Log in

Relevant bibliographies by topics / Hypoxic pulmonary vasoconstriction; HPV

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers

Academic literature on the topic 'Hypoxic pulmonary vasoconstriction; HPV'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Hypoxic pulmonary vasoconstriction; HPV.'

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.

Journal articles on the topic "Hypoxic pulmonary vasoconstriction; HPV"

1

Evans, A. Mark. "Hypoxic pulmonary vasoconstriction." Essays in Biochemistry 43 (August 10, 2007): 61–76. http://dx.doi.org/10.1042/bse0430061.

Full text

Abstract:

HPV (hypoxic pulmonary vasoconstriction) is the critical and distinguishing characteristic of the arteries that feed the lung. In marked contrast, systemic arteries dilate in response to hypoxia to meet the metabolic demands of the tissues they supply. Physiologically, HPV contributes to ventilation–perfusion matching in the lung by diverting blood flow to oxygen-rich areas. However, when alveolar hypoxia is global, as in diseases such as emphysema and cystic fibrosis, HPV leads to HPH (hypoxic pulmonary hypertension) and right heart failure. HPV is driven by the intrinsic response to hypoxia of two different cell types, namely the pulmonary arterial smooth muscle and endothelial cells. These are representatives of a group of specialized cells, commonly referred to as oxygen-sensing cells, which are defined by their acute sensitivity to relatively small changes in PO2 and have evolved to monitor oxygen supply and alter respiratory and circulatory function, as well as the capacity of the blood to transport oxygen. Upon exposure to hypoxia, mitochondrial oxidative phosphorylation is inhibited in all such cells and this, in part, mediates cell activation. In the case of pulmonary arteries, constriction is triggered via: (i) calcium release from the smooth muscle sarcoplasmic reticulum and consequent store-depletion-activated calcium entry into the smooth muscle cells and, (ii) the modulation of transmitter release from the pulmonary artery endothelium, which leads to further constriction of the smooth muscle by increasing the sensitivity of the contractile apparatus to calcium.

APA, Harvard, Vancouver, ISO, and other styles

2

Moudgil, Rohit, Evangelos D. Michelakis, and Stephen L. Archer. "Hypoxic pulmonary vasoconstriction." Journal of Applied Physiology 98, no. 1 (2005): 390–403. http://dx.doi.org/10.1152/japplphysiol.00733.2004.

Full text

Abstract:

Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, through disease, and by desire, in our quest for altitude. Hypoxic pulmonary vasoconstriction (HPV) is a widely conserved, homeostatic, vasomotor response of resistance pulmonary arteries to alveolar hypoxia. HPV mediates ventilation-perfusion matching and, by reducing shunt fraction, optimizes systemic Po2. HPV is intrinsic to the lung, and, although modulated by the endothelium, the core mechanism is in the smooth muscle cell (SMC). The Redox Theory for the mechanism of HPV proposes the coordinated action of a redox sensor (the proximal mitochondrial electron transport chain) that generates a diffusible mediator [a reactive O2 species (ROS)] that regulates an effector protein [voltage-gated potassium (Kv) and calcium channels]. A similar mechanism for regulating O2 uptake/distribution is partially recapitulated in simpler organisms and in the other specialized mammalian O2-sensitive tissues, including the carotid body and ductus arteriosus. Inhibition of O2-sensitive Kv channels, particularly Kv1.5 and Kv2.1, depolarizes pulmonary artery SMCs, activating voltage-gated Ca2+ channels and causing Ca2+ influx and vasoconstriction. Downstream of this pathway, there is important regulation of the contractile apparatus' sensitivity to calcium by rho kinase. Controversy remains as to whether hypoxia decreases or increases ROS and which electron transport chain complex generates the ROS (I and/or III). Possible roles for cyclic adenosine diphosphate ribose and an unidentified endothelial constricting factor are also proposed by some groups. Modulation of HPV has therapeutic relevance to cor pulmonale, high-altitude pulmonary edema, and sleep apnea. HPV is clinically exploited in single-lung anesthesia, and its mechanisms intersect with those of pulmonary arterial hypertension.

APA, Harvard, Vancouver, ISO, and other styles

3

Lumb, Andrew B., and Peter Slinger. "Hypoxic Pulmonary Vasoconstriction." Anesthesiology 122, no. 4 (2015): 932–46. http://dx.doi.org/10.1097/aln.0000000000000569.

Full text

Abstract:

Abstract Hypoxic pulmonary vasoconstriction (HPV) represents a fundamental difference between the pulmonary and systemic circulations. HPV is active in utero, reducing pulmonary blood flow, and in adults helps to match regional ventilation and perfusion although it has little effect in healthy lungs. Many factors affect HPV including pH or Pco2, cardiac output, and several drugs, including antihypertensives. In patients with lung pathology and any patient having one-lung ventilation, HPV contributes to maintaining oxygenation, so anesthesiologists should be aware of the effects of anesthesia on this protective reflex. Intravenous anesthetic drugs have little effect on HPV, but it is attenuated by inhaled anesthetics, although less so with newer agents. The reflex is biphasic, and once the second phase becomes active after about an hour of hypoxia, this pulmonary vasoconstriction takes hours to reverse when normoxia returns. This has significant clinical implications for repeated periods of one-lung ventilation.

APA, Harvard, Vancouver, ISO, and other styles

4

Sylvester, J. T., Larissa A. Shimoda, Philip I. Aaronson, and Jeremy P. T. Ward. "Hypoxic Pulmonary Vasoconstriction." Physiological Reviews 92, no. 1 (2012): 367–520. http://dx.doi.org/10.1152/physrev.00041.2010.

Full text

Abstract:

It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

APA, Harvard, Vancouver, ISO, and other styles

5

Weissmann, Norbert, Robert Voswinckel, Thorsten Hardebusch, et al. "Evidence for a role of protein kinase C in hypoxic pulmonary vasoconstriction." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (1999): L90—L95. http://dx.doi.org/10.1152/ajplung.1999.276.1.l90.

Full text

Abstract:

Hypoxic pulmonary vasoconstriction (HPV) matches lung perfusion to ventilation, thus optimizing gas exchange. NADPH oxidase-related superoxide anion generation has been suggested as part of the signaling response to hypoxia. Because protein kinase (PK) C activation can occur during hypoxia and PKC activation is known to be critical for NADPH oxidase stimulation in different cell types, we probed the role of PKC in hypoxic vasoconstriction in intact rabbit lungs. Control vasoconstrictor responses were elicited by angiotensin II (ANG II) and the stable thromboxane analog U-46619. Portions of the experiments were performed while NO synthesis and prostanoid generation were blocked with N G-monomethyl-l-arginine and acetylsalicylic acid to avoid confounding effects due to interference with these vasoactive mediators. The PKC inhibitor H-7 (10–50 μM) caused dose-dependent inhibition of HPV, but this agent lacked specificity because ANG II- and U-46619-induced vasoconstrictions were correspondingly suppressed. In contrast, low concentrations of the specific PKC inhibitor bisindolylmaleimide I (BIM; 1–15 μM) strongly inhibited the hypoxic vasoconstriction without any interference with the responses to the pharmacological agents. Superimposable dose-inhibition curves were also obtained for BIM when lung NO synthesis and prostanoid generation were blocked throughout the experiments. Under either condition, BIM did not affect normoxic vascular tone. The PKC activator farnesylthiotriazole (FTT), ascertained to stimulate rabbit NADPH oxidase by provocation of alveolar macrophage superoxide anion generation in vitro, caused rapid-onset, transient pressor responses in normoxic lungs. After FTT, the hypoxic vasoconstrictor response was totally suppressed, in contrast to the largely maintained pressor responses to ANG II and U-46619. The lungs became refractory even to delayed hypoxic challenges after FTT application. In conclusion, these data support the concept that activation of PKC is involved in the transduction pathway forwarding pulmonary vasoconstriction in response to alveolar hypoxia.

APA, Harvard, Vancouver, ISO, and other styles

6

Tabeling, Christoph, Hanpo Yu, Liming Wang, et al. "CFTR and sphingolipids mediate hypoxic pulmonary vasoconstriction." Proceedings of the National Academy of Sciences 112, no. 13 (2015): E1614—E1623. http://dx.doi.org/10.1073/pnas.1421190112.

Full text

Abstract:

Hypoxic pulmonary vasoconstriction (HPV) optimizes pulmonary ventilation-perfusion matching in regional hypoxia, but promotes pulmonary hypertension in global hypoxia. Ventilation-perfusion mismatch is a major cause of hypoxemia in cystic fibrosis. We hypothesized that cystic fibrosis transmembrane conductance regulator (CFTR) may be critical in HPV, potentially by modulating the response to sphingolipids as mediators of HPV. HPV and ventilation-perfusion mismatch were analyzed in isolated mouse lungs or in vivo. Ca2+ mobilization and transient receptor potential canonical 6 (TRPC6) translocation were studied in human pulmonary (PASMCs) or coronary (CASMCs) artery smooth muscle cells. CFTR inhibition or deficiency diminished HPV and aggravated ventilation-perfusion mismatch. In PASMCs, hypoxia caused CFTR to interact with TRPC6, whereas CFTR inhibition attenuated hypoxia-induced TRPC6 translocation to caveolae and Ca2+ mobilization. Ca2+ mobilization by sphingosine-1-phosphate (S1P) was also attenuated by CFTR inhibition in PASMCs, but amplified in CASMCs. Inhibition of neutral sphingomyelinase (nSMase) blocked HPV, whereas exogenous nSMase caused TRPC6 translocation and vasoconstriction that were blocked by CFTR inhibition. nSMase- and hypoxia-induced vasoconstriction, yet not TRPC6 translocation, were blocked by inhibition or deficiency of sphingosine kinase 1 (SphK1) or antagonism of S1P receptors 2 and 4 (S1P2/4). S1P and nSMase had synergistic effects on pulmonary vasoconstriction that involved TRPC6, phospholipase C, and rho kinase. Our findings demonstrate a central role of CFTR and sphingolipids in HPV. Upon hypoxia, nSMase triggers TRPC6 translocation, which requires its interaction with CFTR. Concomitant SphK1-dependent formation of S1P and activation of S1P2/4 result in phospholipase C-mediated TRPC6 and rho kinase activation, which conjointly trigger vasoconstriction.

APA, Harvard, Vancouver, ISO, and other styles

7

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije. "Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange." Journal of Applied Physiology 81, no. 4 (1996): 1535–43. http://dx.doi.org/10.1152/jappl.1996.81.4.1535.

Full text

Abstract:

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije.Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange. J. Appl. Physiol. 81(4): 1535–1543, 1996.—Several reports have suggested that hypoxic pulmonary vasoconstriction (HPV) might result in deterioration of pulmonary gas exchange in severe hypoxia. We therefore investigated the effects of HPV on gas exchange in normal and diseased lungs. We incorporated a biphasic HPV stimulus-response curve observed in intact dogs (S. Brimioulle, P. Lejeune, J. L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl. Physiol. 77: 476–480, 1994) into a 50-compartment lung model (J. B. West, Respir. Physiol. 7: 88–110, 1969) to control the amount of blood flow directed to each lung compartment according to the local hypoxic stimulus. The resulting model accurately reproduced the blood gas modifications caused by HPV changes in dogs with acute lung injury. In single lung units, HPV had a moderate protective effect on alveolar oxygenation, which was maximal at near-normal alveolar[Formula: see text] (75–80 Torr), mixed venous[Formula: see text] (35 Torr), and[Formula: see text] at which hemoglobin is 50% saturated (24 Torr). In simulated diseased lungs associated with 40–60 Torr arterial [Formula: see text], however, HPV increased arterial [Formula: see text]by 15–20 Torr. We conclude that HPV can improve arterial oxygenation substantially in respiratory failure.

APA, Harvard, Vancouver, ISO, and other styles

8

Kandhi, Sharath, Bin Zhang, Ghezal Froogh, et al. "EETs promote hypoxic pulmonary vasoconstriction via constrictor prostanoids." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 2 (2017): L350—L359. http://dx.doi.org/10.1152/ajplung.00038.2017.

Full text

Abstract:

To test the hypothesis that epoxyeicosatrienoic acids (EETs) facilitate pulmonary responses to hypoxia, male wild-type (WT) and soluble-epoxide hydrolase knockout (sEH-KO) mice, and WT mice chronically fed a sEH inhibitor ( t-TUCB; 1 mg·kg−1·day−1) were used. Right ventricular systolic pressure (RVSP) was recorded under control and hypoxic conditions. The control RVSP was comparable among all groups. However, hypoxia elicited increases in RVSP in all groups with predominance in sEH-KO and t-TUCB-treated mice. 14,15-EEZE (an EET antagonist) attenuated the hypoxia-induced greater elevation of RVSP in sEH-deficient mice, suggesting an EET-mediated increment. Exogenous 5,6-; 8,9-, or 14,15-EET (0.05 ng/g body wt) did not change RVSP in any conditions, but 11,12-EET enhanced RVSP under hypoxia. Isometric tension was recorded from pulmonary arteries isolated from WT and sEH-KO mice, vessels that behaved identically in their responsiveness to vasoactive agents and vessel stretch. Hypoxic pulmonary vasoconstriction (HPV, expressed as increases in hypoxic force) was significantly greater in vessels of sEH-KO than WT vessels; the enhanced component was inhibited by EEZE. Treatment of WT vessels with 11,12-EET enhanced HPV to the same level as sEH-KO vessels, confirming EETs as primary players. Inhibition of cyclooxygenases (COXs) significantly enhanced HPV in WT vessels, but attenuated HPV in sEH-KO vessels. Blocking/inhibiting COX-1, prostaglandin H2 (PGH2)/thromboxane A2 (TXA2) receptors and TXA synthase prevented the enhanced HPV in sEH-KO vessels but had no effects on WT vessels. In conclusion, an EET-dependent alteration in PG metabolism that favors the action of vasoconstrictor PGH2 and TXA2 potentiates HPV and hypoxia-induced elevation of RVSP in sEH-deficient mice.

APA, Harvard, Vancouver, ISO, and other styles

9

Grimmer, Benjamin, and Wolfgang M. Kuebler. "The endothelium in hypoxic pulmonary vasoconstriction." Journal of Applied Physiology 123, no. 6 (2017): 1635–46. http://dx.doi.org/10.1152/japplphysiol.00120.2017.

Full text

Abstract:

Hypoxic pulmonary vasoconstriction (HPV) in combination with hypercapnic pulmonary vasoconstriction redistributes pulmonary blood flow from poorly aerated to better ventilated lung regions by an active process of local vasoconstriction. Impairment of HPV results in ventilation-perfusion mismatch and is commonly associated with various lung diseases including pneumonia, sepsis, or cystic fibrosis. Although several regulatory pathways have been identified, considerable knowledge gaps persist, and a unifying concept of the signaling pathways that underlie HPV and their impairment in lung diseases has not yet emerged. In the past, conceptual models of HPV have focused on pulmonary arterial smooth muscle cells (PASMC) acting as sensor and effector of hypoxia in the pulmonary vasculature. In contrast, the endothelium was considered a modulating bystander in this scenario. For an ideal design, however, the oxygen sensor in HPV should be located in the region of gas exchange, i.e., in the alveolar capillary network. This concept requires the retrograde propagation of the hypoxic signal along the endothelial layer of the vascular wall and subsequent contraction of PASMC in upstream arterioles that is elicited via temporospatially tightly controlled endothelial-smooth muscle cell crosstalk. The present review summarizes recent work that provides proof-of-principle for the existence and functional relevance of such signaling pathway in HPV that involves important roles for connexin 40, epoxyeicosatrienoic acids, sphingolipids, and cystic fibrosis transmembrane conductance regulator. Of translational relevance, implication of these molecules provides for novel mechanistic explanations for impaired ventilation/perfusion matching in patients with pneumonia, sepsis, cystic fibrosis, and presumably various other lung diseases.

APA, Harvard, Vancouver, ISO, and other styles

10

Starr, I. R., W. J. E. Lamm, B. Neradilek, N. Polissar, R. W. Glenny, and M. P. Hlastala. "Regional hypoxic pulmonary vasoconstriction in prone pigs." Journal of Applied Physiology 99, no. 1 (2005): 363–70. http://dx.doi.org/10.1152/japplphysiol.00822.2004.

Full text

Abstract:

Hypoxic pulmonary vasoconstriction (HPV) is known to affect regional pulmonary blood flow distribution. It is unknown whether lungs with well-matched ventilation (V̇)/perfusion (Q̇) have regional differences in the HPV response. Five prone pigs were anesthetized and mechanically ventilated (positive end-expiratory pressure = 2 cmH2O). Two hypoxic preconditions [inspired oxygen fraction (FiO2) = 0.13] were completed to stabilize the animal's hypoxic response. Regional pulmonary blood Q̇ and V̇ distribution was determined at various FiO2 (0.21, 0.15, 0.13, 0.11, 0.09) using the fluorescent microsphere technique. Q̇ and V̇ in the lungs were quantified within 2-cm3 lung pieces. Pieces were grouped, or clustered, based on the changes in blood flow when subjected to increasing hypoxia. Unique patterns of Q̇ response to hypoxia were seen within and across animals. The three main patterns (clusters) showed little initial difference in V̇/Q̇ matching at room air where the mean V̇/Q̇ range was 0.92–1.06. The clusters were spatially located in cranial, central, and caudal portions of the lung. With decreasing FiO2, blood flow shifted from the cranial to caudal regions. We determined that pulmonary blood flow changes, caused by HPV, produced distinct response patterns that were seen in similar regions across our prone porcine model.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Hypoxic pulmonary vasoconstriction; HPV"

1

Jones, Richard David. "Hypoxia and the pulmonary circulation." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301608.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Jahn, Nora, Regis R. Lamberts, Cornelius J. Busch, et al. "Inhaled carbon monoxide protects timedependently from loss of hypoxic pulmonary vasoconstriction in endotoxemic mice." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-185283.

Full text

Abstract:

Background: Inhaled carbon monoxide (CO) appears to have beneficial effects on endotoxemia-induced impairment of hypoxic pulmonary vasoconstriction (HPV). This study aims to specify correct timing of CO application, it’s biochemical mechanisms and effects on inflammatory reactions. Methods: Mice (C57BL/6; n = 86) received lipopolysaccharide (LPS, 30 mg/kg) intraperitoneally and subsequently breathed 50 ppm CO continuously during defined intervals of 3, 6, 12 or 18 h. Two control groups received saline intraperitoneally and additionally either air or CO, and one control group received LPS but breathed air only. In an isolated lung perfusion model vasoconstrictor response to hypoxia (FiO2 = 0.01) was quantified by measurements of pulmonary artery pressure. Pulmonary capillary pressure was estimated by double occlusion technique. Further, inflammatory plasma cytokines and lung tissue mRNA of nitric-oxide-synthase-2 (NOS-2) and heme oxygenase-1 (HO-1) were measured. Results: HPV was impaired after LPS-challenge (p < 0.01). CO exposure restored HPV-responsiveness if administered continuously for full 18 h, for the first 6 h and if given in the interval between the 3rd and 6th hour after LPS-challenge (p < 0.05). Preserved HPV was attributable to recovered arterial resistance and associated with significant reduction in NOS-2 mRNA when compared to controls (p < 0.05). We found no effects on inflammatory plasma cytokines. Conclusion: Low-dose CO prevented LPS-induced impairment of HPV in a time-dependent manner, associated with a decreased NOS-2 expression.

APA, Harvard, Vancouver, ISO, and other styles

3

Robertson, Blair E. "Hypoxic pulmonary vasoconstriction." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303043.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Albarwani, Sulayma. "Hypoxic pulmonary vasoconstriction." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386771.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Hague, Dominic. "Acute hypoxic pulmonary vasoconstriction." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322196.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Cannon, Donal Patrick. "The pulmonary circulation and hypoxic pulmonary vasoconstriction." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670366.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Hambræus, Jonzon Kristina. "Hypoxic pulmonary vasoconstriction and nitric oxide /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4266-8/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Baxter, Lynne Morrell. "Oxygen sensing, mitochondria and hypoxic pulmonary vasoconstriction." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428772.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Dipp, Michelle. "The role of calcium sensitisation in hypoxic pulmonary vasoconstriction." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:d14ca3ef-c5b8-4a4c-b9d4-5a1ee086cb4a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Lerche, Phillip. "Pulmonary blood flow distribution and hypoxic pulmonary vasoconstriction in pentobarbital-anesthetized horses." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1135278396.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Hypoxic pulmonary vasoconstriction; HPV"

1

Yuan, Jason X. J., ed. Hypoxic Pulmonary Vasoconstriction. Kluwer Academic Publishers, 2004. http://dx.doi.org/10.1007/b105332.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Yuan, Jason X.-J., 1963-, ed. Hypoxic pulmonary vasoconstriction: Cellular and molecular mechanisms. Kluwer Academic Pub., 2004.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Yuan, Jason X. J. Hypoxic Pulmonary Vasoconstriction:: Cellular and Molecular Mechanisms (Developments in Cardiovascular Medicine). Springer, 2004.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.

Full text

Abstract:

Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.

APA, Harvard, Vancouver, ISO, and other styles

5

Hedenstierna, Göran, and João Batista Borges. Normal physiology of the respiratory system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0071.

Full text

Abstract:

The lungs contain 200–300 million alveoli that are reached via 23 generations of airways. The volume in the lungs after an ordinary expiration is called functional residual capacity (FRC) and is approximately 3–4 L. The lung is elastic and force (pressure) is needed to expand it and to overcome the resistance to gas flow in the airways. This pressure can be measured as pleural minus alveolar pressure. The inspired volume goes mainly to dependent, lower lung regions, but with increasing age and in obstructive lung disease airways may close in dependent lung regions during expiration, impeding oxygenation of the blood. With lowered functional residual capacity,airways may be continuously closed with subsequent gas adsorbtion from the closed off alveoli. Perfusion of the lung goes also mainly to dependent regions, but there is in addition, possibly more important, a non-gravitational inhomogeneity. A ventilation-perfusion mismatch may ensue that impedes oxygenation and CO2 removal, but can to some extent be corrected for by hypoxic pulmonary vasoconstriction.

APA, Harvard, Vancouver, ISO, and other styles

6

Davidson, Andrew, Adrian Bosenberg, and Stephen Stayer. Neonatal anaesthesia. Edited by Jonathan G. Hardman and Neil S. Morton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0070.

Full text

Abstract:

Neonatal anaesthesia requires an understanding of how neonates differ from adults and older children in anatomy, physiology, and pharmacology. There are also pathological and surgical conditions in neonates that are associated with unique anaesthesia challenges. Organ systems are generally immature, reducing the clearance of many drugs, while different water and fat content results in altered volumes of distribution. Pharmacological management is further complicated by a lack of basic pharmacokinetic data for the use of most anaesthetic drugs in neonates. At birth, there is a transition from a fetal circulation. Some aspects of fetal physiology can persist and have an impact on anaesthesia care, for example, exaggerated hypoxic pulmonary vasoconstriction. Small size, organ immaturity, and reduced physiological reserve can also result in rapid changes to cardiovascular or respiratory status during surgery. Neonates are also very vulnerable to injury, particularly pulmonary or neurological damage. Even brief episodes of over-inflation or hyperoxia may have long-lasting effects on the lung. Safe neonatal anaesthesia thus requires appropriate equipment and ventilators, careful monitoring, and the rapid management of changes in circulatory or respiratory status. Neonates that need surgery often have other significant co-morbidities; for example, prematurity, sepsis, congenital cardiac disease, or a wide variety of syndromes. Safe anaesthesia requires a careful preoperative assessment looking for such co-morbidities and a good understanding of how these may have an impact on anaesthesia.

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Hypoxic pulmonary vasoconstriction; HPV"

1

Weir, E. Kenneth, Jesús A. Cabrera, Douglas A. Peterson, Saswati Mahapatra, and Zhigang Hong. "Hypoxic Pulmonary Vasoconstriction." In Textbook of Pulmonary Vascular Disease. Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-87429-6_46.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Mark Evans, A., and Jeremy P. T. Ward. "Hypoxic Pulmonary Vasoconstriction – Invited Article." In Advances in Experimental Medicine and Biology. Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2259-2_40.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Traber, D. L., and L. D. Traber. "Hypoxic Pulmonary Vasoconstriction and the Pulmonary Microcirculation." In Yearbook of Intensive Care and Emergency Medicine 2002. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56011-8_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Traber, D. L., and L. D. Traber. "Hypoxic Pulmonary Vasoconstriction and the Pulmonary Microcirculation." In Intensive Care Medicine. Springer New York, 2002. http://dx.doi.org/10.1007/978-1-4757-5551-0_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Post, J. M., E. K. Weir, S. L. Archer, and J. R. Hume. "Redox Regulation of K+ Channels and Hypoxic Pulmonary Vasoconstriction." In Ion Flux in Pulmonary Vascular Control. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2397-0_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Weir, E. Kenneth, Jésus A. Cabrera, Saswati Mahapatra, Douglas A. Peterson, and Zhigang Hong. "The Role of Ion Channels in Hypoxic Pulmonary Vasoconstriction." In Advances in Experimental Medicine and Biology. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Yamaguchi, Kazuhiro, Koichiro Asano, Tomoaki Takasugi, et al. "Roles of Antioxidant Enzymes in Erythrocytes on Hypoxic Pulmonary Vasoconstriction." In Advances in Experimental Medicine and Biology. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2468-7_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Waypa, Gregory B., and Paul T. Schumacker. "Role for Mitochondrial Reactive Oxygen Species in Hypoxic Pulmonary Vasoconstriction." In Signalling Pathways in Acute Oxygen Sensing. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035009.ch14.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

de Stoppelaar, E. I., F. G. Leicher, G. J. Rees, W. Erdmann, N. S. Faithfull, and H. van der Zee. "Hypoxic Pulmonary Vasoconstriction in the Newborn Pig — An Experimental Model." In Advances in Experimental Medicine and Biology. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-3291-6_64.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Weissmann, Norbert, Ralph T. Schermuly, Hossein A. Ghofrani, et al. "Hypoxic Pulmonary Vasoconstriction-Triggered by an Increase in Reactive Oxygen Species?" In Signalling Pathways in Acute Oxygen Sensing. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035009.ch15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Hypoxic pulmonary vasoconstriction; HPV"

1

Prieto-Lloret, Jesus, michelle Connolly, Jeremy P. Ward, and philip I. aaronson. "Primary Role Of Intracellular Calcium Release Via Ryanodine Receptors And Not Calcium Entry In HPV During Hypoxic Pulmonary Vasoconstriction In Non-Preconstricted Rat Intrapulmonary Arteries." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5494.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Albert, Tyler J., and Erik R. Swenson. "Peripheral Chemoreceptor Responsiveness And Hypoxic Pulmonary Vasoconstriction In Humans." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5033.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Petersen, Bodil, Cornelius J. Busch, Kenneth D. Bloch, and Warren M. Zapol. "Arginase Inhibition Restores Hypoxic Pulmonary Vasoconstriction In Endotoxemic Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4830.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Duan, X., Y. Chen, and J. Wang. "Tetramethylpyrazine Reduces Hypoxic Vasoconstriction and Attenuates the Development of Pulmonary Hypertension." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3869.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Fuchs, B., M. Rupp, A. Dietrich, et al. "Regulation of TRPC6 in the Acute Phase of Hypoxic Pulmonary Vasoconstriction." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6241.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Tabeling, Christoph, Hanpo Yu, Liming Wang, et al. "Cystic fibrosis transmembrane conductance regulator and sphingolipids regulate hypoxic pulmonary vasoconstriction." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4905.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Burrowes, Kelly, Alys Clark, and Merryn Tawhai. "Further Evidence For The Role Of Hypoxic Pulmonary Vasoconstriction During Bronchoconstriction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2067.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Burrowes, Kelly S., Annalisa J. Swan, Alys R. Clark, et al. "Predicting The Influence Of Hypoxic Pulmonary Vasoconstriction On The Distribution Of Pulmonary Blood Flow." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2304.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Blissenbach, Birgit, Martin Krönke, Tobias Merz, Christos T. Nakas, and Jacqueline Pichler Hefti. "Effects of hypobaric hypoxia on circulating microRNA expression and hypoxic pulmonary vasoconstriction." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa3012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Connolly, Michelle, Jeremy P. T. Ward, and Philip I. Aaronson. "Intracellular Ca2+ In Rat Isolated Pulmonary Artery During Hypoxic Pulmonary Vasoconstriction In The Absence Of Pretone." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6282.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!