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PubMed2005

Sheathotomy without separation of venule overlying arteriole at occlusion site in uncommon branch retinal vein occlusion.

Two cases of uncommon branch retinal vein occlusion (BRVO) with vein overlying artery at occlusion site that can be found in less than 1% who underwent retinal venule sheathotomy without separation of retinal vessel for decompression of BRVO were reported. Both patients had macular hemorrhage, edema, and area of macular capillary nonperfusion. Visual acuity (VA) worsened to 6/60 in both cases. The retinal venules were dissected around the crossing site without separation of retinal vessels. Intraoperative dilation, pulsation and restoration of downstream blood flow of the involved venules were observed. In the first patient, at 1 day, 2 weeks, and 6 weeks postoperatively, VA improved to 6/36, 6/9, and 6/6, respectively, and remained unchanged at 12 months postoperatively. In the second patient, VA improved to 6/24 on the first day postoperatively and improved to 6/18 at 1 week follow up and continuously improved to nearly normal at 2 months postoperatively then patient lost contact. Postoperative fundus fluorescein angiogram showed dilated and improved perfusion with decreased macular edema in both cases. Optical coherent tomography confirmed remarkable reduction of retinal thickness (from 874 microns preoperatively to 420 microns at 1 week postoperatively) in the second patient. Retinal venule sheathotomy without separation of retinal vessel for decompression of BRVO with venule overlying arteriole at occlusion site could be effective for improving VA and decreased macular edema.

Adult↗
PubMed1992

Behavior of postcapillary venule pericytes during postnatal angiogenesis.

Autogeneic bone marrow was implanted into an artificially created cavity in a segment of rat sciatic nerve, after removal of nerve fascicles, without damaging the epineurium or surrounding microcirculation. Under these conditions, the bone marrow induces capillary growth and forms granulation tissue from surrounding tissues, the behavior of pericytes being studied in the preformed (preexisting) postcapillary venules of the latter. Beginning 20 h after bone marrow implantation, the pericytes of the preexisting postcapillary venules hypertrophy, with shortening of their processes, prominent nucleoli, dispersal of ribosomes into their free form, fragmentation of basal lamina, and increased DNA synthesis. The number of contact surfaces between pericytes and endothelium is noticeably lower than in controls. Many pericytes are in mitosis. Cells with a shape transitional between pericytes and interstitial fibroblast-like cells appear. In some cases, Monastral Blue (MB) was used as a marker of the cells in preexisting venule walls of the graft bed. In the earlier stages of the experiment, the MB labelling is restricted to the cytoplasm of pericytes and endothelial cells of postcapillary venules, and to the macrophages that occur in the space between pericytes and endothelium. Furthermore, the marker continues to be observed, at a later stage, in some of the following cells: pericytes and endothelial cells of the newly formed vessels, macrophages migrating into the interstitium, transitional cells between pericytes and fibroblasts, and typical fibroblasts of the granulation tissue. The present study provides greater evidence that preformed microvasculature pericytes are substantially activated during postnatal angiogenesis and granulation tissue formation, suggesting that they may contribute to the origin of new pericytes and fibroblasts.

Aging↗
PubMed1979

Effect of gonadectomy and oestrogen administration on the response of lymph-node post-capillary venules to infection with Toxoplasma gondii.

The effects of gonadectomy and oestrogen administration on the response of lymph-node post-capillary venules to infection with Toxoplasma gondii have been studied in mice. The endothelial cells of the post-capillary venules were significantly higher in the female than in the male controls. Oophorectomy had no significant effect while orchidectomy increased the height of the cells. However, hexoestrol administration resulted in a rise of the height to maximum levels in the female and in the male gonadectomised animals. The endothelial cells of male and female control and gonadectomised mice were higher after infection with Toxoplasma while in the infected hexoestrol-treated animals, lower cells were seen. The number of lymphocytes passing through the post-capillary venule wall was increased by gonadectomy and decreased by hexoestrol administration in both sexes. The same pattern was seen in the infected groups. The influence of sex hormones on the post-capillary venules and its possible contribution to the differences seen in the immune response between the two sexes is discussed.

Animals↗
PubMed1979

An electron microscopic study of the changes induced by oestrogens on the lymph-node post-capillary venules.

The changes induced in the lymph-node post-capillary venules of male and female mice, 1, 2, 4, 7, 10 and 14 days after oestrogen administration were studied in 1 micron sections and with the electron microscope. The endothelial cells of the post-capillary venules are higher in female than in male control mice. On the first and second days after Hexoestrol administration there is an increase in the number of ribosomes and polyribosomes lying free in the cytoplasm of the endothelial cells. These cells were significantly increased in height between day 2 and day 7, in both male and female Hexoestrol-receiving mice, remaining at high levels thereafter. The increase in height was accompanied by an increase in the Golgi elements which occupied the major part of the cytoplasm of the endothelial cells. Lysosomes, multivesicular bodies and signs of phagocytosis were more often seen. In contrast, the numbers of lymphocytes passing through the post-capillary venule wall were significantly decreased, probably due to a direct effect of Hexoestrol on the thymus. The relation of an oestrogenic effect on the ultrastructure of the post-capillary venules to the sex differences seen in the immune response is discussed. The possibility that this may constitute a part of a general oestrogenic effect on the reticuloendothelial system is also considered.

Animals↗
PubMed1993

Influence of dextrans on platelet distribution in arterioles and venules.

Dextrans bind to the surface of platelets, red blood cells and endothelium. We investigated whether a low doses (30 mg/kg IV) of 40-kDa (Dx40), neutral, 500-kDa (Dx500) or sulphated, 500-kDa (Dx500S) dextrans influence platelet distribution in rabbit mesenteric arterioles and venules (diameter 17-33 microns). Intravital fluorescence videomicroscopy was used to visualize platelets labelled in vivo with acridine red. Their concentration distribution determined within a thin optical section about the median vessel plane was expressed relative to the mean concentration in that vessel. In arterioles, Dx500 and Dx500S increased the relative platelet concentration in the centre [radial position (R): 0.0-0.4 R] from 0.60 to 1.07 (P < 0.001) and 1.20 (P < 0.003), and reduced it near the wall (0.8-0.9 R) from 1.59 to 0.93 (P < 0.02) and 0.95 (P < 0.03) respectively. In venules a similar, but non-significant, effect was observed. Dx40 did not change platelet distribution in arterioles, but decreased their concentration in venules in the centre from 1.08 to 0.71 (P < 0.03) and increased it at the wall from 0.89 to 1.27 (P < 0.04). The deformability of red blood cells was unchanged, but their aggregation tendency increased approximately two-fold after Dx500 and Dx500S injection, while Dx40 had no influence. Leucocyte margination in venules did not affect platelet distribution. Dextran injection did not change microvascular flow velocity or plasma viscosity, suggesting that the observed changes in arteriolar platelet distribution were caused by binding of dextran to the surface of platelets and/or red blood cells.

Animals↗
PubMed1992

Effects of SC-41930 on leukocyte adherence and emigration in rat mesenteric venules.

This study demonstrates that SC-41930, 7-[3-(4-acetyl-3-methoxy-2-propylphenoxy)-propoxy]-3,4-dihydro-8-p ropyl-2H-1-benzopyran-2-carboxylic acid, an orally active LTB4 receptor antagonist, reduces LTB4-induced leukocyte adhesion and emigration in rat mesenteric venules. The mesentery of Sprague-Dawley rats was prepared for intravital microscopic examination and venules of 25-35 microns were chosen for evaluation. In control animals, LTB4 (20 nM) was superfused over the mesentery for 30 min. In the treatment group SC-41930 (5 microM) was superfused for 30 min, followed by a 30 min superfusion with SC-41930 and LTB4. The LTB4-induced increase in leukocyte adherence and emigration in postcapillary venules was significantly attenuated by pretreatment with SC-41930. Other experiments demonstrated that platelet-activating-factor-induced leukocyte adherence was not affected by SC-41930. These results indicate that SC-41930 is a potent inhibitor of LTB4-induced leukocyte-endothelial cell adhesive interactions in postcapillary venules.

Animals↗
PubMed1989

Anti-high endothelial venule monoclonal antibody HECA-452 recognizes plasmacytoid T cells and delineates an "extranodular" compartment in the reactive lymph node.

So-called plasmacytoid T cells represent a subset of monocyte related cells, which share with endothelium the CD36+ CD11b- (OKM5+ OKM1-) phenotype. The reactivity of plasmacytoid T cells with rat monoclonal antibody HECA-452, highly specific for high endothelial venules, was analyzed in reactive lymph nodes. In all cases, HECA-452 not only labelled the endothelium of high endothelial venules, but also strongly reacted with singular and clustered plasmacytoid T cells. The HECA-452 positivity for high endothelial venules and plasmacytoid T cells visualized a lymph node compartment extending from the subcapsular sinus to the corticomedullary junction. This compartment surrounded the composite nodule and was designated the "extranodular" compartment. The co-occurrence of plasmacytoid T cells and high endothelial venules in this extranodular compartment, together with their immunophenotypical similarities, may be indicative of functional co-operations.

Antibodies, Monoclonal↗
PubMed2003

Role of Rho kinase and actin filament in the increased vascular permeability of skin venules in rats after scalding.

OBJECTIVE: To investigate the role of the Small GTPase Rho and endothelial cytoskeleton in the increased vascular permeability of rat skin after scalding. METHODS: Rats were subjected to scalding local ventral skin and a venule was isolated from scalded skin and cannulated by micropipette. The venular permeability was measured with a fluorescence ratio technique and expressed with the permeability coefficient to albumin (P(a)). The venular F-actin filaments were observed by staining with rhodamine phalloidin and laser confocal scanning microscopy. A specific Rho kinase inhibitor Y-27632 was added into vessel bathing solution or preincubated with vessels to evaluate the role of Rho kinase in regulating of vascular barrier function. RESULTS: Scalding increased P(a) value of skin venule about threefold compared to normal skin venules (P<0.01) and was maintained for 120 min. Inhibition of Rho kinase with Y-27632 (30 micromol/l in low-concentration group; 60 micromol/l in high-concentration group) significantly attenuated the hyperpermeability responses to scalding in a dose dependent fashion. A prominent peripheral actin rim (PAR) existed at the outer area of endothelial cells and apparently delineated the cell-to-cell borders. In the control group, the PARs were arranged smoothly and fairly continuously. However, occasionally PARs did show focal interruption with focal fluorescein isothiocyanate (FITC)-albumin leakage. In the burned group, PARs were less organized and accompanied by a large amount of FITC-albumin leakage. Inhibition of Rho kinase with Y-27632 dramatically reduced P(a) value with recovery of actin filament arrangement in venule after scalding. CONCLUSION: Burn leads to dermal venular permeability increase with endothelial cytoskeleton depolymerization and disruption. Rho signal transduction pathway is involved in these responses.

Actins↗
PubMed1978

Open junctions in the endothelium of the postcapillary venules of the diaphragm.

We have previously established that approximately 30% of the endothelial junctions in the pericytic venules of the mouse diaphragm are open to a gap of approximately 30--60 A, and are fully permeated by hemeundecapeptide (H11P) (mol diam approximately 20 A). To estimate the size limit for molecules that can permeate these junctions, we have administered graded tracers intravenously and studied their behavior at the level of pericytic venules in bipolar microvascular fields (BMFs) in the mouse diaphragm. Horseradish peroxidase (HRP) (mol diam approximately 50 A) permeated only approximately 50% of the open junctions of the venular endothelium. Outflow through venular junctions appeared to be modest since the tracer remained restricted to the perivenular spaces. Hemoglobin (Hb, mol diam 64 x 55 x 50 A) permeated only a few (less than 5%), and ferritin (mol diam 110 A), practically none, of the endothelial junctions of the pericytic venules. The findings suggest that under normal conditions the size limit for permeant molecules for open venular junctions is approximately 60 A. Replicas of freeze-fracture preparations from appropriate regions in BMF showed that the intercellular junctions of the venular endothelium have the same organization as previously described for the corresponding segments of the microvasculature in the omentum and mesentery: discontinuous creases or grooves either free of or marked by few intramembrane particles only. Administration of histamine (topically or systemically) and 5-hydroxytryptamine (5-HT) (topically) resulted in typical focal separations of the endothelial junctions and intramural deposits of large tracer particles (carbon black) in the postcapillary venules.

Animals↗
PubMed1993

Effects of Ruscus extract on the internal diameter of arterioles and venules of the hamster cheek pouch microcirculation.

In the present study, we investigated (a) the effects of the extract of Ruscus aculeatus, which is used to increase peripheral venous tone, on the diameter of arterioles (ID range 10-70 microns) and venules (ID range 20-135 microns) of hamster cheek pouch microvasculature in vivo and (b) the influence of temperature on the observed effects. For microcirculatory measurements, the preparations were placed under an intravital microscope and coupled to a closed-circuit TV (ccTV) system. The TV monitor display was used to obtain arteriolar and venular ID recordings (always at the same site) by an image shearing device. For systemic intravenous (i.v.) administration, the measurements were performed every 10 min, before (control) and after injection of the extract (5 mg/kg). During topical application, the extract was tested, in different concentrations, at 25 degrees, 36.5 degrees, and 40 degrees C. Systemic i.v. administration of Ruscus extract evoked venular constriction and did not affect the arteriolar diameter or mean arterial pressure (MAP). Topical application of Ruscus extract elicited concentration- and temperature-dependent responses in the vessels. At 25 degrees C, arterioles and venules dilated; at 36.5 degrees C, the arterioles remained unchanged while the venules constricted, and at 40 degrees C, the arterioles remained unchanged or constricted depending on the concentration used while the venules further constricted. The effects of Ruscus extract observed in vivo at the microcirculatory level further support the data previously reported on larger vessels and on patients with venous insufficiency.

Administration, Topical↗
PubMed1991

Blood vessels in human immunodeficiency virus-related lymphoadenopathy: high endothelial venules and lymphocyte migration.

The vasculature of 25 lymph nodes of patients with human immunodeficiency virus-related lymphadenopathy was investigated morphometrically. The number of small vessels, the morphological features of high endothelial venules and the migratory index of the lymphocytes passing through the high endothelial venules, as well as the stage-dependent change of each parameter, were analysed. Twenty reactive lymph nodes served as controls. The total number of vessels in the HIV-infected lymph nodes was relatively stable. However, the small vessels with flat endothelium increased in number, while the number of high endothelial venules decreased as the disorder progressed, and the decrease in the lymphocyte migration seemed to precede the change in the morphology of high endothelial venules. The presumptive role of these alterations in the pathogenesis of the investigated disorder is emphasized.

AIDS-Related Complex↗
PubMed1985

Electrical resistance of arterioles and venules in the hamster cheek pouch.

The electrical resistance of the vascular endothelium was determined on single microvessels in the hamster cheek pouch in order to obtain information about this variable in a mammalian preparation. So far, the technique has only been applied to frog microvessels. The technique consists of injection of current into the vascular lumen via a microelectrode and recording of the ensuing intravascular potential distribution by a second microelectrode. Cable theory was used for the analysis. The average diameter of the vessels under study was 41 micron for arterioles and 28 micron for venules. The average resistance of the vessel wall at 37 degrees C was 19 omega cm2 and 3.3 omega cm2, respectively. For the venules this is somewhat lower than what has been recorded on muscle capillaries (Olesen & Crone 1983) in the frog at room temperature, whilst the values on arterioles are rather similar. The calculated sodium permeabilities, PNa+, were for arterioles 4 X 10(-5) cm X s-1 and for venules 23 X 10(-5) cm X s-1. The high permeability values for arterioles and venules indicate that the vascular exchange function may not be limited to capillaries only.

Action Potentials↗
PubMed1993

The influence of vasopressin on the arterioles and venules of skeletal muscle of the rat during systemic hypoxia.

1. In rats anaesthetized with Saffan, the spinotrapezius muscle was prepared for in vivo microscopy. Systemic hypoxia (breathing 8% O2 for 3 min) induced a fall in arterial pressure and tachycardia, together with constriction in some arterioles and venules of each section of the vascular tree and dilatation in others. 2. The vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)-arginine vasopressin (20 mg kg-1 I.V.) preferentially attenuated constrictor responses induced by hypoxia in both arterioles and venules, but had no significant effect on the dilator responses. Analysis of responses in individual sections of the vascular tree suggested that the V1-receptor antagonist reduced hypoxia-induced constrictor responses in proximal arterioles (> 13 microns diameter) though not in terminal arterioles (< 13 microns), but reduced hypoxia-induced constrictor responses in both the proximal and distal venules (9-130 microns). 3. Infusion of vasopressin at 1.4, 2.8, 5.7 and 11.4 ng min-1 kg-1 i.v. for 3 min, expected to produce plasma concentrations within the range 28-228 pg ml-1, evoked rises in arterial pressure together with decreases in heart rate. There was also vasoconstriction in the proximal arterioles of spinotrapezius that was graded with vasopressin concentration (5-35% decrease in diameter). 4. Infusion of vasopressin at 1.4 mg min-1 kg-1 i.v. for 3 min with the intention of producing a plasma concentration likely to be reached or exceeded during 8% O2, evoked constriction of all proximal arterioles, though not of terminal arterioles, and constriction of all venous vessels. The magnitude of the constriction induced by vasopressin in vessels that dilated during hypoxia was just as great as in those that constricted during hypoxia. 5. We propose that vasopressin released during systemic hypoxia exerts a constrictor influence upon the proximal arterioles and all sections of the venous tree of skeletal muscle. In individual arterioles and venules the constrictor influence of vasopressin and catecholamines may be overcome by the influence of locally released vasodilator metabolites.

Animals↗
PubMed2004

The protein kinase MEK1/2 mediate vascular endothelial growth factor- and histamine-induced hyperpermeability in porcine coronary venules.

Mitogen-activated protein kinases (MAPKs) have been implicated in the signal transduction of the endothelial response to growth factors and inflammatory stimuli. The objective of this study was to test the hypothesis that the p42/44 MAPK pathway plays a common role in mediating the microvascular hyperpermeability response to vascular endothelial growth factor (VEGF) and histamine. The apparent permeability coefficient of albumin was measured in isolated and perfused coronary venules. Application of VEGF induced a rapid increase in venular permeability, and the effect was blocked by PD98059 and UO126, selective inhibitors of the mitogen-activated protein kinase kinase MEK1/2, in a dose-dependent pattern. The same MEK1/2 inhibitors dose-dependently attenuated the increase in venular permeability caused by histamine. In addition, the increases in venular permeability caused by agents that are known to activate the nitric oxide pathway, including the calcium ionophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase G activator 8-bromo-cGMP, were significantly attenuated in venules pretreated with the MEK1/2 inhibitors. Furthermore, transfection of venules with active MEK1 increased baseline permeability. In contrast, transfection of active ERK1, a downstream target of MEK1/2, did not significantly alter the basal permeability of venules. Moreover, inhibition of ERK1/2 with a specific inhibiting peptide did not prevent the hyperpermeability response to VEGF or histamine. The results suggest that activation of MEK1/2 may play a central role in the signal transduction of microvascular hyperpermeability in response to growth factors and inflammatory mediators.

Animals↗
PubMed2006

A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion.

The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in four different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thickness-to-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules.

Animals↗
PubMed1987

Rat venule mechanical characteristics during venous pressure elevation.

The purpose of this study was to compare the in vivo mechanical characteristics during venous pressure elevation of two sizes of venules in the intestinal muscularis of anesthetized Wistar rats. The two venules studied were the first-order venule (1V), ID = 71.2 +/- 3.3 microns [12] (means +/- SE [n]) and the small collecting vein (SCV), ID = 134.4 +/- 9.1 microns [12]. Vessel diameters and servonull pressures were measured as venous pressure was elevated with a snare about the vein of the isolated segment. The distension characteristics of the two vessels were significantly different, with the 1V evidencing greater strains (percent change from control diameter) and in vivo distensibilities [D = (delta lumen area/lumen area)/delta pressure] than the SCV at all pressure elevations above control. The 1V and SCV mean wall elastic moduli (calculated using Rhodin's measurements of venule control wall thickness) reflected these differences: the initial 1V wall Young's modulus was low and changed little during the vessel distension, whereas the SCV modulus was greater at control and increased sharply with strain in a nonlinear fashion. Although a portion of these differences can be attributed to different initial hoop wall stress levels, the SCV elastic modulus was significantly greater than the 1V modulus at comparable levels of wall stress. Both active and passive factors may contribute to these in vivo differences in elastic modulus, but this experiment does not distinguish between them.

Animals↗
PubMed1987

Venule distension properties in Wistar, Wistar-Kyoto, and spontaneously hypertensive rats.

The purpose of this study was to determine whether venule distension characteristics are modified in denervated venules in the spontaneously hypertensive rat (SHR) during the developmental stage of hypertension. The distension of denervated first-order venules (1V) and small collecting veins (SCV) in the intestine of 7- to 8-wk-old SHR, Wistar-Kyoto (WKY), and Wistar rats were measured with intravital microscopy during venous pressure elevation. Diameter strain and distensibility were calculated for the 1V and SCV from vessel diameter and servo-null pressure. The Wistar 1V underwent larger strains and distensibilities than the WKY or SHR vessels, which had similar characteristics. For the SCV, the Wistar and WKY strains and distensibilities were similar, with the SHR different from these at only certain pressure elevations. Thus no consistent patterns of altered distension characteristics were found in denervated SHR SCV or 1V compared with its controls. This study does not distinguish between changes in local active and passive factors in the vessel wall which may influence distension. Our results may be consistent with disease mechanisms in the 7- to 8-wk-old SHR which leave these local factors unchanged or with mechanisms which have local venular effects that counterbalance each other, leaving the distension behavior of the denervated venules unchanged.

Animals↗
PubMed1992

Concentration profile of blood platelets differs in arterioles and venules.

Platelet distribution was investigated in 21 venules (V) and 10 arterioles (A) of the rabbit mesentery (vessel diam 15-33 microns). Circulating platelets were labeled in vivo with the dye acridine red and observed with fluorescence video microscopy. Only platelets flowing in a thin (5-7 microns) optical section located about the median plane of the vessel were used. The relative position of each platelet, i.e., the distance of its centroid to the left vessel wall divided by the local vessel diameter, was determined. In addition, in 10 venules leukocyte margination was inhibited by intravenous injection of dextran sulfate (500,000 mol wt; 30 mg/kg body wt). The number of platelets per unit volume (i.e., platelet density) relative to the mean density was significantly higher in the vessel center of V (1.04) than of A (0.55; P less than 0.005). In contrast, near the wall this density was significantly higher in A compared with V. Mean values were as follows: at radial position (R) = 0.9-1.0, 0.30 in A and 0.11 in V (P greater than 0.05); at R = 0.8-0.9, 1.63 in A and 0.84 in V (P less than 0.002); at R = 0.7-0.8, 1.60 in A and 1.36 in V (P greater than 0.05); at R = 0.6-0.7, 1.16 in A and 1.60 in V (P less than 0.02); and at R = 0.5-0.6, 0.92 in A and 1.36 in V (P less than 0.02). These differences in platelet distribution between arterioles and venules are not caused by the presence of leukocyte margination in venules.

Animals↗