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Journal articles on the topic 'Postcapillary venule'
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1
Parazynski, S. E., B. J. Tucker, M. Aratow, A. Crenshaw, and A. R. Hargens. "Direct measurement of capillary blood pressure in the human lip." Journal of Applied Physiology 74, no. 2 (1993): 946–50. http://dx.doi.org/10.1152/jappl.1993.74.2.946.
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In this study, we developed and tested a new procedure for measuring microcirculatory blood pressures above heart level in humans. Capillary and postcapillary venule blood pressures were measured directly in 13 human subjects by use of the servo-nulling micropressure technique adapted for micropuncture of lip capillaries. Pressure waveforms were recorded in 40 separate capillary vessels and 14 separate postcapillary venules over periods ranging from 5 to 64 s. Localization and determination of capillary and postcapillary vessels were ascertained anatomically before pressure measurements. Capillary pressure was 33.2 +/- 1.5 (SE) mmHg in lips of subjects seated upright. Repeated micropunctures of the same vessel gave an average coefficient of variation of 0.072. Postcapillary venule pressure was 18.9 +/- 1.6 mmHg. This procedure produces a direct and reproducible means of measuring microvascular blood pressures in a vascular bed above heart level in humans.
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Kim, Sangho, Aleksander S. Popel, Marcos Intaglietta, and Paul C. Johnson. "Aggregate formation of erythrocytes in postcapillary venules." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (2005): H584—H590. http://dx.doi.org/10.1152/ajpheart.00690.2004.
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The purpose of the present study was to obtain information on erythrocyte aggregate formation in vivo. The movements of erythrocytes in postcapillary venules of the rat spinotrapezius muscle at various flow rates were recorded with a high-speed video camera before and after infusion of dextran 500. To distinguish aggregates, the following criteria were used: 1) a fixed distance (4 μm) between the center points of two adjacent cells, 2) lack of visible separation between the adjacent cells, and 3) movement of the adjacent cells in the same direction. Without dextran 500 infusion, 11 and 5% of erythrocytes formed aggregates in low (33.2 ± 28.3 s) and high pseudoshear (144.2 ± 58.3 s) conditions, respectively, based on the above criteria. After dextran 500 infusion, 53% of erythrocytes satisfied the criteria in the low pseudoshear condition (26.5 ± 17.0 s) and 13% of erythrocytes met the criteria in the high pseudoshear condition (240.0 ± 85.9 s), indicating erythrocyte aggregation is strongly associated with shear rate. Approximately 90% of aggregate formation occurred in a short time period (0.15–0.30 s after entering the venule) in a region 15 to 30 μm from the entrance. The time delay may reflect rheological entrance conditions in the venule.
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Diaz-Flores, Lucio, Ricardo Gutierrez, and Hilda Varela. "Behavior of postcapillary venule pericytes during postnatal angiogenesis." Journal of Morphology 213, no. 1 (1992): 33–45. http://dx.doi.org/10.1002/jmor.1052130105.
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Kim, Sangho, Janet Zhen, Aleksander S. Popel, Marcos Intaglietta, and Paul C. Johnson. "Contributions of collision rate and collision efficiency to erythrocyte aggregation in postcapillary venules at low flow rates." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H1947—H1954. http://dx.doi.org/10.1152/ajpheart.00764.2006.
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Red blood cell aggregation at low flow rates increases venous vascular resistance, but the process of aggregate formation in these vessels is not well understood. We previously reported that aggregate formation in postcapillary venules of the rat spinotrapezius muscle mainly occurs in a middle region between 15 and 30 μm downstream from the entrance. In light of the findings in that study, the main purpose of this study was to test two hypotheses by measuring collision frequency along the length of the venules during low flow. We tested the hypothesis that aggregation rarely occurs in the initial 15-μm region of the venule because collision frequency is very low. We found that collision frequency was lower than in other regions, but collision efficiency (the ratio of aggregate formation to collisions) was almost nil in this region, most likely because of entrance effects and time required for aggregation. Radial migration of red blood cells and Dextran 500 had no effect on collision frequency. We also tested the hypothesis that aggregation was reduced in the distal venule region because of the low aggregability of remaining nonaggregated cells. Our findings support this hypothesis, since a simple model based on the ratio of aggregatable to nonaggregatable red blood cells predicts the time course of collision efficiency in this region. Collision efficiency averaged 18% overall but varied from 0 to 52% and was highest in the middle region. We conclude that while collision frequency influences red blood cell aggregate formation in postcapillary venules, collision efficiency is more important.
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Iwamoto, S., J. Li, T. Omi, S. Ikemoto, and E. Kajii. "Identification of a novel exon and spliced form of Duffy mRNA that is the predominant transcript in both erythroid and postcapillary venule endothelium." Blood 87, no. 1 (1996): 378–85. http://dx.doi.org/10.1182/blood.v87.1.378.378.
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Abstract The Duffy gene has been shown not to be split by introns, even in its 5′ untranslated region, and to be expressed not only in erythroid but in postcapillary venule endothelium of almost every organ in the body. To further investigate the transcriptional start position in erythroid and postcapillary venule endothelium, we performed 5′-rapid amplification of cDNA ends (5′-RACE). While every positive clone of 5′- RACE encoded the identical sequence of previously identified cDNA downstream from nucleotide 203, the upstream sequences were different. The upstream sequences corresponded to the sequence from nucleotide - 279 to -308/-357 in erythroblasts and from -279 to -355/-383 in lung and were regarded as comprising a novel exon. This novel exon encoded seven residues initiated with a methionine, linked to nucleotide 203 in- frame and in agreement with the GT-AG splicing rule. The major erythroid transcriptional start position was identified in human erythroleukemia cells by primer extension and in bone marrow by ribonuclease protection analysis at 34 bases upstream from the first ATG codon. Distinctively, in lung and kidney, the transcription was started at 82 bases upstream from the ATG. Both Northern blotting and reverse transcription-polymerase chain reaction followed by Southern analysis indicated a predominance of the novel spliced form of mRNA of about 50- to 200-fold comparing with the unspliced form, in every studied organ and erythroid lineage cells. The spliced form of cDNA has been transfected into a human erythroleukemic cell line, K562, and the expressed protein reacted with Duffy-specific murine monoclonal antibody Fy6. These studies indicate that the product from the spliced form of mRNA is the major product of the Duffy gene in the erythroid lineage and postcapillary venule endothelium.
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Iwamoto, S., J. Li, T. Omi, S. Ikemoto, and E. Kajii. "Identification of a novel exon and spliced form of Duffy mRNA that is the predominant transcript in both erythroid and postcapillary venule endothelium." Blood 87, no. 1 (1996): 378–85. http://dx.doi.org/10.1182/blood.v87.1.378.bloodjournal871378.
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The Duffy gene has been shown not to be split by introns, even in its 5′ untranslated region, and to be expressed not only in erythroid but in postcapillary venule endothelium of almost every organ in the body. To further investigate the transcriptional start position in erythroid and postcapillary venule endothelium, we performed 5′-rapid amplification of cDNA ends (5′-RACE). While every positive clone of 5′- RACE encoded the identical sequence of previously identified cDNA downstream from nucleotide 203, the upstream sequences were different. The upstream sequences corresponded to the sequence from nucleotide - 279 to -308/-357 in erythroblasts and from -279 to -355/-383 in lung and were regarded as comprising a novel exon. This novel exon encoded seven residues initiated with a methionine, linked to nucleotide 203 in- frame and in agreement with the GT-AG splicing rule. The major erythroid transcriptional start position was identified in human erythroleukemia cells by primer extension and in bone marrow by ribonuclease protection analysis at 34 bases upstream from the first ATG codon. Distinctively, in lung and kidney, the transcription was started at 82 bases upstream from the ATG. Both Northern blotting and reverse transcription-polymerase chain reaction followed by Southern analysis indicated a predominance of the novel spliced form of mRNA of about 50- to 200-fold comparing with the unspliced form, in every studied organ and erythroid lineage cells. The spliced form of cDNA has been transfected into a human erythroleukemic cell line, K562, and the expressed protein reacted with Duffy-specific murine monoclonal antibody Fy6. These studies indicate that the product from the spliced form of mRNA is the major product of the Duffy gene in the erythroid lineage and postcapillary venule endothelium.
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Mayrovitz, H. N. "Leukocyte rolling: a prominent feature of venules in intact skin of anesthetized hairless mice." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 1 (1992): H157—H161. http://dx.doi.org/10.1152/ajpheart.1992.262.1.h157.
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Leukocyte (white blood cell; WBC) rolling in postcapillary venules is a frequently reported phenomenon in the microvasculature of experimental preparations. In most reports where this phenomenon has been systematically studied the confounding effects of various procedures associated with tissue preparation have been present. Thus there is sparse information on the extent of WBC rolling under fairly normal conditions. Here observations and features of this phenomenon in venules in the intact skin microvasculature of the homozygous hairless mouse ear are described. One venule in each of 10 mice was observed and continuously video recorded for 90 min. The parameters determined (mean +/- SD) were diameter, 15.9 +/- 3.1 microns; red blood cell velocity, 359 +/- 227 micron/s; flux of rolling WBCs, 3.2 +/- 2.6/min; velocity of rolling WBCs, 9.6 +/- 1.1 micron/s; systemic WBC count (CWBC), 3,220 +/- 1,072/microliters; and total WBC flux, estimated as the product of CWBC and calculated venule blood flow, 8.5 +/- 3.0/min. Overall, 44.8 +/- 13.8% of the total WBC flux exhibited rolling with a velocity that was 3.6 +/- 2.9% of the red blood cell velocity. During the total 15-h combined observation time, no WBCs were seen to be adherent. These findings establish that in small venules of normal skin, WBC rolling is common, since on the average nearly one of two WBCs delivered to the venule exhibits rolling. Furthermore, because the translational rolling speed is very low, they contribute to the marginated pool, which, according to the present data, might be better termed the “rolling” pool.
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Cooper, Stephanie M., and Milton R. Sims. "Evidence of acute inflammation in the periodontal ligament subsequent to orthodontic tooth movement in rats." Australasian Orthodontic Journal 11, no. 2 (1989): 107–9. http://dx.doi.org/10.2478/aoj-1989-0022.
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Abstract Experimental orthodontic tooth extrusion can result in red cell diapedesis through the PDL vascular wall. Diapedesis is an early sign of acute inflammation. At the ultrastructural level, red cell migration is demonstrated occurring through the endothelial junction of a postcapillary-sized venule. This phenomenon is considered to be indicative of unphysiological tooth loading..
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Mulivor, A. W., and H. H. Lipowsky. "Role of glycocalyx in leukocyte-endothelial cell adhesion." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (2002): H1282—H1291. http://dx.doi.org/10.1152/ajpheart.00117.2002.
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The binding of fluorescently labeled microspheres (FLMs, 0.1-μm diameter) coated with antibody (1a29) to ICAM-1 was studied in postcapillary venules during topical application of the chemoattractant N-formylmethionyl-leucyl-phenylalanine (fMLP). FLM adhesion to endothelial cells (ECs) increased dramatically from 50 to 150 spheres per 100-μm length of venule after superfusion of the mesentery with fMLP and equaled or exceeded levels of leukocyte (WBC) adhesion. Removal of the EC glycocalyx by micropipette infusion of the venule with heparinase increased FLM-EC adhesion to levels attained with fMLP. Subsequent application of fMLP did not increase FLM adhesion further, suggesting that the FLMs saturated all ICAM-1 binding sites. Perfusion with heparinase after suffusion with fMLP significantly increased FLM-EC adhesion above levels attained with fMLP. However, WBC adhesion fell because of possible removal of selectins necessary to maintain WBC rolling at the wall. It is concluded that the glycocalyx serves as a barrier to adhesion and that its shedding during natural activation of ECs may be an essential part of the inflammatory response.
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Joyce, N. C., M. F. Haire, and G. E. Palade. "Contractile proteins in pericytes. I. Immunoperoxidase localization of tropomyosin." Journal of Cell Biology 100, no. 5 (1985): 1379–86. http://dx.doi.org/10.1083/jcb.100.5.1379.
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In these studies we have compared the relative amounts and isoforms of tropomyosin in capillary and postcapillary venule pericytes, endothelial cells, and vascular smooth muscle cells in four rat microvascular beds: heart, diaphragm, pancreas, and the intestinal mucosa. The results, obtained by in situ immunoperoxidase localization, indicate that (a) tropomyosin is present in capillary and postcapillary venule pericytes in relatively high concentration; (b) the tropomyosin content of pericytes appears to be somewhat lower than in vascular smooth muscle cells but higher than in endothelia and other vessel-associated cells; and (c) pericytes, unlike endothelia and other nonmuscle cells, contain detectable levels of tropomyosin immunologically related to the smooth muscle isoform. These results and our previous findings concerning the presence of a cyclic GMP-dependent protein kinase (Joyce, N., P. DeCamilli, and J. Boyles, 1984, Microvasc. Res. 28:206-219) in pericytes demonstrate that these cells contain significant amounts of at least two proteins important for contraction regulation. Taken together, the evidence suggests that pericytes are contractile elements related to vascular smooth muscle cells, possibly involved, as are the latter, in the regulation of blood flow through the microvasculature.
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Taherzadeh, Morteza, Asit K. Das, and John B. Warren. "Nifedipine increases microvascular permeability via a direct local effect on postcapillary venules." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (1998): H1388—H1394. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1388.
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Calcium-channel antagonist drugs are prescribed widely for angina and hypertension. A limiting side effect is edema, which can make heart failure worse. We show that nifedipine, a dihydropyridine-type calcium-channel antagonist, can increase vascular permeability in rat skeletal muscle and skin when injected locally. In nifedipine-injected cremaster muscle, the copper content, used to quantify Monastral blue dye accumulation, was 15.0 ± 2.4 μg/g compared with 5.3 ± 0.7 μg/g in control preparations ( P < 0.05). The injection of nifedipine in rat skin in vivo increased local plasma leakage in injected sites from 5.5 ± 1.1 μl in control sites to 9.9 ± 2.5, 17.0 ± 2.4, 24.3 ± 5.9, and 23.3 ± 5.4 μl in sites injected with 10−10, 10−9, 10−8, or 10−7.2 mol/site, respectively ( P < 0.05 in each case compared with control). Vascular labeling techniques using light microscopy, electron microscopy, and microanalysis show that the microvascular site of leakage is not from capillaries but from postcapillary venules of 12–36 μm in diameter, the same site that controls the edema response in inflammation. Nifedipine can act within the microcirculation to increase the permeability of the postcapillary venule.
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Oliani, Sonia M., Mark J. Paul-Clark, Helen C. Christian, Roderick J. Flower, and Mauro Perretti. "Neutrophil Interaction with Inflamed Postcapillary Venule Endothelium Alters Annexin 1 Expression." American Journal of Pathology 158, no. 2 (2001): 603–15. http://dx.doi.org/10.1016/s0002-9440(10)64002-3.
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Aliyarbayova, Aygun Aliyar, Tamilla Amiraslan Sultanova, Gulnara Huseyn Sadiqova, Nigar Tariyel Guliyeva, Shahla Adalat Huseynova, and Shahana Qazanfar Qurbanova. "HISTOMORPHOLOGICAL EVALUATION OF VENOUS VESSELS IN THE SPINAL GANGLIA. ANIMAL MODEL OF STUDY." Deutsche internationale Zeitschrift für zeitgenössische Wissenschaft 62 (August 19, 2023): 19–27. https://doi.org/10.5281/zenodo.8265663.
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We present the morphological (histological and ultrastructural) peculiarities of venous vessels of spinal ganglia, especially the specific properties of extracapsular vessels under light and electron microscopic study. The research performed on male rat's spinal ganglia. The object of research fixated by intravascular perfusion, then embedded in Epon - Araldite blocks according to general methods accepted in microscopy. Also, from spinal ganglia taken after intra aortal administration of ink solution dissolved in 10% gelatin, prepared blocks. Obtained semithin and total cryostat section investigated under microscopes. The current study demonstrates cellular structure of venous vessels walls, source, formation and direction of venous vessels of spinal ganglia.
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Cameron, J., M. R. Sims, and W. J. Sampson. "Ultrastructural changes in postcapillary-sized venule morphology in aged mouse periodontal ligament." Australasian Orthodontic Journal 17, no. 1 (2001): 8–16. http://dx.doi.org/10.2478/aoj-2001-0002.
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Abstract The aim of this study was to compare the postcapillary-sized venule (PCV) morphology of four young ALCA mice (35 days) and four colony-related aged mice (365 days) using the transmission electron microscope (TEM). Right and left mandibular first molar mesial roots with associated periodontal ligament (PDL) and bony socket, were used for TEM assessment. Five PCV profiles were selected at each 160µm interval, from the alveolar crest to the tooth apex. PCV profile dimensions were measured on standardised micrographs magnified x2900. Age affects were tested using multiple regression analysis. The number of PCV profiles in the tooth third of the PDL was higher in aged mice (p < 0.01) and comprised predominantly apericytic vessels (p < 0.001). The number of PCV profiles increased significantly (p < 0.001) in aged mice in the PDL middle circumferential third halfway down the molar root. Age had no significant affect on PCV diameter. Aged PDL permeability studies are needed to investigate whether the changes in aged PCV profile number are associated with functional modification of the PDL microvasculature.
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Hayden, Melvin R. "The Brain Endothelial Cell Glycocalyx Plays a Crucial Role in the Development of Enlarged Perivascular Spaces in Obesity, Metabolic Syndrome, and Type 2 Diabetes Mellitus." Life 13, no. 10 (2023): 1955. http://dx.doi.org/10.3390/life13101955.
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The brain endothelial cell (BEC) glycocalyx (ecGCx) is a BEC surface coating consisting of a complex interwoven polysaccharide (sweet husk) mesh-like network of membrane-bound proteoglycans, glycoproteins, and glycosaminoglycans (GAGs) covering the apical luminal layer of the brain endothelial cells. The ecGCx may be considered as the first barrier of a tripartite blood–brain barrier (BBB) consisting of (1) ecGCx; (2) BECs; and (3) an extravascular compartment of pericytes, the extracellular matrix, and perivascular astrocytes. Perturbations of this barrier allow for increased permeability in the postcapillary venule that will be permissive to both fluids, solutes, and proinflammatory peripherally derived leukocytes into the perivascular spaces (PVS) which result in enlargement as well as increased neuroinflammation. The ecGCx is known to have multiple functions, which include its physical and charge barrier, mechanical transduction, regulation of vascular permeability, modulation of inflammatory response, and anticoagulation functions. This review discusses each of the listed functions in detail and utilizes multiple transmission electron micrographs and illustrations to allow for a better understanding of the ecGCx structural and functional roles as it relates to enlarged perivascular spaces (EPVS). This is the fifth review of a quintet series that discuss the importance of EPVS from the perspective of the cells of brain barriers. Attenuation and/or loss of the ecGCx results in brain barrier disruption with increased permeability to proinflammatory leukocytes, fluids, and solutes, which accumulate in the postcapillary venule perivascular spaces. This accumulation results in obstruction and results in EPVS with impaired waste removal of the recently recognized glymphatic system. Importantly, EPVS are increasingly being regarded as a marker of cerebrovascular and neurodegenerative pathology.
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Lauridsen, Holly M., Jordan S. Pober, and Anjelica L. Gonzalez. "A composite model of the human postcapillary venule for investigation of microvascular leukocyte recruitment." FASEB Journal 28, no. 3 (2013): 1166–80. http://dx.doi.org/10.1096/fj.13-240986.
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Davis, M. J. "Microvascular control of capillary pressure during increases in local arterial and venous pressure." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (1988): H772—H784. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h772.
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The extent to which capillary hydrostatic pressure might be protected from increases in local arterial and venous pressure was examined in the wing microcirculation of unanesthetized pallid bats (Antrozous pallidus). Arterial inflow and venous outflow pressures to the wing were elevated using a box technique to increase pressure around the body of the animal in steps of 12 mmHg between 0 and +60 mmHg for 3-min periods. During this time, hydrostatic pressure, diameter, and red cell velocity in single microvessels were continuously recorded. All branching orders of arterioles constricted significantly during increases in box pressure (Pb), while capillaries and venules dilated. First-order arteriole and venule pressures increased 1:1 with Pb. Capillary pressures increased by only a fraction of Pb up to +36 mmHg, but at higher Pb, the change in capillary pressure was equivalent to the change in Pb. Calculations of vascular resistance indicate that changes in both pre- and postcapillary resistance in this tissue act to prevent increases in capillary pressure during moderate, but not during large, increases in arterial and venous pressure.
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Bowen, B. R., C. Fennie, and L. A. Lasky. "The Mel 14 antibody binds to the lectin domain of the murine peripheral lymph node homing receptor." Journal of Cell Biology 110, no. 1 (1990): 147–53. http://dx.doi.org/10.1083/jcb.110.1.147.
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Murine and human leukocytes express surface glycoproteins, termed homing receptors (HRs), containing lectin-like, EGF-like (egf), and complement binding-like domains, that apparently endow these cells with the ability to home to peripheral lymph nodes (pln's) by virtue of an adhesive interaction with the pln postcapillary venule endothelium. The murine pln HR was initially characterized with a rat monoclonal antibody, Mel 14, that was specific for the murine form of the receptor. This work demonstrated that Mel 14 blocked the binding of murine lymphocytes to pln endothelium both in vitro and in vivo, a result consistent with the possibility that this monoclonal antibody recognizes a region of the HR that is involved with endothelium recognition and adhesion. In addition, this antibody also blocked the binding to the HR of PPME, a polyphosphomannan carbohydrate known to inhibit lymphocyte-pln endothelium interactions, suggesting that Mel 14 may recognize the lectin domain of the pln HR. Here we show that, while Mel 14 recognized truncated HR containing both the lectin and egf domains, antibody recognition was lost when the lectin domain alone was expressed. Chimeric molecules, in which regions of the lectin domain of the non-Mel 14-reactive human pln HR were replaced with homologous regions of the murine pln HR, demonstrated that the Mel 14 recognition site is within the NH2-terminal 53 amino acids of the lectin domain. These results suggest that the Mel 14 monoclonal antibody recognizes a determinant within the lectin domain of the pln HR whose conformation may be dependent upon the presence of the egf domain. Since Mel 14 efficiently blocks lymphocyte-endothelial interactions, these results support the hypothesis that the pln HR lectin domain may be directly involved with binding of lymphocytes to a carbohydrate ligand on the pln postcapillary venule endothelium.
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Zhang, Lin, Min Zeng, and Bingmei M. Fu. "Inhibition of endothelial nitric oxide synthase decreases breast cancer cell MDA-MB-231 adhesion to intact microvessels under physiological flows." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (2016): H1735—H1747. http://dx.doi.org/10.1152/ajpheart.00109.2016.
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Nitric oxide (NO) at different concentrations may promote or inhibit tumor growth and metastasis under various conditions. To test the hypothesis that tumor cells prefer to adhere to the locations with a higher endothelial NO production in intact microvessels under physiological flows and to further test that inhibiting NO production decreases tumor cell adhesion, we used intravital fluorescence microscopy to measure NO production and tumor cell adhesion in postcapillary venules of rat mesentery under normal and reduced flow conditions, and in the presence of an endothelial nitric oxide synthase (eNOS) inhibitor, NG-monomethyl-l-arginine (l-NMMA). Rats (SD, 250–300 g) were anesthetized. A midline incision (∼2 inch) was made in the abdominal wall, and the mesentery was taken out from the abdominal cavity and spread over a coverslip for the measurement. An individual postcapillary venule (35–50 μm) was first loaded with 4,5-diaminofluorescein diacetate (DAF-2 DA), a fluorescent indictor for NO. Then the DAF-2 intensity was measured for 30 min under a normal or reduced flow velocity, with and without perfusion with MDA-MB-231 breast cancer cells, and in the presence of l-NMMA. We found that tumor cells prefer to adhere to the microvessel locations with a higher NO production such as curved portions. Inhibition of eNOS by l-NMMA attenuated the flow-induced NO production and reduced tumor cell adhesion. We also found that l-NMMA treatment for ∼40 min reduced microvessel permeability to albumin. Our results suggest that inhibition of eNOS is a good approach to preventing tumor cell adhesion to intact microvessels under physiological flows.
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Cai, Bin, Jie Fan, Min Zeng, Lin Zhang, and Bingmei M. Fu. "Adhesion of malignant mammary tumor cells MDA-MB-231 to microvessel wall increases microvascular permeability via degradation of endothelial surface glycocalyx." Journal of Applied Physiology 113, no. 7 (2012): 1141–53. http://dx.doi.org/10.1152/japplphysiol.00479.2012.
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To investigate the effect of tumor cell adhesion on microvascular permeability ( P) in intact microvessels, we measured the adhesion rate of human mammary carcinoma MDA-MB-231, the hydraulic conductivity (Lp), the P, and reflection coefficient (σ) to albumin of the microvessels at the initial tumor cell adhesion and after ∼45 min cell perfusion in the postcapillary venules of rat mesentery in vivo. Rats (Sprague-Dawley, 250–300 g) were anesthetized with pentobarbital sodium given subcutaneously. A midline incision was made in the abdominal wall, and the mesentery was gently taken out and arranged on the surface of a glass coverslip for the measurement. An individual postcapillary venule was perfused with cells at a rate of ∼1 mm/s, which is the mean blood flow velocity in this type of microvessels. At the initial tumor cell adhesion, which was defined as one adherent cell in ∼100- to 145-μm vessel segment, Lp was 1.5-fold and P was 2.3-fold of their controls, and σ decreased from 0.92 to 0.64; after ∼45-min perfusion, the adhesion increased to ∼5 adherent cells in ∼100- to 145-μm vessel segment, while Lp increased to 2.8-fold, P to 5.7-fold of their controls, and σ decreased from 0.92 to 0.42. Combining these measured data with the predictions from a mathematical model for the interendothelial transport suggests that tumor cell adhesion to the microvessel wall degrades the endothelial surface glycocalyx (ESG) layer. This suggestion was confirmed by immunostaining of heparan sulfate of the ESG on the microvessel wall. Preserving of the ESG by a plasma glycoprotein orosomucoid decreased the P to albumin and reduced the tumor cell adhesion.
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Johns, Douglas G., Zhaohui Ao, Robert N. Willette, Colin H. Macphee, and Stephen A. Douglas. "Role of p38 MAP kinase in postcapillary venule leukocyte adhesion induced by ischemia/reperfusion injury." Pharmacological Research 51, no. 5 (2005): 463–71. http://dx.doi.org/10.1016/j.phrs.2004.11.008.
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Vergnolle, Nathalie. "Proteinase-Activated Receptor-2-Activating Peptides Induce Leukocyte Rolling, Adhesion, and Extravasation In Vivo." Journal of Immunology 163, no. 9 (1999): 5064–69. http://dx.doi.org/10.4049/jimmunol.163.9.5064.
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Abstract Proteinase-activated receptor 2 (PAR2) has been suggested to play a role in inflammatory reactions. Because leukocyte-endothelial cell interactions are critical events during inflammatory reactions, and because PAR2 is expressed both on endothelium and leukocytes, we have examined the effects of PAR2-activating peptides (PAR2-APs) on leukocyte rolling and adhesion in mesenteric venules and on leukocyte recruitment into the peritoneal cavity. Using intravital microscopy, leukocyte rolling, flux, and adhesion in rat mesenteric postcapillary venules were quantified. Topical addition of PAR2-APs (10 μM) for 1 min to the superfused venule induced a significant increase in leukocyte rolling and adherence. The increase in leukocyte adherence was not affected by pretreatment with a mast cell stabilizer (sodium cromoglycate) nor by prior degranulation of mast cells with compound 48/80. Nonetheless, both leukocyte rolling and adhesion were completely inhibited by pretreatment with a platelet-activating factor receptor antagonist (WEB 2086). Intraperitoneal injections of a selective PAR2-AP (SLIGRL-NH2) caused a significant increase in leukocyte migration into the peritoneal cavity. The effect of SLIGRL-NH2 on peritoneal leukocyte infiltration was completely inhibited by WEB 2086. These data suggest that PAR2 activation could contribute to several early events in the inflammatory reaction, including leukocyte rolling, adherence, and recruitment, by a mechanism dependent on platelet-activating factor release.
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Lacorre, Delphine-Armelle, Espen S. Baekkevold, Ignacio Garrido, et al. "Plasticity of endothelial cells: rapid dedifferentiation of freshly isolated high endothelial venule endothelial cells outside the lymphoid tissue microenvironment." Blood 103, no. 11 (2004): 4164–72. http://dx.doi.org/10.1182/blood-2003-10-3537.
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Abstract Endothelial cells display remarkable heterogeneity in different organs and vascular beds. Although many studies suggest that tissues “speak” to endothelial cells, endothelial cell diversity remains poorly characterized at the molecular level. Here, we describe a novel strategy to characterize tissue-specific endothelial cell phenotypes and to identify endothelial cell genes that are under the control of the local microenvironment. By comparing post-capillary high endothelial venule endothelial cells (HEVECs), freshly isolated from human tonsils without any cell culture step, with HEVECs cultured for 2 days, we found that HEVECs rapidly lost their specialized characteristics when isolated from the lymphoid tissue microenvironment. Striking changes occurred as early as after 48 hours, with complete loss of the postcapillary venule–specific Duffy antigen receptor for chemokines (DARCs) and the HEV-specific fucosyltransferase Fuc-TVII. DNA microarray analysis identified several other candidate HEV genes that were rapidly down-regulated ex vivo, including type XV collagen, which we characterized as a novel, abundant HEV transcript in situ. Together, our results demonstrate that blood vessel type–specific and tissue-specific characteristics of endothelial cells are under the control of their microenvironment. Therefore, even short-term primary cultures of human endothelial cells may not adequately mimic the differentiated endothelial cell phenotypes existing in vivo.
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Ritter, L. S., and P. F. McDonagh. "Low-flow reperfusion after myocardial ischemia enhances leukocyte accumulation in coronary microcirculation." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 3 (1997): H1154—H1165. http://dx.doi.org/10.1152/ajpheart.1997.273.3.h1154.
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During early reperfusion after myocardial ischemia, the mechanisms responsible for leukocyte accumulation in the heart are unclear. We examined the effects of reducing coronary blood flow during reperfusion on leukocyte accumulation in coronary capillaries and postcapillary venules. Isolated rat hearts were perfused for 30 min and then subjected to 30 min of 37 degrees C, no-flow ischemia. The deposition of fluorescently labeled leukocytes was observed directly in coronary capillaries and venules using intravital microscopy after 5, 20, and 35 min of reperfusion. Blood cell velocity was measured in venules after 5 min of reperfusion (R5), and shear rate (s-1) was calculated. Four groups were studied: nonischemic control (NIC) hearts and postischemic hearts reperfused at full flow (I/R100) and at 50 and 10% of full flow (I/R50 and I/R10, respectively). In I/R100 hearts, there was a significant increase in leukocyte trapping in capillaries compared with the NIC group (R5: 5.7 +/- 0.6 vs. 2.0 +/- 0.4 leukocytes/capillary field, respectively; P < 0.05). However, the increase in leukocyte adhesion to venules was not statistically significant compared with NIC (R5: 3.2 +/- 0.4 vs. 1.5 +/- 0.6 leukocytes/100-micron venule, respectively; P < 0.2). In I/R50 hearts, a further increase in leukocyte accumulation occurred in the capillaries but not in the venules. However, in I/R10 hearts, there was a statistically significant increase in both capillaries (R5: 9.2 +/- 0.8; P < 0.05) and venules (R5: 4.4 +/- 0.5; P < 0.05). When leukocyte margination in coronary venules was examined as a function of venular shear rate, a significant correlation (r = 0.99, P < 0.05) was found. These results suggest that, after ischemia, a reduction in reflow enhances leukocyte trapping in capillaries and that leukocyte adhesion in venules is inversely related to shear rate. Enhanced leukocyte accumulation may in turn increase the leukocyte contribution to early reperfusion injury in the heart.
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Peti-Peterdi, János, Gergely Kovács, Péter Hamar, and László Rosivall. "Hemodynamics of gastric microcirculation in rats." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (1998): H1404—H1410. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1404.
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Recently, we described a novel preparation of rat stomach for vascular micropuncture studies. The aim of the present study was to directly measure basic microvascular parameters along the length of the gastric vasculature. Blood vessels were identified, and intravascular pressure was measured with a servo-null transducer, vessel dimensions with videometry, blood flow with microspheres, and plasma colloid osmotic pressure with an osmometer. When systemic arterial pressure was 100–110 mmHg, intravascular pressures in small arteries, primary, secondary, and tertiary submucosal arterioles, mucosal terminal arterioles, and muscle arterioles were 77.8 ± 2.6, 74.6 ± 2.5, 54.1 ± 1.8, 34.4 ± 1.6, 32.4 ± 1.2, and 30.5 ± 1.4 (SE) mmHg, respectively. Intravascular pressures in collecting veins, secondary and primary submucosal venules, muscle venules, and small veins were 26.6 ± 1.1, 21.8 ± 1.6, 17.1 ± 0.8, 18.2 ± 0.9, and 14.4 ± 0.6 mmHg, respectively. Capillary pressure in the mucosa (28 mmHg), as estimated by interpolation between terminal arteriole and collecting venule pressures, was significantly higher than in the muscle layer (23.6 ± 1.4 mmHg). A total of 155 vessels from 25 animals were sampled. Relative blood flows were 16 ± 3% in the muscle and 84 ± 3% in the mucosa-submucosa. Analysis of filtration forces in these two different capillary beds suggests that gastric mucosal capillaries are primarily a filtering network, whereas muscle capillaries are in fluid balance. Calculated resistance ratios indicate low precapillary but relatively high postcapillary vascular resistance in the gastric mucosa.
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Uz, Zühre, Thomas M. van Gulik, Mehtap D. Aydemirli, et al. "Identification and quantification of human microcirculatory leukocytes using handheld video microscopes at the bedside." Journal of Applied Physiology 124, no. 6 (2018): 1550–57. http://dx.doi.org/10.1152/japplphysiol.00962.2017.
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Leukocyte recruitment and adhesion to the endothelium are hallmarks of systemic inflammation that manifest in a wide range of diseases. At present, no method is available to directly measure leukocyte kinetics at the bedside. In this study, we validate a new method to identify and quantify microcirculatory leukocytes observed by handheld vital microscopy (HVM) using space-time diagram (STD) analysis. Video clips ( n = 59) containing one capillary-postcapillary venule unit where leukocytes could be observed emanating from a capillary into a venule in cardiac surgery patients ( n = 20) were included. STD analysis and manual counting were used to quantify the number of leukocytes (total, rolling, and nonrolling). Pearson’s correlation and Bland-Altman analysis were used to determine agreement between the STDs and manual counting. For reproducibility, intra- and interobserver coefficients of variation (CVs) were assessed. Leukocyte (rolling and nonrolling) and red blood cell velocities were assessed. The STDs and manual counting procedures for the quantification of rolling leukocytes showed good agreement ( r = 0.8197, P < 0.0001), with a Bland-Altman analysis mean difference of −0.0 (−6.56; 6.56). The overall intraobserver CV for the STD method was 1.5%. The overall interobserver CVs for the STD and the manual method were 5.6% and 9.4%, respectively. The nonrolling velocity was significantly higher than the rolling velocity (812 ± 519 µm/s vs. 201 ± 149 µm/s, P = 0.001). STD results agreed with the manual counting procedure results, had a better reproducibility, and could assess the leukocyte velocity. STD analysis using bedside HVM imaging presented a new methodology for quantifying leukocyte kinetics and functions in the microcirculation. NEW & NOTEWORTHY In this study, we introduce space-time diagram analysis of sublingual microcirculation imaging using handheld vital microscopy to identify and quantify the presence and kinetics of human microcirculatory leukocytes. We validated the methodology by choosing anatomical units consisting of a capillary connected to a venule, which allowed precise identification of leukocytes.
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Harris, Norman R. "Reperfusion-induced changes in capillary perfusion and filtration: effects of hypercholesterolemia." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (1999): H669—H675. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h669.
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Fluid filtration rate ( J v/ S) and red blood cell velocity ( V RBC) in individual mesenteric capillaries of normocholesterolemic (NC) and hypercholesterolemic (HC) rats were measured before and after ischemia and reperfusion (I/R). In NC rats, a correlation was found between baseline J v/ Sand the percent of the feeding arteriole length that was paired (<15 μm) with a postcapillary venule (A-V pairing), but not in the HC group. Additionally, in NC rats only, a correlation was found between baseline V RBC and A-V pairing. In capillaries in which A-V pairing was substantial (>20%), V RBCdropped after reperfusion in the HC group (54% of baseline; P < 0.05), but not in the NC group (79%). The decrease in V RBC in HC rats could be attenuated by a P-selectin antibody (PB1.3). PB1.3 was also able to attenuate the increase in I/R-induced capillary J v/ Sin HC rats (median increase = 1.26-fold vs. 1.53-fold without PB1.3). These data suggest a role for A-V pairing in capillary perfusion in NC rats and a potential role for P-selectin in I/R-induced microvascular dysfunction in HC rats.
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Kubo, Hajime, Takashi Fujiwara, Lotta Jussila, et al. "Involvement of vascular endothelial growth factor receptor-3 in maintenance of integrity of endothelial cell lining during tumor angiogenesis." Blood 96, no. 2 (2000): 546–53. http://dx.doi.org/10.1182/blood.v96.2.546.
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Abstract Vascular endothelial growth factor (VEGF) plays a major role in tumor angiogenesis. VEGF-C, however, is thought to stimulate the growth of lymphatic vessels because an expression of its specific receptor, VEGF receptor-3 (VEGFR-3), was demonstrated to be restricted to lymphatic vessels. Here we demonstrate that the inactivation of VEGFR-3 by a novel blocking monoclonal antibody (mAb) suppresses tumor growth by inhibiting the neo-angiogenesis of tumor-bearing tissues. Although VEGFR-3 is not expressed in adult blood vessels, it is induced in vascular endothelial cells of the tumor-bearing tissues. Hence, VEGFR-3 is another receptor tyrosine kinase involved in tumor-induced angiogenesis. Micro-hemorrhage in the tumor-bearing tissue was the most conspicuous histologic finding specific to AFL4 mAb-treated mice. Scanning microscopy demonstrated disruptions of the endothelial lining of the postcapillary venule, probably the cause of micro-hemorrhage and the subsequent collapse of the proximal vessels. These findings suggest the involvement of VEGFR-3 in maintaining the integrity of the endothelial lining during angiogenesis. Moreover, our results suggest that the VEGF-C/VEGFR-3 pathway may serve another candidate target for cancer therapy.
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Kubo, Hajime, Takashi Fujiwara, Lotta Jussila, et al. "Involvement of vascular endothelial growth factor receptor-3 in maintenance of integrity of endothelial cell lining during tumor angiogenesis." Blood 96, no. 2 (2000): 546–53. http://dx.doi.org/10.1182/blood.v96.2.546.014k12_546_553.
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Vascular endothelial growth factor (VEGF) plays a major role in tumor angiogenesis. VEGF-C, however, is thought to stimulate the growth of lymphatic vessels because an expression of its specific receptor, VEGF receptor-3 (VEGFR-3), was demonstrated to be restricted to lymphatic vessels. Here we demonstrate that the inactivation of VEGFR-3 by a novel blocking monoclonal antibody (mAb) suppresses tumor growth by inhibiting the neo-angiogenesis of tumor-bearing tissues. Although VEGFR-3 is not expressed in adult blood vessels, it is induced in vascular endothelial cells of the tumor-bearing tissues. Hence, VEGFR-3 is another receptor tyrosine kinase involved in tumor-induced angiogenesis. Micro-hemorrhage in the tumor-bearing tissue was the most conspicuous histologic finding specific to AFL4 mAb-treated mice. Scanning microscopy demonstrated disruptions of the endothelial lining of the postcapillary venule, probably the cause of micro-hemorrhage and the subsequent collapse of the proximal vessels. These findings suggest the involvement of VEGFR-3 in maintaining the integrity of the endothelial lining during angiogenesis. Moreover, our results suggest that the VEGF-C/VEGFR-3 pathway may serve another candidate target for cancer therapy.
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Cureton, Elizabeth L., Alexander Q. Ereso, Gregory P. Victorino, et al. "Local Secretion of Urocortin 1 Promotes Microvascular Permeability during Lipopolysaccharide-Induced Inflammation." Endocrinology 150, no. 12 (2009): 5428–37. http://dx.doi.org/10.1210/en.2009-0489.
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Abstract Urocortin 1 (Ucn1) is a neuropeptide that regulates vascular tone and is implicated in both the vascular and immune cell-mediated responses to inflammation. The role of Ucn1 in regulating microvascular permeability has not been determined. We hypothesized that local Ucn1 release promotes microvascular permeability and that this effect augments the local gastrointestinal vascular response to lipopolysaccharide (LPS)-induced systemic inflammation. We measured hydraulic (Lp) and macromolecule permeability in mesenteric venules. We show that a continuous infusion of 10−7m Ucn1 in a postcapillary venule increased Lp 2-fold over baseline, as did LPS-induced inflammation. However, simultaneous infusion of Ucn1 and LPS markedly increased Lp by 7-fold. After local knockdown of Ucn1 using RNA interference, infusion of Ucn1 with LPS resulted in return to 2-fold increase, confirming that Ucn1 synergistically augments hydraulic permeability during inflammation. LPS and Ucn1 treatment also resulted in increased numbers of interstitial microspheres, which colocalized with CD31+ immune cells. Ucn1 activity is mediated through two receptor subtypes, CRH-R1 and CRH-R2. CRH-R1 receptor blockade exacerbated, whereas CRH-R2 receptor blockade decreased the LPS-induced increase in Lp. Finally, treatment with the c-JUN N-terminal kinase (JNK) antagonist SP600125 during infusion of LPS, but not Ucn1, decreased Lp. These findings suggest that Ucn1 increases microvascular permeability and acts synergistically with LPS to increase fluid and macromolecule losses during inflammation. Knockdown of endogenous Ucn1 during inflammation attenuates synergistic increases in Lp. Ucn1’s effect on Lp is partially mediated by the CRH-R2 receptor and acts independently of the c-JUN N-terminal kinase signal transduction pathway.
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Cayrol, Corinne, Chrystelle Lacroix, Catherine Mathe, et al. "The THAP–zinc finger protein THAP1 regulates endothelial cell proliferation through modulation of pRB/E2F cell-cycle target genes." Blood 109, no. 2 (2006): 584–94. http://dx.doi.org/10.1182/blood-2006-03-012013.
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Abstract We recently cloned a novel human nuclear factor (designated THAP1) from postcapillary venule endothelial cells (ECs) that contains a DNA-binding THAP domain, shared with zebrafish E2F6 and several Caenorhabditis elegans proteins interacting genetically with retinoblastoma gene product (pRB). Here, we show that THAP1 is a physiologic regulator of EC proliferation and cell-cycle progression, 2 essential processes for angiogenesis. Retroviral-mediated gene transfer of THAP1 into primary human ECs inhibited proliferation, and large-scale expression profiling with microarrays revealed that THAP1-mediated growth inhibition is due to coordinated repression of pRB/E2F cell-cycle target genes. Silencing of endogenous THAP1 through RNA interference similarly inhibited EC proliferation and G1/S cell-cycle progression, and resulted in down-regulation of several pRB/E2F cell-cycle target genes, including RRM1, a gene required for S-phase DNA synthesis. Chromatin immunoprecipitation assays in proliferating ECs showed that endogenous THAP1 associates in vivo with a consensus THAP1-binding site found in the RRM1 promoter, indicating that RRM1 is a direct transcriptional target of THAP1. The similar phenotypes observed after THAP1 overexpression and silencing suggest that an optimal range of THAP1 expression is essential for EC proliferation. Together, these data provide the first links in mammals among THAP proteins, cell proliferation, and pRB/E2F cell-cycle pathways.
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Kanameishi, Shuto, Sachiko Ono, Yuki Honda Keith, Ryota Asahina, Tetsuya Honda та Kenji Kabashima. "Lymphotoxin β receptor signaling mediates the formation of high endothelial venule-like vessels in atopic dermatitis-like skin lesions in mice". Journal of Immunology 208, № 1_Supplement (2022): 48.06. http://dx.doi.org/10.4049/jimmunol.208.supp.48.06.
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Abstract High endothelial venules (HEVs) are specialized blood vessels contribute to the trafficking of lymphocytes into secondary lymphoid organs by expressing a group of L-selectin ligands called peripheral node addressins (PNAd). In lymph nodes (LNs), lymphotoxin β receptor (LTβR) signaling from dendritic cells (DCs) is essential for the formation of HEVs. On the other hand, PNAd+ HEV-like vessels are observed in the skin under certain inflammatory conditions, such as atopic dermatitis (AD). However, the characteristics and the formation mechanism of HEV-like vessels in the inflammatory skin remains unclear. To address these issues, we first identified PNAd+ HEV-like vessels in the skin using a calcipotriol-induced mouse AD model. HEV-like vessels were located in the postcapillary venules abundant in cellular organelles, which were similar to HEVs in LNs. Blockade of LTβR-signaling by administration of LTβR-Fc fusion protein markedly decreased the formation of HEV-like vessels in the AD-like skin. Analysis using published single-cell RNA-seq data of human AD skin revealed that T cells and DCs highly expressed LTB, a gene encoding LTβ. The expression of LTB was highlighted in T cells by RNAscope in both human AD lesions and mouse AD-like skin. The formation of HEV-like vessels in AD-like skin was normal in Ltbfl/flCD11cCre mice, but was partially impaired in Ltbfl/flCD4Cre mice. Collectively, HEV-like vessels in the inflammatory skin show similar characteristics to HEVs in LNs, and LTβR signaling, partly by LTβ from T cells, is responsible for their formation.
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Kishi, Masashi, Hiroshi Tanaka, Akitoshi Seiyama, et al. "Pentoxifylline attenuates reperfusion injury in skeletal muscle after partial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 5 (1998): H1435—H1442. http://dx.doi.org/10.1152/ajpheart.1998.274.5.h1435.
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Leukocytes have been shown to contribute to ischemia-reperfusion injury in skeletal muscle. Pentoxifylline (PTXF), a xanthine-derived phosphodiesterase inhibitor, has received recent attention because of its action on leukocytes. To clarify the effects of PTXF in reperfusion injury, we measured the resting transmembrane potential difference ( E m) and evaluated postcapillary venule microcirculation using intravital microscopy in rat skeletal muscle during ischemia and reperfusion. The infrarenal aorta was clamped for 90 min and then reperfused for 60 min. Persistent depolarization of the resting E m was observed in an ischemia-reperfusion (IR) group and was significantly repolarized in a PTXF group during the reperfusion period. The tissue water content was significantly reduced in the PTXF group, although no difference was noted in the tissue lactate content. Flowing erythrocyte velocity and wall shear rate in the PTXF group were significantly higher than in the IR group during the reperfusion period but without significant differences in vessel diameter and hemoglobin oxygenation. Blood flow measured by laser-Doppler flowmeter was also significantly improved in the PTXF group. Furthermore, the adherent leukocyte count was significantly reduced in the PTXF group during this same period. These results indicate that PTXF attenuated reperfusion-associated membrane injury and tissue edema and that PTXF suppressed leukocyte adhesion and improved hindlimb blood flow during the reperfusion period.
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Hnatjuk, Mychailo, Serhii Konovalenko, Myroslav Kritsak, et al. "MORPHOLOGICAL FEATURES OF THE STRUCTURAL REARRANGEMENT OF THE HEMOMICROCIRCULATORY BED OF THE HEART CHAMBERS IN DIABETES AND POST-RESECTION PULMONARY HYPERTENSION." Clinical anatomy and operative surgery 23, no. 2 (2024): 23–31. http://dx.doi.org/10.24061/1727-0847.23.2.2024.25.
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Damage to the cardiovascular system and diabetes are recognized as the most common global pathologies that often lead to disability and premature death. Foreign and domestic scientists believe that the study of the structure of the human heart and experimental animals are important social, medical and biological directions in connection with the wide spread and growth of cardiovascular diseases and various types of diabetes.Aim. To carry out a morphometric assessment of the features of the structural rearrangement of the hemomicrocirculatory channel of the heart chambers in diabetes and post-resection pulmonary hypertension.Material and methods. The hearts of 48 white male rats, which were divided into three groups, were morphologically studied. The 1st group included 12 intact animals, the 2nd – 12 rats with experimental streptozotocin- induced diabetes, the 3rd – 12 experimental animals with post-resection pulmonary hypertension, the 4th – 12 rats with experimental streptozotocin- induced diabetes and post-resection pulmonary hypertension. The model of experimental diabetes was reproduced by injecting rats with streptozotocin intraperitoneally once at a dose of 50 mg/kg, having previously dissolved it in 0.1 M citrate buff er solution (pH-4.5). Postresection pulmonary hypertension in experimental animals was modeled by right- sided pulmonectomy. Animals were euthanized by bloodletting under thiopental anesthesia 28 days after the start of the experiment. Pieces were cut from the ventricles of the heart, which were fi xed in a 10 % formalin solution, passed through ethyl alcohols of increasing concentration and placed in paraffi n. Microtome sections after depara ffi nization were stained with various dyes. In the left and right ventricles of the heart, the diameters of the studied structures were measured: arterioles, precapillary arterioles, capillaries, postcapillary venules, venules. Quantitative indicators were processed statistically.The results. During the morphological and morphometric studies of the hemomicrocirculatory bed of the ventricles of the heart in conditions of diabetes and post-resection pulmonary hypertension, changes in the quantitative morphological indicators of the elements of the studied heart bed were observed compared to the control ones. The diameter of arterioles of the right ventricle in streptozotocin-i nduced diabetes statistically signifi cantly (p<0.001) decreased by 4.2 %, in post-resection pulmonary hypertension – by 19.9 % (p<0.001), in combined lesions (diabetes and pulmonary hypertension) this morphometric indicator increased respectively – by 30.9 % (р<0.001). It should be noted that the diameter of the hemocapillaries of the right ventricle decreased by 4.7 % with a signifi cant diff erence (p<0.01) in the second group of observations, and by 18.8 % and 30.1 % in post-resection pulmonary arterial hypertension and combined damage. which indicated deterioration of blood supply to the right ventricle.In the simulated experimental conditions, the diameter of the venule of the hemomicrocirculatory channel of the right ventricle of the heart also increased signifi cantly. Thus, in the second studied group of animals (with streptozotocin- induced diabetes), the diameter of the venules was statistically signifi cantly (p<0.001) larger by 3.2 %. In the 3rd experimental group, the diameter of the studied venules of the right ventricle in post-resection pulmonary hypertension changed more. At the same time, the indicated quantitative morphological indicator increased by 16.8 % (р<0.001). In the 4th group of observations (when post-resection pulmonary hypertension is combined with diabetes), the obtained results exceeded the similar control indicator by 24.7 % (р<0.001), which indicated a violation of blood outfl ow in the postcapillary area of the hemomicrocirculatory channel of the right ventricle.Conclusion. Diabetes mellitus and post-resection pulmonary hypertension lead to a pronounced structural rearrangement of the hemomicrocirculatory bed and other structural components of the heart. The detected pathomorphological changes dominated in the right ventricle in post-resection pulmonary hypertension in combination with diabetes.
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Raffetto, Joseph D. "Which dressings reduce inflammation and improve venous leg ulcer healing." Phlebology: The Journal of Venous Disease 29, no. 1_suppl (2014): 157–64. http://dx.doi.org/10.1177/0268355514529225.
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Chronic venous leg ulcers (VLU) affect around 1% of the adult population in the Western world. The impact of VLU is both social and economic, with significant expenditures on active venous ulcers to provide medical treatment and eventual healing. At the core of VLU is venous hypertension which affects the venous macrocirculation. The changes incurred in venous hemodynamics leads to microcirculatory changes affecting the postcapillary venule and surrounding tissues. Inflammation by leukocytes affecting the venous endothelium, promotes a complex cascade and activation of adhesion molecules expression, chemokines and cytokines released, altered growth factor responses, and activation of protease (e.g. tPA) and proteinase (e.g. MMPs) activity that causes dysregulation and compromise of tissue integrity with eventual dermal damage and ulcer development. A critical component to treating VLU is correcting the abnormal venous hemodynamics and compression therapy. Unfortunately, VLU recurrence ranges between 30–70%, and other modalities in therapy along with compression are required. The goal for adjuvant products is to restore the balance from an inflammatory chronic wound to that of a reparative wound that will promote provisional matrix and epithelialization. There are many products on the market that can be used as adjuvant to compression therapy, but it must be recognized that there is a paucity of clinical trials that have evaluated the clinical effectiveness of specific products with clearly defined end points, and most importantly a healed VLU with a low recurrence rate. This review will discuss the fundamentals of VLU inflammation, and evaluate the available literature that may have benefit in reducing inflammation and lead to effective VLU healing.
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Hayden, Melvin R. "A Closer Look at the Perivascular Unit in the Development of Enlarged Perivascular Spaces in Obesity, Metabolic Syndrome, and Type 2 Diabetes Mellitus." Biomedicines 12, no. 1 (2024): 96. http://dx.doi.org/10.3390/biomedicines12010096.
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The recently described perivascular unit (PVU) resides immediately adjacent to the true capillary neurovascular unit (NVU) in the postcapillary venule and contains the normal-benign perivascular spaces (PVS) and pathological enlarged perivascular spaces (EPVS). The PVS are important in that they have recently been identified to be the construct and the conduit responsible for the delivery of metabolic waste from the interstitial fluid to the ventricular cerebrospinal fluid for disposal into the systemic circulation, termed the glymphatic system. Importantly, the outermost boundary of the PVS is lined by protoplasmic perivascular astrocyte endfeet (pvACef) that communicate with regional neurons. As compared to the well-recognized and described neurovascular unit (NVU) and NVU coupling, the PVU is less well understood and remains an emerging concept. The primary focus of this narrative review is to compare the similarities and differences between these two units and discuss each of their structural and functional relationships and how they relate not only to brain homeostasis but also how they may relate to the development of multiple clinical neurological disease states and specifically how they may relate to obesity, metabolic syndrome, and type 2 diabetes mellitus. Additionally, the concept and importance of a perisynaptic astrocyte coupling to the neuronal synapses with pre- and postsynaptic neurons will also be considered as a perisynaptic unit to provide for the creation of the information transfer in the brain via synaptic transmission and brain homeostasis. Multiple electron microscopic images and illustrations will be utilized in order to help explain these complex units.
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Chin, Y. H., J. P. Cai, and X. M. Xu. "Transforming growth factor-beta 1 and IL-4 regulate the adhesiveness of Peyer's patch high endothelial venule cells for lymphocytes." Journal of Immunology 148, no. 4 (1992): 1106–12. http://dx.doi.org/10.4049/jimmunol.148.4.1106.
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Abstract The adhesion of lymphocytes to endothelial cells lining the postcapillary high endothelial venules (HEV) is the first step in their emigration from the bloodstream into lymph nodes and Peyer's patches (PP). We have recently shown that the adhesiveness of cultured rat lymph node and PP HEV cells for thoracic duct lymphocytes can be increased significantly by pretreatment with TNF-alpha, IFN-gamma, and IL-4. In the present study we investigated the role of transforming growth factor-beta 1 (TGF-beta) on the adhesiveness of nonstimulated and cytokine-stimulated PP HEV cells for rat lymphocytes. The results indicated that at picomolar concentrations, TGF-beta significantly (p less than 0.001) decreased the ability of PP HEV cells to adhere 51Cr-labeled rat lymphocytes. Maximal inhibition was observed with a TGF-beta dose of 0.5 ng/ml and an incubation time of 6 to 12 h. TGF-beta did not affect the morphology of HEV cells and had no adverse effect on their viability. Moreover, the decrease in HEV adhesiveness by TGF-beta was reversible, with lymphocyte binding returning to control level 24 h after removal of the cytokine. The specificity of TGF-beta was confirmed by the ability of neutralizing anti-TGF-beta 1 antibody, but not control serum, to abolish the inhibitory properties of the cytokine. In addition, TGF-beta completely abrogated the increased adhesiveness of PP HEV cells normally induced by TNF-alpha or IFN-gamma. In contrast, TGF-beta had no effect on the stimulating effects of IL-4. Moreover, preincubation of PP HEV cells with TGF-beta did not alter the ability of these cells to respond to IL-4. Importantly, the adhesion of rat lymphocytes to IL-4-stimulated PP HEV cells can be blocked by pretreatment of lymphocytes with the PP-homing receptor-specific 1B.2.6 antibody whereas pretreatment of human mononuclear cells with anti-very late activation antigen-4 alpha antibody inhibited only partially the binding of these cells to the IL-4-stimulated PP HEV monolayers. Taken together, these findings strongly suggest that TGF-beta and IL-4 play important regulatory roles in lymphocyte-HEV adhesion and that the stimulatory effect of IL-4 is mediated at least in part through the increased expression of organ-specific ligands on HEV cells.
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Hadley, T. J., Z. H. Lu, K. Wasniowska, et al. "Postcapillary venule endothelial cells in kidney express a multispecific chemokine receptor that is structurally and functionally identical to the erythroid isoform, which is the Duffy blood group antigen." Journal of Clinical Investigation 94, no. 3 (1994): 985–91. http://dx.doi.org/10.1172/jci117465.
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Pappu, Vijay, and Prosenjit Bagchi. "Hydrodynamic interaction between erythrocytes and leukocytes affects rheology of blood in microvessels." Biorheology: The Official Journal of the International Society of Biorheology 44, no. 3 (2007): 191–215. http://dx.doi.org/10.1177/0006355x2007044003003.
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Hydrodynamic interaction between erythrocytes (RBC) and leukocytes (WBC) in a microvessel of size 20–40 micron, typical of a postcapillary venule, is studied using a two-dimensional computational model. The model is based on immersed boundary method, and it takes into consideration the particulate nature of blood by explicitly modeling individual blood cell, and cell deformation. Due to their highly flexible nature, RBC drift away from the wall and toward the center of a vessel creating a cell-free layer. It is shown here that the lateral motion of RBC is strongly affected in presence of a WBC, and is dependent on whether the WBC is non-adherent or firmly adhered. When the WBC is non-adherent, some RBC, depending on their initial radial locations and vessel size, may be deflected closer toward the wall, resulting in a decrease in the cell-free layer. The apparent viscosity of the whole blood containing both RBC and WBC is computed, and shown to be much higher than that containing RBC only. The increased viscosity cannot be accounted for by the contribution due to WBC only. This observation is in agreement with a previous in vivo measurement. Here we show that the additional flow resistance is due to the decrease in the cell-free layer resulting from the WBC-RBC interaction. It can be accounted for by a two-layer model of blood when the reduced values of the cell-free layer thickness are used. When the WBC is firmly adhered, RBC easily move away from the wall, and the cell-free layer is not significantly changed. In such cases, the major contribution to whole blood viscosity comes from the WBC alone. The hydrodynamic interaction between WBC and RBC, though it exists, does not contribute significantly when WBC are adhered.
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Lee, T. C., D. S. Long, and R. J. Clarke. "Effect of endothelial glycocalyx layer redistribution upon microvessel poroelastohydrodynamics." Journal of Fluid Mechanics 798 (June 10, 2016): 812–52. http://dx.doi.org/10.1017/jfm.2016.337.
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The endothelial glycocalyx layer (EGL) is a macromolecular layer that lines the inner surface of blood vessels. It is believed to serve a number of physiological functions in the microvasculature, including protection of the vessel walls from potentially harmful levels of fluid shear, as a molecular sieve that acts to regulate transendothelial mass transport, and as a transducer of mechanical stress from the vessel lumen. To best fulfil some of its roles, it has been suggested that the EGL redistributes, so that it is thickest at the cell–cell junctions. It has also been suggested that the majority of mechanotransduction occurs through the solid phase of the EGL, rather than via its fluid phase. The difficulties associated with measuring the distribution of the EGL in vivo make these hypotheses difficult to confirm experimentally. Consequently, to gauge the impact of EGL redistribution from a theoretical standpoint, we compute the flow through a porous-lined microvessel, the endothelial surface of which has been informed by confocal microscopy images of a postcapillary venule. Following earlier studies, we model the poroelastohydrodynamics of the EGL using biphasic mixture theory, taking advantage of a recently developed boundary integral representation of these equations to solve the coupled poroelastohydrodynamics using the boundary element method. However, the low permeabilities of the EGL mean that viscous effects are confined to thin layers, thereby also enabling an asymptotic treatment of the dynamics in this limit. In this asymptotic regime, we also consider a two-layer Stokes flow model for the lumen flow to approximate the effect of red blood cells within the lumen. We demonstrate that redistribution of the EGL can have a substantial impact upon microvessel haemodynamics. We also confirm that the bulk of the mechanical stress is indeed carried through the solid phase of the EGL.
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Issekutz, T. B. "Effects of six different cytokines on lymphocyte adherence to microvascular endothelium and in vivo lymphocyte migration in the rat." Journal of Immunology 144, no. 6 (1990): 2140–46. http://dx.doi.org/10.4049/jimmunol.144.6.2140.
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Abstract The first step in the migration of lymphocytes out of the blood is adherence of lymphocytes to endothelial cells (EC) in the postcapillary venule. It is thought that in inflammatory reactions cytokines activate the endothelium to promote lymphocyte adherence and migration into the inflammatory site. Injection of IFN-gamma, IFN-alpha/beta, and TNF-alpha into the skin of rats stimulated the migration of small peritoneal exudate lymphocytes (sPEL) into the injection site, and these cytokines mediated lymphocyte recruitment to delayed-type hypersensitivity, sites of virus injection, and in part to LPS. The effect of cytokines on lymphocyte adherence to rat microvascular EC was examined. IFN-gamma, IFN-alpha/beta, IL-1, TNF-alpha, and TNF-beta increased the binding of small peritoneal exudate lymphocyte (sPEL) to EC. IFN-gamma was more effective and stimulated adherence at much lower concentrations than the other cytokines. IL-2 did not increase lymphocyte adherence. LPS strongly stimulated lymphocyte binding. Treatment of EC, but not sPEL, enhanced adhesion, and 24 h of treatment with IFN-gamma and IL-1 induced near maximal adhesion. Lymph node lymphocytes, which migrate poorly to inflammatory sites, adhered poorly to unstimulated and stimulated EC, whereas sPEL demonstrated significant spontaneous adhesion which was markedly increased by IFN-gamma, IL-1, and LPS. Spleen lymphocytes showed an intermediate pattern of adherence. Combinations of IFN-gamma and TNF-alpha were additive in stimulating sPEL-EC adhesion. Depletion of sPEL and spleen T cells by adherence to IFN-gamma stimulated EC decreased the in vivo migration of the lymphocytes to skin sites injected with IFN-gamma, IFN-alpha/beta, TNF-alpha, poly I:C, LPS, and to delayed-type hypersensitivity reactions by 50%, and significantly increased the migration of these cells to normal lymph nodes, as compared to unfractionated lymphocytes. Thus the cytokines and lymphocytes involved in migration to cutaneous inflammation in the rat stimulate lymphocyte adhesion to rat EC in vitro, and IFN-gamma stimulated EC appear to promote the selective adhesion of inflammatory site-seeking lymphocytes.
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Juchem, Gerd, Dominik R. Weiss, Maria Knott, et al. "Regulation of coronary venular barrier function by blood borne inflammatory mediators and pharmacological tools: insights from novel microvascular wall models." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (2012): H567—H581. http://dx.doi.org/10.1152/ajpheart.00360.2011.
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We hypothesized that postcapillary venules play a central role in the control of the tightness of the coronary system as a whole, particularly under inflammatory conditions. Sandwich cultures of endothelial cells and pericytes of precapillary arteriolar or postcapillary venular origin from human myocardium as models of the respective vascular walls (sandwich cultures of precapillary arteriolar or postcapillary venular origin) were exposed to thrombin and components of the acutely activatable inflammatory system, and their hydraulic conductivity ( LP) was registered. LP of SC-PAO remained low under all conditions (3.24 ± 0.52·10−8cm·s−1·cmH2O−1). In contrast, in the venular wall model, PGE2, platelet-activating factor (PAF), leukotriene B4 (LTB4), IL-6, and IL-8 induced a prompt, concentration-dependent, up to 10-fold increase in LP with synergistic support when combined. PAF and LTB4 released by metabolically cooperating platelets, and polymorphonuclear leucocytes (PMNs) caused selectively venular endothelial cells to contract and to open their clefts widely. This breakdown of the barrier function was preventable and even reversible within 6–8 h by the presence of 50 μM quercetin glucuronide (QG). LTB4 synthesis was facilitated by biochemical involvement of erythrocytes. Platelets segregated in the arterioles and PMNs in the venules of blood-perfused human myocardium (histological studies on donor hearts refused for heart transplantation). Extrapolating these findings to the coronary microcirculation in vivo would imply that the latter's complex functionality after accumulation of blood borne inflammatory mediators can change rapidly due to selective breakdown of the postcapillary venular barrier. The resulting inflammatory edema and venulo-thrombosis will severely impair myocardial performance. The protection afforded by QG could be of particular relevance in the context of cardiosurgical intervention.
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Saltzman, Darin J., Andras Toth, Amy G. Tsai, Marcos Intaglietta, and Paul C. Johnson. "Oxygen tension distribution in postcapillary venules in resting skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (2003): H1980—H1985. http://dx.doi.org/10.1152/ajpheart.00322.2002.
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We tested the hypothesis that blood flow is distributed among capillary networks in resting skeletal muscle in such a manner as to maintain uniform end-capillary Po2. Oxygen tension in venules draining two to five capillaries was obtained by using the phosphorescence decay methodology in rat spinotrapezius muscle. For 64 postcapillary venules among 18 networks in 10 animals, the mean Po2 was 30.1 Torr (range, 9.7–43.5 Torr) with a coefficient of variation (CV; standard deviation/mean) of 0.26. Oxygen levels of postcapillary venules within a single network or single animal, however, displayed a much smaller CV (0.064 and 0.094, respectively). By comparison, the CV of blood flow in 57 postcapillary venules of 17 networks in 9 animals was 1.27 with a mean flow of 0.011 ± 0.014 nl/s and a range of 3.7 × 10–4 to 6.5 × 10–2 nl/s. Blood flow of postcapillary venules within single networks displayed a lower CV (mean, 0.51), whereas that in individual animals was 0.78. Results indicate that among venular networks, heterogeneity of oxygen tension is less than that of blood flow and within venular networks the heterogeneity of oxygen tension is much less than that of blood flow. In addition, postcapillary Po2 was independent of flow among venules in which both were measured. Results of this study may be attributable to three factors: 1) O2 diffusion between adjacent capillaries and venules, 2) structural remodeling in regions of lower Po2, and 3) O2-dependent local control mechanisms.
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Kanwar, S., RC Woodman, MC Poon, et al. "Desmopressin induces endothelial P-selectin expression and leukocyte rolling in postcapillary venules." Blood 86, no. 7 (1995): 2760–66. http://dx.doi.org/10.1182/blood.v86.7.2760.2760.
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Abstract Desmopressin, (DDAVP; 1-desamino-8-D-arginine vasopressin) increases the release and activity of von Willebrand factor (vWF); however, its effects on the other major constituent of endothelial Weibel-Palade bodies, P-selectin, has not been investigated. DDAVP-induced P-selectin expression may explain DDAVP's efficacy in bleeding disorders in which vWF levels are normal. Therefore, the objective of this study is to assess the effect of DDAVP on P-selectin expression on endothelial cells of postcapillary venules in vivo and on human umbilical vein endothelium in vitro, and to determine whether DDAVP has direct effects on leukocyte behavior in postcapillary venules. DDAVP (0.1 and 1.0 microgram/mL) induced a significant but transient increase in P-selectin expression on human umbilical vein endothelial cells as well as on rat and human platelets. Immunohistochemical analysis of rat postcapillary venules showed that in contrast to saline, DDAVP injection (1 microgram/kg, intravenous) induced significant endothelial P-selectin expression. DDAVP administration also induced a rapid and significant increase in leukocyte rolling in rat mesenteric venules in vivo. This response was entirely dependent on P-selectin, as an anti-P-selectin antibody rapidly reversed the DDAVP-induced increase in leukocyte rolling. DDAVP induced leukocyte rolling in medium (20 to 40 microns) and large (> 40 microns), but not small (< 20 microns), postcapillary venules. In animals that were treated with DDAVP, there was a steady and significant increase in leukocyte adhesion. This study shows that DDAVP can directly induce P-selectin expression on endothelium in vitro and in vivo and that the latter response is capable of supporting prolonged leukocyte rolling in rat postcapillary venules.
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Kanwar, S., RC Woodman, MC Poon, et al. "Desmopressin induces endothelial P-selectin expression and leukocyte rolling in postcapillary venules." Blood 86, no. 7 (1995): 2760–66. http://dx.doi.org/10.1182/blood.v86.7.2760.bloodjournal8672760.
Full textAbstract:
Desmopressin, (DDAVP; 1-desamino-8-D-arginine vasopressin) increases the release and activity of von Willebrand factor (vWF); however, its effects on the other major constituent of endothelial Weibel-Palade bodies, P-selectin, has not been investigated. DDAVP-induced P-selectin expression may explain DDAVP's efficacy in bleeding disorders in which vWF levels are normal. Therefore, the objective of this study is to assess the effect of DDAVP on P-selectin expression on endothelial cells of postcapillary venules in vivo and on human umbilical vein endothelium in vitro, and to determine whether DDAVP has direct effects on leukocyte behavior in postcapillary venules. DDAVP (0.1 and 1.0 microgram/mL) induced a significant but transient increase in P-selectin expression on human umbilical vein endothelial cells as well as on rat and human platelets. Immunohistochemical analysis of rat postcapillary venules showed that in contrast to saline, DDAVP injection (1 microgram/kg, intravenous) induced significant endothelial P-selectin expression. DDAVP administration also induced a rapid and significant increase in leukocyte rolling in rat mesenteric venules in vivo. This response was entirely dependent on P-selectin, as an anti-P-selectin antibody rapidly reversed the DDAVP-induced increase in leukocyte rolling. DDAVP induced leukocyte rolling in medium (20 to 40 microns) and large (> 40 microns), but not small (< 20 microns), postcapillary venules. In animals that were treated with DDAVP, there was a steady and significant increase in leukocyte adhesion. This study shows that DDAVP can directly induce P-selectin expression on endothelium in vitro and in vivo and that the latter response is capable of supporting prolonged leukocyte rolling in rat postcapillary venules.
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Ichimura, Hideo, Kaushik Parthasarathi, Andrew C. Issekutz, and Jahar Bhattacharya. "Pressure-induced leukocyte margination in lung postcapillary venules." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 3 (2005): L407—L412. http://dx.doi.org/10.1152/ajplung.00048.2005.
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Although pressure elevation in lung postcapillary venules increases endothelial P-selectin expression, the extent to which P-selectin causes lung leukocyte margination remains controversial. To address this issue, we optically viewed postcapillary venules of the isolated blood-perfused rat lung by real-time fluorescence imaging. To determine leukocyte margination in single postcapillary venules, we quantified the fluorescence of leukocytes labeled in situ with rhodamine 6G (R6G). Although baseline fluorescence was sparse, a 10-min pressure elevation by 10 cmH2O markedly increased R6G fluorescence. Both stopping blood flow during pressure elevation and eliminating leukocytes from the perfusion blocked the fluorescence increase, affirming that these fluorescence responses were attributable to pressure-induced leukocyte margination. A P-selectin-blocking MAb and the L- and P-selectin blocker fucoidin each inhibited the fluorescence increase, indicating that P-selectin was critical for inducing margination. Time-dependent imaging of blood-borne fluorescent beads revealed reduction of plasma velocity during pressure elevation. After pressure returned to baseline, a similar reduction of plasma velocity, established by manually decreasing the perfusion rate, prolonged margination. Our findings show that in lung postcapillary venules, the decrease in plasma velocity critically determines pressure-induced leukocyte margination.
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Wynne, Susan E., Laurence J. Walsh, and Gregory J. Seymour. "Specialized Postcapillary Venules in Human Gingival Tissue." Journal of Periodontology 59, no. 5 (1988): 328–31. http://dx.doi.org/10.1902/jop.1988.59.5.328.
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Taherzadeh, M., and JB Warren. "Nifedipine Induced Oedema Forms via Postcapillary Venules." Clinical Science 92, s36 (1997): 9P. http://dx.doi.org/10.1042/cs092009pb.
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Kadyrovich, Khaidarov Nodir, Shomurodov Kahramon Erkinovich, and Kamalova Malika Ilhomovna. "Microscopic Examination Of Postcapillary Cerebral Venues In Hemorrhagic Stroke." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 08 (2021): 69–73. http://dx.doi.org/10.37547/tajmspr/volume03issue08-11.
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Hemorrhagic stroke among acute cerebral circulatory disorders is characterized by severe neurological complications and the need to choose between surgical intervention or therapeutic therapy. According to the World Health Organization (WHO)". Globally, stroke deaths will reach 7.8 million by 2030 unless an aggressive global response to the epidemic is put in place" 1. Subarachnoid haemorrhage, which accounts for half of the non-traumatic intracerebral haemorrhage, affects the most active and able-bodied population. The most important medical and social objectives are to monitor the course of the disease from the first hours after the onset of stroke, to prescribe adequate treatment in a timely manner, and to reduce mortality and disability rates [5,9].
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Cooper, Dianne, Janice Russell, Keith D. Chitman, Matthew C. Williams, Robert E. Wolf, and D. Neil Granger. "Leukocyte dependence of platelet adhesion in postcapillary venules." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (2004): H1895—H1900. http://dx.doi.org/10.1152/ajpheart.01000.2003.
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Reperfusion of ischemic tissues results in development of a proinflammatory, prothrombogenic phenotype, culminating in the recruitment of leukocytes and platelets within postcapillary venules. Recent studies have indicated an interdependence of platelet and leukocyte adhesion, suggesting that heterotypic blood cell interactions may account for postischemic platelet recruitment. The objectives of this study were to 1) determine whether ischemia-reperfusion (I/R)-induced platelet recruitment is leukocyte dependent and 2) quantify the contributions of leukocytes and endothelial cells in this platelet recruitment. Intravital microscopy was used to monitor the recruitment of fluorescently labeled platelets in postcapillary venules of the small intestine after 45-min ischemia and 4-h reperfusion. To assess the leukocyte dependence of platelet adhesion, platelets from wild-type mice were infused into mice deficient in neutrophils and/or lymphocytes and mice deficient in key leukocyte adhesion molecules (CD18 and ICAM-1). These antileukocyte strategies resulted in significantly reduced platelet recruitment. Simultaneous visualization of platelets and leukocytes enabled quantification of leukocyte-dependent and endothelium-dependent platelet adhesion. It was observed that in wild-type animals 74% of I/R-induced platelet adhesion was a result of platelet-leukocyte interactions. Although the majority of adherent platelets were associated with leukocytes, <50% of adherent leukocytes were platelet bearing, suggesting that not all adherent leukocytes support platelet adhesion. These results are consistent with leukocytes playing a major role in supporting I/R-induced platelet adhesion.