscess adjacent to the larynx; left lung consolidation; mild swelling, darkening, and congestion of the liver with accentuation of the lobular pattern; and edema and congestion of the distal small and large intestines. Histologic examination identified necrotizing bronchopneumonia, necrotizing hepatitis, nephritis, and enterocolitis. Eosinophilic intranuclear inclusions were detected in syncytial cells and degenerate bronchial epithelium in the lungs and in some hepatocytes associated with necrotic foci. Bacterial cultures of the lung, liver, and laryngeal abscess failed to detect any significant pathogen. Lung and liver tested positive for equine herpesvirus with neuropathogenic marker by real-time PCR. Subsequently, equine herpesvirus was isolated in tissue culture, and the entire viral DNA polymerase gene (ORF30) was sequenced. The zebra lung isolate had a very close nucleotide and amino acid sequence identity to equid alphaherpesvirus 9 (EHV-9; 99.6% and 99.8%, respectively) in contrast to the neuropathogenic T953 strain of EHV-1 (94.7% and 96.6%, respectively). Although zebras are considered the natural host for EHV-9, we document an unusual acute systemic, fatal EHV-9 infection in a 2-y-old Grant’s zebra.
19
Yang, Fan, Lu Deng, MuHu Chen, Ying Liu, and Jianpeng Zheng. "6-Gingerol Ameliorates Sepsis Induced Acute Lung Injury by Regulating Nuclear Factor-κB and Nuclear-Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Signaling Pathways." Current Topics in Nutraceutical Research 19, no. 3 (November 19, 2020): 255–60. http://dx.doi.org/10.37290/ctnr2641-452x.19:255-260.
Full textAbstract:
Acute lung injury initiated systemic inflammation leads to sepsis. Septic mice show a series of degenerative changes in lungs as demonstrated by pulmonary congestion, alveolar collapse, inflammatory cell infiltration, and increased wet-todry weight in lungs. 6-Gingerol ameliorates histopathological changes and clinical outcome of the sepsis. The increase in the levels of tumor necrosis factor-α, interleukin-1 beta, interleukin-6, and interleukin-18 in septic mice were reduced by administration with 6-Gingerol. Also, 6-Gingerol attenuates sepsis-induced increase of malonaldehyde and decrease of catalase, superoxide, and glutathione. Enhanced phospho-p65, reduced nuclear factor erythropoietin-2-related factor 2, and heme oxygenase 1 in septic mice were reversed by administration with 6-Gingerol. In conclusion, 6-Gingerol demonstrates anti-inflammatory and antioxidant effects against sepsis associated acute lung injury through inactivation of nuclear factor-kappa B and activation of nuclear-factor erythroid 2-related factor 2 pathways.
20
Szidon, J. Peter. "Pathophysiology of the Congested Lung." Cardiology Clinics 7, no. 1 (February 1989): 39–48. http://dx.doi.org/10.1016/s0733-8651(18)30455-7.
Full text
21
Cottrill, Carol M., William N. O'Connor, Robert Fitz, and Mark N. Gillespie. "Pulmonary vascular remodeling in rats with unilaterally banded lobar pulmonary veins." Cardiology in the Young 2, no. 2 (April 1992): 121–28. http://dx.doi.org/10.1017/s1047951100000731.
Full textAbstract:
AbstractAlthough pulmonary vascular disease occurs in association with pulmonary venous obstruction, a model of pulmonary vascular lesions in this setting in small laboratory animals has yet to be described. The objective of this study was to determine if unilateral banding of pulmonary veins in the rat would produce pulmonary vascular disease that mimicked key aspects of the human disorder. Rats were anesthetized and, after mechanical ventilation and thoracotomy, one of the four pulmonary veins was banded to reduce its external diameter by approximately 65–75% to 0.8 mm. Additional animals, sham-operated controls, were treated identically except for venous banding. Mortality did not differ between groups and was less than 20%. Eight weeks after surgical preparation, moderate pulmonary hypertension was demonstrated with a mean pressure in the pulmonary artery of 24.9 mm Hg (range 19.25 – 30.0) in the banded group versus 18.7 mm Hg (range 16.6 – 19.3) for sham-operated animals. Pulmonary cineangiography in rats with banded pulmonary veins demonstrated marked pulmonary congestion and a prolonged residence time of contrast medium in the capillary circulation of the lung region subjected to banding. Angiographically, non-banded lungs were similar to shams. Histopathology of the vein-banded region revealed venous congestion, arterialization of veins, perivenular edema, and sparse to moderate inflammation. Prominent bronchial vessels, pulmonary arterial medial and occasional intimal thickening, and periarterial inflammation were also observed in banded regions. Similar inflammation around pulmonary arterial and pulmonary venous vessels was noted in contralateral lung lobes but not in sham-operated control rats. Morphometric evaluation of all muscular pulmonary arteries from 50–200μ external diameter accompanying airways to the level of terminal and respiratory bronchioles indicated that the medial area in lung regions subjected to venous banding was over three times greater than in shams. Pulmonary arteries from the contralateral, unbanded lungs of treated animals also exhibited a two-fold increase in medial area. These findings indicate that a modest degree of pulmonary venous banding in rats produces congestion and causes alterations in lung vessels which are reminiscent of those observed in humans with pulmonary venous outflow obstruction. Such a model in a cost-effective laboratory animal should be useful for delineating the specific mechanisms underlying these alterations.
22
Uzal, Francisco A., Birgit Puschner, John M. Tahara, and Robert W. Nordhausen. "Gossypol Toxicosis in a Dog Consequent to Ingestion of Cottonseed Bedding." Journal of Veterinary Diagnostic Investigation 17, no. 6 (November 2005): 626–29. http://dx.doi.org/10.1177/104063870501700622.
Full textAbstract:
Six dogs died after accidental ingestion of cottonseed bedding. No clinical signs of illness were observed prior to death. A full diagnostic workup was performed on one of these dogs. At necropsy, the lungs were congested and edematous, and the liver was firm, congested, and had a marked reticular pattern. There was also moderate ascites. Histopathologic examination revealed multifocal myocardial degeneration and necrosis, severe pulmonary edema, and chronic passive congestion of the lungs, heart, liver, and kidneys. Transmission electron microscopy of the myocardium revealed disruption of myofibrils, chromatin condensation, and disrupted and swollen mitochondria. The cottonseed bedding contained 1,600 mg/kg of free gossypol, a concentration considered toxic for monogastric animals. The stomach content revealed the presence of gossypol, thus confirming ingestion of cottonseed. Gossypol poisoning in dogs is extremely rare and has not yet been associated with cottonseed bedding. This first documented case of gossypol poisoning in a dog, caused by the ingestion of cottonseed bedding, demonstrates how specific toxicological analysis is crucial in reaching an accurate diagnosis.
23
Kanchana, Madurai Padmanabhan, Muthu Prabha Sellamuthu, and Revathy Mahendran. "A rare case report of congenital high airway obstruction syndrome presenting in a 23 weeks foetus." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 3 (February 27, 2018): 1277. http://dx.doi.org/10.18203/2320-1770.ijrcog20180938.
Full textAbstract:
Congenital High Airway Obstruction Syndrome or CHAOS is a blockage of the foetus’s trachea or larynx due to many factors including narrowing of the airway, a web-like membrane or even tracheal atresia. In the uterus, the foetal lungs constantly produce fluid and as a result of this airway blockage in the trachea, the lung fluid cannot escape out of the foetal mouth. Because of this the foetus’s lungs become distended with fluid and over distended lungs can put pressure on the heart and affect the heart’s ability to function. If the heart cannot function effectively hydrops or congestive heart failure can occur. We present a rare case of CHAOS diagnosed prenatally at about 23 weeks by USG in our hospital.
24
Doerschuk, C. M., and H. S. Sekhon. "Pulmonary blood volume and edema in postpneumonectomy lung growth in rats." Journal of Applied Physiology 69, no. 3 (September 1, 1990): 1178–82. http://dx.doi.org/10.1152/jappl.1990.69.3.1178.
Full textAbstract:
After pneumonectomy in young animals, the contralateral lung undergoes compensatory growth and generally attains the same weight and air space volume as both lungs in age-matched controls. In this study, we determined the contribution of lung edema and increased blood volume to the weight gain in rats. Three weeks after pneumonectomy (n = 18) or sham pneumonectomy (n = 17), the pulmonary blood volume and the extravascular water and albumin were evaluated by use of 51Cr-labeled erythrocytes and 125I-labeled albumin. The air space volume, blood-free lung weights, and DNA and protein content were also compared. The data show that the total pulmonary blood volumes and the blood volume per gram of blood-free dry lung were similar in pneumonectomized and age-matched sham controls. The total extravascular albumin and the extravascular albumin per gram of blood-free dry lung were also similar as well as the extravascular lung water, wet-to-dry weight ratios, DNA and protein content, and air space volumes. These data indicate that the increased weight of the postpneumonectomy lung was due to cellular and stromal proliferation. The blood volume and interstitial fluid increased in proportion to the increase in lung parenchyma. Neither vascular congestion nor increased extravascular protein and water contributed to the observed weight gain.
25
AL-Samarrae, Ekram A. A. "Evaluation of transfer factor protective efficacy against Tuberculosis in Guinea Pigs." Iraqi Journal of Veterinary Medicine 29, no. 2 (December 31, 2005): 112–21. http://dx.doi.org/10.30539/iraqijvm.v29i2.857.
Full textAbstract:
Transfer factor has been prepared from sensitized guinea pigs against heatkilled Mycobacterium bovis antigen and protective efficacy were evaluated inguinea pigs that gave 1 ml of transfer factor equivalent 5x108 cell / ml of sensitizedand normal cell donor; then challenged with dose 0.01 mg / animal of virulentMycobacterium bovis, After 40 days of challenge all animals were sacrificied.Histologically: - TFs recipient group showed a mono-nuclear cellsinfiltration’s (Lymphocytes & Macrophages) with a mild emphysema of lungs, andliver showed mononuclear cells ,a small necrotic foci in the lymphocytic organs(spleen & lymph nodes); the kidney showed mononuclear cells in glomeruli andurinary tubules ;While the TFn recipient group were an areas of caseated necroticmaterials surrounded by macrophages &Lymphocytes, congestion of internalorgans (Liver and Spleen) and Sever congestion with hemorrhage of alveoli tissue,sever emphysema & consolidation in lung kidney showed tuberculle foci inglomeruli and around urinary tubules .There were no pathgenomic changes in heart muscles of TFs recipient group whilea mild congestion in TFn recipient group.
26
Sarhan, Osama M., Antrix Jain, Hamed M. A. Mutwally, Gamal H. Osman, Sung Yun Jung, Tawfik Issa, and Mohamed Elmogy. "Impact Effect of Methyl Tertiary-Butyl Ether “Twelve Months Vapor Inhalation Study in Rats”." Biology 9, no. 1 (December 20, 2019): 2. http://dx.doi.org/10.3390/biology9010002.
Full textAbstract:
We investigated the early risk of developing cancer by inhalation of low doses (60 µL/day) of methyl tertiary butyl ether (MTBE) vapors using protein SDS-PAGE and LC-MS/MS analysis of rat sera. Furthermore, histological alterations were assessed in the trachea and lungs of 60 adult male Wistar rats. SDS-PAGE of blood sera showed three protein bands corresponding to 29, 28, and 21 kDa. Mass spectroscopy was used to identify these three bands. The upper and middle protein bands showed homology to carbonic anhydrase 2 (CA II), whereas the lower protein band showed homology with peroxiredoxin 2. We found that exposure to MTBE resulted in histopathological alterations in the trachea and the lungs. The histological anomalies of trachea and lung showed that the lumen of trachea, bronchi, and air alveoli packed with free and necrotic epithelial cells (epithelialization). The tracheal lamina propria of lung demonstrated aggregation of lymphoid cells, lymphoid hyperplasia, hemorrhage, adenomas, fibroid degeneration, steatosis, foam cells, severe inflammatory cells with monocytic infiltration, edema, hemorrhage. Occluded, congested, and hypertrophied lung arteries in addition, degenerated thyroid follicles, were observed. The hyaline cartilage displayed degeneration, deformation, and abnormal protrusion. In conclusion, our results suggest that inhalation of very low concentrations of the gasoline additive MTBE could induce an increase in protein levels and resulted in histopathological alterations of the trachea and the lungs.
27
Shafi, Majid, Shayaib A. Kamil, Masood S. Mir, S. Adil, Showkat A. Shah, and Mir Manzoor. "In vivo evaluation of ziram induced acute toxicity on pathomorphology of broiler chicken." Journal of Applied and Natural Science 8, no. 4 (December 1, 2016): 2206–11. http://dx.doi.org/10.31018/jans.v8i4.1113.
Full textAbstract:
Fungicides are usually used in agriculture and often find their way in poultry feed. Therefore, a study was undertaken to study the in vivo effect of one such fungicide (ziram) induced intoxication on pathomorphology of broiler chicken. After 2 weeks of age the birds were given fungicide (Ziram) in feed as a single oral dose of 100 mg/kg body weight. Out of 10 birds, 3 died due to ziram intoxication (30% mortality rate). Birds that died rapidly showed pronounced neurological signs like convulsions. The carcasses of ziram intoxicated birds appeared dehydrated and their mucous membrane was pale in colour. Marked vascular congestion was observed in brain on gross examination. The livers showed congestion and haemorrhages with necrotic foci. Kidneys and lungs had ecchymotic haemorrhages and heart revealed gelatinization of pericardium, distention and pericarditis. Atrophy of bursa of Fabricius and thymus; hypertrophy of thyroid was found. Histopathological examination revealed neuronal degeneration and necrosis associated with mild gliosis in brain. Lungs, pericardium and epicardium had severe congestion and there was degeneration with separation of myofibers. Glomeruli were congested and frequently revealed hypercellularity. There were sinusoidal congestion and varying degrees of hepatocellular degeneration. Bursa revealed mild depletion of lymphoid cells in few lobules while as thymus showed hypoplasia with depletion of lymphocytes. Thyroid had mild mononuclear cell infiltration and caecum showed marked necrosis and denudation of the mucosa. In conclusion, the depletion of lymphoid tissue from lymphoid organs was suggestive of immunosuppressive and immunomodulatory effects of ziram toxicity in broiler chicken.
28
Souza, Mariana C., Tatiana A. Padua, and Maria G. Henriques. "Endothelial-Leukocyte Interaction in Severe Malaria: Beyond the Brain." Mediators of Inflammation 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/168937.
Full textAbstract:
Malaria is the most important parasitic disease worldwide, accounting for 1 million deaths each year. Severe malaria is a systemic illness characterized by dysfunction of brain tissue and of one or more peripheral organs as lungs and kidney. The most severe and most studied form of malaria is associated with cerebral complications due to capillary congestion and the adhesion of infected erythrocytes, platelets, and leukocytes to brain vasculature. Thus, leukocyte rolling and adhesion in the brain vascular bed during severe malaria is singular and distinct from other models of inflammation. The leukocyte/endothelium interaction and neutrophil accumulation are also observed in the lungs. However, lung interactions differ from brain interactions, likely due to differences in the blood-brain barrier and blood-air barrier tight junction composition of the brain and lung endothelium. Here, we review the importance of endothelial dysfunction and the mechanism of leukocyte/endothelium interaction during severe malaria. Furthermore, we hypothesize a possible use of adjunctive therapies to antimalarial drugs that target the interaction between the leukocytes and the endothelium.
29
Rahman, T., S. Khalequezzaman, S. Ahsan, J. Alam, and MK Sarker. "A case report of congenital high airway obstruction syndrome (CHAOS) caused by complete laryngeal obstruction." Pulse 7, no. 1 (May 7, 2015): 38–41. http://dx.doi.org/10.3329/pulse.v7i1.23248.
Full textAbstract:
CHAOS or Congenital High Airway Obstruction Syndrome is a blockage of the fetuss trachea or larynx due to a number of factors including narrowing of the airway, a web-like membrane or even tracheal atresia. In the uterus, the fetal lungs constantly produce fluid and as a result of this airway blockage in the trachea, the lung fluid cannot escape out of the fetal mouth. Because of this the fetuss lungs become distended with fluid and over distended lungs can put pressure on the heart and affect the hearts ability to function. If the heart cannot beat effectively hydrops or congestive heart failure can occur. We present a case of CHAOS with hydrops and associated anomalies, determined prenatally at about 21 weeks by MRI in our hospital.Pulse Vol.7 January-December 2014 p.38-41
30
Khaleel, Hadeel Kamil. "Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine." Baghdad Science Journal 16, no. 3(Suppl.) (September 22, 2019): 0719. http://dx.doi.org/10.21123/bsj.2019.16.3(suppl.).0719.
Full textAbstract:
The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.
31
Lagishetty, Venu, Prasanna Tamarapu Parthasarathy, Oluwakemi Phillips, Jutaro Fukumoto, Young Cho, Itsuko Fukumoto, Huynh Bao, et al. "Dysregulation of CLOCK gene expression in hyperoxia-induced lung injury." American Journal of Physiology-Cell Physiology 306, no. 11 (June 1, 2014): C999—C1007. http://dx.doi.org/10.1152/ajpcell.00064.2013.
Full textAbstract:
Hyperoxic acute lung injury (HALI) is characterized by inflammation and epithelial cell death. CLOCK genes are master regulators of circadian rhythm also implicated in inflammation and lung diseases. However, the relationship of CLOCK genes in hyperoxia-induced lung injury has not been studied. This study will determine if HALI alters CLOCK gene expression. To test this, wild-type and NALP3−/− mice were exposed to room air or hyperoxia for 24, 48, or 72 h. In addition, mice were exposed to different concentrations of hyperoxia (50, 75, or 100% O2) or room air for 72 h. The mRNA and protein levels of lung CLOCK genes, based on quantitative PCR and Western blot analysis, respectively, and their target genes are significantly elevated in mice exposed to hyperoxia compared with controls. Alterations in CLOCK genes are associated with increased inflammatory markers in bronchoalveolar lavage fluid of hyperoxic mice compared with controls. Histological examination of mice lungs exposed to hyperoxia show increased inflammation and alveolar congestion compared with controls. Our results indicate sequential increase in CLOCK gene expression in lungs of mice exposed to hyperoxia compared with controls. Additionally, data suggest a dose-dependent increase in CLOCK gene expression with increased oxygen concentrations. To validate if the expression changes related to CLOCK genes are indeed associated with inflammation, NALP3−/− was introduced to analyze loss of function in inflammation. Western blot analysis showed significant CLOCK gene downregulation in NALP3−/− mice compared with wild-type controls. Together, our results demonstrate that hyperoxia-mediated lung inflammation is associated with alterations in CLOCK gene expression.
32
Edwards, Suzanne, J. David Small, Joachim Dieter Geratz, Lorraine K. Alexander, and Ralph S. Baric. "An Experimental Model for Myocarditis and Congestive Heart Failure after Rabbit Coronavirus Infection." Journal of Infectious Diseases 165, no. 1 (January 1, 1992): 134–40. http://dx.doi.org/10.1093/infdis/165.1.134.
Full textAbstract:
Abstract In a model for virus-induced myocarditis and congestive heart failure, rabbit coronavirus infection was divided into acute (days 2–5) and subacute (days 6–12) phases on the basis of day of death and pathologic findings. During the acute phase, the principal histologic lesions were degeneration and necrosis of myocytes, myocytolysis, interstitial edema, and hemorrhage. The severity of these changes increased in the subacute phase. Pleural effusion and congestion of the lungs and liver were also present at this time. Myocarditis was detected by day 9 and peaked by day 12. Heart weights and heart weight-to-body weight ratios were increased, and dilation of the right ventricular cavity became prominent early in infection and persisted. In contrast, dilation of the left ventricle occurred late in the subacute stage. Virus was isolated from infected hearts between days 2 and 12. These data suggest that rabbit coronavirus infection progresses to myocarditis and congestive heart failure.
33
Pritchard, Kirkwood A., Jingsong Ou, Zhijun Ou, Yang Shi, James P. Franciosi, Paul Signorino, Sushma Kaul, et al. "Hypoxia-induced acute lung injury in murine models of sickle cell disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 4 (April 2004): L705—L714. http://dx.doi.org/10.1152/ajplung.00288.2002.
Full textAbstract:
Vaso-occlusive events are the major source of morbidity and mortality in sickle cell disease (SCD); however, the pathogenic mechanisms driving these events remain unclear. Using hypoxia to induce pulmonary injury, we investigated mechanisms by which sickle hemoglobin increases susceptibility to lung injury in a murine model of SCD, where mice either exclusively express the human α/sickle β-globin (hαβS) transgene (SCD mice) or are heterozygous for the normal murine β-globin gene and express the hαβStransgene (mβ+/-, hαβS+/-; heterozygote SCD mice). Under normoxia, lungs from the SCD mice contained higher levels of xanthine oxidase (XO), nitrotyrosine, and cGMP than controls (C57BL/6 mice). Hypoxia increased XO and nitrotyrosine and decreased cGMP content in the lungs of all mice. After hypoxia, vascular congestion was increased in lungs with a greater content of XO and nitrotyrosine. Under normoxia, the association of heat shock protein 90 (HSP90) with endothelial nitric oxide synthase (eNOS) in lungs of SCD and heterozygote SCD mice was decreased compared with the levels of association in lungs of controls. Hypoxia further decreased association of HSP90 with eNOS in lungs of SCD and heterozygote SCD mice, but not in the control lungs. Pretreatment of rat pulmonary microvascular endothelial cells in vitro with xanthine/XO decreased A-23187-stimulated nitrite + nitrate production and HSP90 interactions with eNOS. These data support the hypotheses that hypoxia increases XO release from ischemic tissues and that the local increase in XO-induced oxidative stress can then inhibit HSP90 interactions with eNOS, decreasing ·NO generation and predisposing the lung to vaso-occlusion.
34
da Luz, Sônia Cristina Almeida, Melissa Falster Daubermann, Gustavo Roberto Thomé, Matheus Mülling dos Santos, Angelica Ramos, Gerson Torres Salazar, João Batista Teixeira da Rocha, and Nilda Vargas Barbosa. "Diphenyl Ditelluride Intoxication Triggers Histological Changes in Liver, Kidney, and Lung of Mice." Analytical Cellular Pathology 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/784612.
Full textAbstract:
Tellurium compounds may be cytotoxic to different cells types. Thus, this work evaluated the effect of diphenyl ditelluride ((PhTe)2), an organotellurium commonly used in organic synthesis, on the morphology of liver, kidney, and lung. Adult mice were acutely (a subcutaneous single dose: 250 μmol/kg) or subchronically (one daily subcutaneous dose: 10 or 50 μmol/kg for 7 and 14 days) exposed to (PhTe)2. Afterwards, the histological analyses of liver, kidney, and lungs were performed. Liver histology revealed that the hepatocytes of mice subchronically exposed to (PhTe)2presented cytoplasmic vacuolization, hydropic degeneration, and hyperchromatic nuclei. Subchronic exposure to 50 μmol/kg (PhTe)2also caused hepatic necrosis. Microvesicular and macrovesicular steatosis were identified in liver of mice acutely exposed to (PhTe)2. Acute and subchronic intoxication with (PhTe)2induced changes on epithelial cells of renal tubules, namely, loss of brush border and cytoplasmatic vacuolization. Atrophy and hypertrophy, cast proteinaceous formation, and acute tubular necrosis were also identified in renal tissue. Mice subchronically exposed to 50 μmol/kg (PhTe)2developed intra-alveolar edema and alveolar wall congestion in some areas of lungs. Acute exposure to (PhTe)2did not cause histological changes in lungs. Our data show that (PhTe)2may be considered a histotoxic agent for liver, kidney, and lung.
35
Patel, Chandni B., Komal Patel, Vasudha M. Bhagat, and Pinkal Shah. "Pattern of histopathological lesions in lung autopsy." International Journal of Research in Medical Sciences 6, no. 1 (December 23, 2017): 279. http://dx.doi.org/10.18203/2320-6012.ijrms20175734.
Full textAbstract:
Background: A large number of pathologic conditions involve the lung parenchyma like inflammatory, neoplastic and others. The lungs are also involved in almost all terminal events of cardiovascular disease. Autopsy is an important and most useful way to find out the condition of internal organs and to evaluate any localized lesions or systemic disease and hence determine cause of death. Aims and objectives of study are to identify the histopathological spectrum of lung disease. To find out frequency of various lung pathologies in respect to age and sex.Methods: This study was retrospective and done on 649 cases of medico legal autopsies. The tissue specimens were fixed and processed. Routine paraffin sectioning was done followed by Hematoxylene and eosin (H and E) staining. Special stains were done whenever required. Relevant clinical and postmortem findings, gross and microscopic examination findings were recorded.Results: After thorough histopathological examinations, of total 649 cases, various pulmonary lesions were identified in 348(53.6%) cases while in 301(46.4%) cases no significant pathology was seen. Most commonly affected age group was 30-49 years 43.1% followed by age group of >60years 17.8%. Majority of diseased were male 285 (81.9%). Most common lung pathology found was Edema and congestion in 93 cases (26.72%), chronic venous congestion in 92 cases (26.44%) pneumonia in 65 cases (18.68%) followed by Tuberculosis/Tuberculous pneumonia in 29 cases (8.3%).Conclusions: In our population, the present study reveals that infectious disease are still the most common cause of mortality, despite recent advances in diagnostic technology, the autopsy has remained an important complementary tool for identifying and understanding pathology of disease.
36
Enia, Giuseppe, Rocco Tripepi, Vincenzo Panuccio, Claudia Torino, Maurizio Garozzo, Giovanni Giorgio Battaglia, and Carmine Zoccali. "Pulmonary Congestion and Physical Functioning in Peritoneal Dialysis Patients." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 32, no. 5 (September 2012): 531–36. http://dx.doi.org/10.3747/pdi.2010.00250.
Full textAbstract:
Purpose Decline in physical function is commonly observed in patients with kidney failure on dialysis. Whether lung congestion, a predictable consequence of cardiomyopathy and fluid overload, may contribute to the low physical functioning of these patients has not been investigated. Methods In 51 peritoneal dialysis (PD) patients, we investigated the cross-sectional association between the physical functioning scale of the Kidney Disease Quality of Life Short Form (KDQOL-SF: Rand Corporation, Santa Monica, CA, USA) and an ultrasonographic measure of lung water recently validated in dialysis patients. The relationship between physical functioning and lung water was also analyzed taking into account the severity of dyspnea measured using the New York Heart Association (NYHA) classification currently used to grade the severity of heart failure. Results Evidence of moderate-to-severe lung congestion was evident in 20 patients, and this alteration was asymptomatic (that is, NHYHA class I) in 11 patients (55%). On univariate analysis, physical functioning was inversely associated with lung water ( r = –0.48, p < 0.001), age ( r = –0.44, p = 0.001), previous cardiovascular events ( r = –0.46, p = 0.001), and fibrinogen ( r = –0.34, p = 0.02). Physical functioning was directly associated with blood pressure, the strongest association being with diastolic blood pressure ( r = 0.38, p = 0.006). The NYHA class correlated inversely with physical functioning ( r = –0.51, p < 0.001). In multiple regression analysis, only lung water and fibrinogen remained independent correlates of physical functioning. The NYHA class failed to maintain its independent association. Conclusions This cross-sectional study supports the hypothesis that symptomatic and asymptomatic lung congestion is a relevant factor in the poor physical functioning of patients on PD.
37
Adili, Ayinuerguli, Adilijiang Kari, Chuanlong Song, and Abulaiti Abuduhaer. "Chelidonine Attenuates Sepsis-Induced Acute Lung Injury via Suppressing Toll-like Receptor 4/Myeloid Differentiation Factor 88/Nuclear Factor-॔B Signaling Pathway in Newborn Mice." Current Topics in Nutraceutical Research 19, no. 1 (July 30, 2020): 120–26. http://dx.doi.org/10.37290/ctnr2641-452x.19:120-126.
Full textAbstract:
We have examined the mechanism underlying amelioration of sepsis-induced acute lung injury by chelidonine in newborn mice. To this end, a sepsis model was established using cecal ligation and puncture in newborn mice. The sepsis-induced acute lung injury was associated with an increased inflammatory infiltration and pulmonary congestion, as well as abnormal alveolar morphology. The lung injury-associated increased tumor necrosis factor-α and interleukin-1β in bronchoalveolar lavage fluid and lung, the markers of inflammatory infiltration and pulmonary congestion, diminished by chelidonine treatment. Chelidonine administration also downregulated protein levels of toll-like receptor 4, myeloid differentiation factor 88, phosphorylated nuclear factor-kappa B, and nuclear factor-kappa B that are elevated in response to sepsis. In conclusion, chelidonine provides a potential therapeutic strategy for newborn mice with acute lung injury.
38
Rahman, MM, J. Alam, MM Rahman, MAHNA Khan, and MG Haider. "Pathology of Pullorum Disease and Molecular Characterization of Its Pthogen." Annals of Bangladesh Agriculture 23, no. 1 (June 15, 2020): 25–35. http://dx.doi.org/10.3329/aba.v23i1.51471.
Full textAbstract:
This experiment was conducted to determine the pathology of pullorum disease of chickens and molecular identification of its pathogen. A total of 108 samples, including swabs from different organs were collected from different commercial layer farms of Gazipur district. The histopathological samples were collected in 10% formalin and the swabs were collected in tetrathionate broth. Samples were subjected to isolation and identification of the causal agent followed by gross and histopathological study of the affected visceral organs. Fifty eight out of 108 cloacal swabs (53.7%) were Salmonella positive. The percentage of Salmonella positive in liver swabs, spleen swabs, lung swabs and intestinal swabs from dead birds were 55.88%, 32.35%, 35.29% and 47.05%, respectively. On average, 52.94% livers of Salmonella affected birds were enlarged, congested and hemorrhagic and necrotic foci was present in 32.35% liver. Unabsorbed and coagulated yolk was found in 70.58% cases. From these 38.24% spleens were swollen and congested and 44.12 % kidneys were enlarged. At histopathology, 52.94% livers showed congestion, focal necrosis with multifocal infiltration of histiocytes in liver parenchyma. Focal necrosis and inflammatory cells were found in 70.58% spleen. Infiltration of heterophils in intestinal mucosa was found in 47.05% cases. 20.58% (7 out of 34) samples were PCR positive for Salmonella Pullorum organism.
Ann. Bangladesh Agric. (2019) 23(1) : 25-35
39
Matthew, E., L. Kutcher, and J. Dedman. "Protection of lungs from hyperoxic injury: gene expression analysis of cyclosporin A therapy." Physiological Genomics 14, no. 2 (July 7, 2003): 129–38. http://dx.doi.org/10.1152/physiolgenomics.00130.2002.
Full textAbstract:
We have previously shown that cyclosporin A (CsA), an inhibitor of protein phosphatase 2B (calcineurin), attenuates hyperoxia-induced reductions in murine lung compliance. CsA protected against hyperoxia-induced changes in neutrophil infiltration, capillary congestion, edema, and hyaline membrane formation. Gene expression studies were conducted to identify the gene expression patterns underlying the protective effects of CsA during hyperoxic lung injury. After 72 h of simultaneous treatment with >95% oxygen and CsA (50 mg·kg−1·day−1), RNA was isolated from murine lungs. RNA from treated and untreated lungs was reverse transcribed to cDNA, competitively hybridized, and used to probe 8,734 complimentary DNAs on the Incyte mouse GEM 1 array. Several known genes and expressed sequence tags (ESTs) showed increased (GenBank accession numbers: AA125385, AA241295, W87197, syntaxin, and cyclin G) or decreased [AA036517, AA267567, AA217009, W82577, uteroglobin, stromal cell-derived factor 1, and surfactant protein C (SP-C)] expression after hyperoxia. Hyperoxia-stimulated reductions in SP-C gene expression were confirmed through Northern blot analysis. The increase in gene expression of one expressed sequence tag (AA125385) with hyperoxia was reversed by CsA treatment. Sequence data demonstrated that this EST has high homology to murine cyclin B1. Western blot analysis did not demonstrate any changes in distal lung cyclin B1 expression after hyperoxia. Protein expression of cyclin B1 in the distal lung was observed in the endothelial cells, bronchiolar epithelial cells, and both the type I and type II alveolar epithelial cells. Further analysis of cyclin B1 may elucidate the protective actions of CsA in hyperoxic injury.
40
Motta, Rodrigo Garcia, Igor Garcia Motta, Antonio Campanha Martinez, Aristeu Vieira da Silva, Antonio Carlos Paes, Lorrayne Souza Araujo Martins, Rodrigo Costa da Silva, and Marcio Garcia Ribeiro. "Unusual caudal vena cava thrombosis in a cow, secondary to Trueperella (Arcanobacterium) pyogenes infection." Pesquisa Veterinária Brasileira 36, no. 7 (July 2016): 587–90. http://dx.doi.org/10.1590/s0100-736x2016000700004.
Full textAbstract:
Abstract: The caudal vena cava thrombosis, or pulmonary thromboembolism, in cattle is correlated with lactic acidosis, caused by diets rich in grains and highly fermentable, associated or not to septic situations, used in feedlots of beef or high-producing dairy cattle. This paper reports an unusual caudal vena cava thrombosis in a cow, secondary to Trueperella (Arcanobacterium) pyogenes infection, resulting in reduced milk production, anorexia, pale mucous membranes, ruminal atony, sternal decubitus and autoauscultation position. The heart was enlarged at necropsy, presence of clots distributed along the thoracic cavity, adherence between lung and pleura, abscesses, emphysema, petechiae, suffusions and ecchymosis in lungs, thickening of the caudal vena cava wall, hepatomegaly with chronic passive congestion ("nutmeg" aspect), and rumenitis. In lab, the actinomycete Trueperella (Arcanobacterium) pyogenes was isolated from liver and lung samples, probably resulting through dissemination of the bacteria of the rumen content, what reaffirms the opportunistic behavior of this actinomycete.
41
Almansour, Mansour, Csaba Laszlo Sajti, Ziad Shraideh, and Bashir Jarrar. "Pulmonary Histological Alterations Induced by 20 nm Silver Nanoparticles." Journal of Nano Research 35 (October 2015): 104–14. http://dx.doi.org/10.4028/www.scientific.net/jnanor.35.104.
Full textAbstract:
Silver nanoparticles (SNPs) are widely invested in nanomedicine and consuming products due to their unique antimicrobial properties. However, little is known about the toxicity of these particles on human health. The present investigation was carried out to investigate the histological alterations induced in the lung tissues by 20±5 nm SNPs. Male albino Wistar rats were exposed to SNPs at a daily dose of 2 mg/kg for 21 days. Lung biopsies from all rats under study were subjected to histopathological examinations. Exposure to 20±5 nm SNPs induced the following pulmonary alterations: thickened alveolar wall, macrophages invasion and inflammatory cells infiltration, lymphatic follicles enlargement, pulmonary edema, alveolar hypersensitivity and interstitial congestion. Occasional atelectasis and fibrocytes proliferation were also detected. The findings of the present work might indicate that SNPs potentially trigger oxidative stress and alterations in the pulmonary tissues that may affect the function of the lungs.
42
Mukaddam-Daher, S., J. Tremblay, N. Fujio, C. Koch, M. Jankowski, E. W. Quillen, and J. Gutkowska. "Alteration of lung atrial natriuretic peptide receptors in genetic cardiomyopathy." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 1 (July 1, 1996): L38—L45. http://dx.doi.org/10.1152/ajplung.1996.271.1.l38.
Full textAbstract:
These studies were designed to characterize the atrial natriuretic peptide (ANF) receptor subtypes [guanylyl cyclase natriuretic peptide receptors (NPR-A, NPR-B) and NPR-C] in lungs of normal hamsters and to evaluate alterations in receptor kinetics in genetic cardiomyopathy (CMO), a model of human congestive heart failure. Lung membranes were obtained from normal and CMO 200-to 230-day-old hamsters. Cross-linking and competitive binding receptor assays using 125I-labeled human ANF showed that lung membranes exhibit NPR, mainly guanylyl cyclase NPR-A and clearance NPR-C receptors. Stimulation of guanylyl cyclase by ANF and C-type natriuretic peptide (CNP) confirmed the presence of NPR-A and NPR-B. The maximum binding capacity of total ANF binding sites (442 +/- 68 vs. 271 +/- 57 fmol/mg protein, P < 0.05) was reduced, but dissociation constant (0.26 +/- 0.04 vs. 0.41 +/- 0.08 nM) was not altered in CMO animals. Similar reductions were observed in the binding sites for brain natriuretic peptide (BNP; 438 +/- 83 vs. 236 +/- 53 fmol/mg protein) and CNP (321 +/- 80 vs. 165 +/- 56 fmol/mg protein, P < 0.05) which may reflect a decline in NPR-A and NPR-B and/or NPR-C. Acid wash improved binding of 125I-labeled rat ANF to lung membranes of both normal and CMO hamsters, but the tendency towards reduced binding in CMO hamsters did not reach statistical significance, implying that downregulation may not have been due only to prior occupancy of the receptors. Transcripts of NPR-A, NPR-B, and NPR-C receptors in hamster lungs were detected by quantitative polymerase chain reaction. Compared with normal controls, the CMO hamster lung NPR-A mRNA was reduced by 50%, but NPR-B mRNA and NPR-C mRNA were not altered. Moreover, CMO hamster lungs showed less activation of guanylyl cyclase by ANF. These studies demonstrate that lung NPR are downregulated in hamster CMO.
43
Hatridge, J., A. Haji, J. R. Perez-Padilla, and J. E. Remmers. "Rapid shallow breathing caused by pulmonary vascular congestion in cats." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2257–64. http://dx.doi.org/10.1152/jappl.1989.67.6.2257.
Full textAbstract:
The vasculature of one lung of unanesthetized spontaneously breathing decerebrate cats was isolated and congested with blood. Such pulmonary vascular congestion (PVC) consistently resulted in a shallow tachypnea associated with expiratory activation of the diaphragm and thyroarytenoid muscles, signifying augmented expiratory braking. With progressive increases in pulmonary vascular pressure, tachypnea and expiratory braking increased progressively and ultimately obscured phasic activity in the diaphragm and thyroarytenoid. Thus the apnea caused by PVC constitutes not an arrest of neural respiratory activity but rather a continuous activation of thoracic inspiratory and laryngeal adductor muscles. When capsaicin, a neurotoxin that activates nonmyelinated afferents, was injected into the pulmonary artery of the isolated lung, it produced changes in timing and distribution of respiratory motor output that resembled those with PVC but were more abrupt in onset. Capsaicin, applied perineurally to the cervical vagi, preferentially blocked the conduction of nonmyelinated afferent fibers. This procedure, which produced little degradation in Hering-Breuer reflexes, eliminated tachypnea and expiratory braking caused by PVC or capsaicin injection. The results indicate that activation of pulmonary vagal afferent fibers of C or A-delta category in unanesthetized cats reflexly modifies the respiratory motor output in a way that resembles the human response to PVC or pulmonary embolism. This is a brain stem reflex.
44
Zorzanelli, Leína, Nair Yukie Maeda, Mariana Meira Clavé, Vera Demarchi Aiello, Marlene Rabinovitch, and Antonio Augusto Lopes. "Serum Cytokines in Young Pediatric Patients with Congenital Cardiac Shunts and Altered Pulmonary Hemodynamics." Mediators of Inflammation 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7672048.
Full textAbstract:
Background and Objective.Inflammation is central in the pathogenesis of pulmonary hypertension. We investigated how serum cytokines correlate with clinical features, hemodynamics, and lung histology in young patients with pulmonary hypertension associated with congenital cardiac shunts.Design.Prospective, observational study.Methods and Results. Patients (n=44) were aged 2.6 to 37.6 months. Group I patients (n=31) were characterized by pulmonary congestion and higher pulmonary blood flow compared to group II (p=0.022), with no need for preoperative cardiac catheterization. Group II patients (n=13) had no congestive features. At catheterization, they had elevated pulmonary vascular resistance (5.7 [4.4–7.4] Wood units·m2, geometric mean with 95% CI). Cytokines were measured by chemiluminescence. Macrophage migration inhibitory factor (MIF) was found to be inversely related to pulmonary blood flow (r=-0.33,p=0.026) and was higher in group II (high pulmonary vascular resistance) compared to group I (high pulmonary blood flow) (p=0.017). In contrast, RANTES chemokine (regulated on activation, normal T cell expressed and secreted) was characteristically elevated in Group I (p=0.022). Interleukin 16 was also negatively related to pulmonary blood flow (rS=-0.33,p=0.029) and was higher in patients with obstructive vasculopathy at intraoperative lung biopsy (p=0.021).Conclusion. Cytokines seem to be important and differentially regulated in subpopulations of young patients with cardiac shunts.
45
Ravikumar, Priya, Cuneyt Yilmaz, Dennis J. Bellotto, D. Merrill Dane, Aaron S. Estrera, and Connie C. W. Hsia. "Separating in vivo mechanical stimuli for postpneumonectomy compensation: imaging and ultrastructural assessment." Journal of Applied Physiology 114, no. 8 (April 15, 2013): 961–70. http://dx.doi.org/10.1152/japplphysiol.01394.2012.
Full textAbstract:
Following right pneumonectomy (PNX), the remaining lung expands and its perfusion more than doubles. Tissue and microvascular mechanical stresses are putative stimuli for compensatory lung growth and remodeling, but their relative contribution remains uncertain. To temporally separate expansion- and perfusion-related stimuli, we replaced the right lung of adult dogs with a customized inflated prosthesis. Four months later, the prosthesis was either acutely deflated (DEF) or kept inflated (INF). Thoracic high-resolution computed tomography (HRCT) was performed pre- and post-PNX before and after prosthesis deflation. Lungs were fixed for morphometric analysis ∼12 mo post-PNX. The INF prosthesis prevented mediastinal shift and lateral lung expansion while allowing the remaining lung to expand 27–38% via caudal elongation, associated with reversible capillary congestion in dependent regions at low inflation and 40–60% increases in the volumes of alveolar sepal cells, matrix, and fibers. Delayed prosthesis deflation led to further significant increases in lung volume, alveolar tissue volumes, and alveolar-capillary surface areas. At postmortem, alveolar tissue volumes were 33% higher in the DEF than the INF group. Lateral expansion explains ∼65% of the total post-PNX increase in left lung volume assessed in vivo or ex vivo, ∼36% of the increase in HRCT-derived (tissue + microvascular blood) volume, ∼45% of the increase in ex vivo septal extravascular tissue volume, and 60% of the increase in gas exchange surface areas. This partition agrees with independent physiological measurements obtained in these animals. We conclude that in vivo signals related to lung expansion and perfusion contribute separately and nearly equally to post-PNX growth and remodeling.
46
Dokic, Z., and W. Pirog. "Emphysematous lesions in the right cranial lung lobe and torsion of the right medial lung lobe in a British shorthair cat: a case report." Veterinární Medicína 60, No. 12 (September 14, 2017): 706–11. http://dx.doi.org/10.17221/8586-vetmed.
Full textAbstract:
A three-year-old male British shorthair cat that had exhibited progressive lethargy and intermittent dyspnoea for 14 days was referred for evaluation of acute respiratory deterioration. Clinical findings included rapid and shallow breathing, pale mucous membranes, sound suppression on the right side, and a subcutaneous haematoma in the right epigastric area. Serum biochemistry analysis showed leukocytosis and thrombocytosis. Radiographs revealed hydropneumothorax, a broken eighth right rib, atelectatic right cranial lung lobe (RCrL), and consolidation of the right middle lobe (RML). Doppler examination revealed sonographic changes in the echotexture of both lobes and venous flow was absent in the twisted RML. Furthermore, bronchoscopy showed proximal narrowing of the cat’s RML bronchus. Exploratory surgery via medial sternotomy confirmed torsion of the RML and identified deteriorated gas-containing lesions in the collapsed RCrL. Both lung lobes were removed by standard lobectomy, and postoperative recovery was without major complications. Histopathological examination diagnosed multiple bullae and blebs, with significant subpleural haemorrhages in the atelectatic RCrL, whereas tissue congestion with haemorrhages, necrosis, and thrombosis typical for lung lobe torsion were observed in the RML. No other underlying aetiology was apparent. Two months post-operatively, the cat presented with similar acute onset of dyspnoea and spontaneous pneumothorax and was euthanised at the owner’s request. The autopsy revealed identical new emphysematous changes in the contra-lateral lung lobes that had been absent at the time of surgery. Emphysematous lesions, regardless of their origin, should be considered in the etiopathology of lung lobe torsion.
47
Oncu, Meral, Kanat Gulle, Erdal Karaoz, Fatih Gultekin, Sureyya Karaoz, Inanc Karakoyun, and Ethem Mumcu. "Effect of chronic fluorosis on lipid peroxidation and histology of lung tissues in first and second generation rats." Toxicology and Industrial Health 22, no. 9 (October 2006): 375–80. http://dx.doi.org/10.1177/0748233706071973.
Full textAbstract:
This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first and second generation rat lung tissues. Sixteen, virgin, female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two experimental groups (control and fluoride supplemented). The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and lactation periods. After the lactation period, young animals (first generation; F1) were exposed to the same amount of NaF in drinking water for four months. At the end of the four-month experimental period, nine randomly-chosen male rats (F1) were sacrificed and lung tissues were removed for histopathological and enzymatic lipid peroxidation examination. The second generation rats were obtained from the remaining rats by the same method. They were also treated similarly. At the end of the four-month experimental period, nine randomly-chosen male rats (F2) were sacrificed, and the lungs were removed for histological and lipid peroxidation examination. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and the lung TBARS levels of fluoride supplemented F1 and F2 rats were higher than controls. There were marked histological changes in the lung tissues of fluoride supplemented F1 and F2 rats, as follows: in F1 rats; loss of alveolar architecture, emphysematous areas, descuamation of alveolar epithelium and alveolar congestion were observed. There were thickened interalveolar septae and congestion of alveolar septal vessels. Intraparenchymal thick-walled vessels were also observed. There were markedly perivascular and intraparenchymal focal mononuclear cell infiltrations. In F2 rats, in addition to these changes, there were lipid cell hyperplasia and increased connective tissue mass in the parenchymal areas. It is concluded that chronic fluorosis causes a marked destruction in lung tissues of F1 and F2 rats by causing lipid peroxidation. Toxicology and Industrial Health 2006; 22: 375-380.
48
Kerem, Alexander, Jun Yin, Stephanie M. Kaestle, Julia Hoffmann, Axel M. Schoene, Baljit Singh, Hermann Kuppe, Mathias M. Borst, and Wolfgang M. Kuebler. "Lung Endothelial Dysfunction in Congestive Heart Failure." Circulation Research 106, no. 6 (April 2, 2010): 1103–16. http://dx.doi.org/10.1161/circresaha.109.210542.
Full text
49
Yang, Mo, En Yu Liang, Li Xia Zhou, Beng H. Chong, and Chunfu Li. "Lung Damage and Thrombocytopenia." Blood 126, no. 23 (December 3, 2015): 4638. http://dx.doi.org/10.1182/blood.v126.23.4638.4638.
Full textAbstract:
Abstract Hematological changes in patients with lung damage were common and included thrombocytopenia (55%) (Yang et al, Int J Mol Med. 2004; Hon et al, Lancet. 2003). A number of potential mechanisms have been investigated. The lungs of patients who died of lung infection show diffuse alveolar damage with pulmonary congestion, edema, formation of hyaline membrane, and fibrosis. Viral infection, oxygen toxicity and/or barotrauma contribute to the lung damage. The lung tissue and pulmonary endothelial cell damage result in platelet activation, aggregation, and thrombi formation at the site of the injury. All these mechanisms may induce the consumption of platelets and megakaryocytes (MK). The association between lung injury and thrombocytopenia was investigated by comparing the MK and platelet counts, and platelet activation using P-selectin as a marker, between the prepulmonary (right atrial) and postpulmonary (left atrial) blood in rats with and without hyperoxic lung injury. In the healthy controls, the postpulmonary blood had lower megakaryocyte count, higher platelet count, but similar P-selectin expression. In contrast, the lung-damaged animals did not show any such differences in either MK or platelet count, but P-selectin expression was greater in the postpulmonary blood. Peripheral platelet and intra-pulmonary MK counts in the lung-damaged rats were significantly lower than those in their respective controls. Intra-pulmonary thrombi or platelet aggregation were detected in the lung-damaged rats but not in the controls. These findings showed that lung damage reduced circulating platelets through (i) failure of the lungs to retain and fragment MK to release platelets, (ii) and platelet activation leading to platelet aggregation, thrombi formation and platelet consumption. The number and morphology of circulating MK were also investigated before, during and after cardiopulmonary bypass (CPB) in 22 patients undergoing routine cardiac surgery. Results showed that: (i) The total number of MK in central venous was higher than those of peripheral arteries during normal circulation (P<0.01). There was significant decrease of Type-4 MK (mature and large MK) number in peripheral arteries compared with that in central venous (P<0.001); and (ii) During CPB, the total MK and Type-4 MK of central venous and peripheral arteries were significant increased when compared with that in normal circulation (P<0.01). Our observation supports that the lungs may remove large MK during normal circulation. This physiological effect would be lost on CPB. On the other hand, the lungs may be the sites of platelet release from mature MK. The inflammation, the long term ventilation and/or oxygen therapy may result in pulmonary fibrosis and other pathological changes. The reduced or morphologically altered pulmonary capillary bed would affect the MK fragmentation in the lung. The increased consumption of platelet and/or the decreased production of platelet may lead to thrombocytopenia. Disclosures Yang: National Natural Science Foundation of China(81270580): Research Funding.
50
Cohen, A. B., M. D. Stevens, E. J. Miller, M. A. Atkinson, G. Mullenbach, R. J. Maunder, T. R. Martin, J. P. Wiener-Kronish, and M. A. Matthay. "Neutrophil-activating peptide-2 in patients with pulmonary edema from congestive heart failure or ARDS." American Journal of Physiology-Lung Cellular and Molecular Physiology 264, no. 5 (May 1, 1993): L490—L495. http://dx.doi.org/10.1152/ajplung.1993.264.5.l490.
Full textAbstract:
We carried out studies to determine whether the neutrophil-activation peptide-2 (NAP-2) plays a role in the recruitment and/or degranulation of neutrophils into the lungs of patients with the adult respiratory distress syndrome (ARDS) or congestive heart failure (CHF). NAP-2 precursors plus NAP-2 (beta-thromboglobulin-like antigen) were measured in lung fluids and plasmas with a radioimmunoassay, and NAP-2 was separated from its precursors by high-performance liquid chromatography. Pulmonary edema fluids (PEFs) from patients with CHF contained higher concentrations of the beta-thromboglobulin-like antigen than PEFs from patients with ARDS, and bronchoalveolar lavage fluids (BALs) from patients with ARDS contained higher concentrations of beta-thromboglobulin-like antigen than BALs from normal subjects. beta-Thromboglobulin-like antigen concentration was 4.1-fold greater in PEFs from patients with CHF than in their plasmas. Chemotactically active NAP-2 was also demonstrated in PEFs but not in plasmas from patients with CHF and ARDS. These data suggest that significant platelet degranulation occurred into the lungs of the patients with CHF and that NAP-2 and other platelet constituents may contribute to fluid formation in patients with CHF.