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PubMed1989

Responses of isolated guinea pig pulmonary venules to hypoxia and anoxia.

Because small pulmonary arteries are believed to be the major site of hypoxic pulmonary vasoconstriction (HPV), pulmonary venular responses to hypoxia have received little attention. Therefore the responses of isolated guinea pig pulmonary venules to hypoxia (bath PO2, 25 Torr) and anoxia (bath PO2, 0 Torr) were characterized. Pulmonary venules [effective lumen radius (ELR), 116 +/- 2 microns] with an adherent layer of parenchyma responded to hypoxia and anoxia with a graded sustained contraction (hypoxia, 0.03 +/- 0.01; anoxia, 0.26 +/- 0.03 mN/mm), whereas paired femoral venules (ELR, 184 +/- 7 microns) contracted to anoxia only (0.05 +/- 0.02 mN/mm). Repeated challenges with hypoxia and anoxia continued to elicit sustained pulmonary venular contractions; femoral venule contractions to anoxia were not repeatable. Hypoxia- and anoxia-induced pulmonary venular contractions were calcium and pH dependent. Dissection of the parenchyma from pulmonary venules did not alter contractions to decreased PO2. Anoxic contractions of pulmonary venules were variably reduced by replacement of the bath fluid; however, the release of a contractile mediator(s) from pulmonary venules during hypoxia or anoxia was not demonstrated. Pulmonary venular responses to hypoxia and anoxia are similar to those induced by hypoxia in vivo, and results obtained from this model may be useful in predicting mechanisms of HPV.

Animals↗
PubMed1991

Interaction of lymphocytes and high endothelial venules in irradiated lymph nodes.

After total-body exposure to various doses of ionizing radiation, the ability of lymphocytes to interact specifically with high endothelial venules of rat cervical and mesenteric lymph nodes was analyzed in frozen sections. Following a radiation dose of 1.5 Gy, high endothelial venules remained intact and the binding of unirradiated lymphocytes to the venules was enhanced relative to unirradiated controls. At radiation doses above 5.0 Gy, damage to high endothelial venules was observed histologically as well as assessed functionally. There was a significant decrease in specific lymphocyte-venule binding and a significant increase in nonspecific binding. These findings suggest that radiation-induced damage to high endothelial venules might play a role in radiation-induced immunosuppression by interfering with the normal passage of lymphocytes from the blood into lymph nodes via a specific interaction between lymphocytes and high endothelial venules.

Animals↗
PubMed1990

Extravasation of lymphocytes via paracortical venules in sheep lymph nodes: visualization using an intracellular fluorescent label.

In rodents and humans, lymphocytes extravasate into lymph nodes via specialized paracortical venules lined with high endothelium (HEV). Sheep and other ruminants do not have morphologically defined HEV in their lymph nodes. It has been assumed that lymphocyte extravasation in these species proceeds via analogous structures; i.e., paracortical venules lined with low to medium endothelium. In this study, lymphocyte suspensions were prepared from surgically excised lymph nodes of sheep and labeled with an intracellular fluorescent dye, H33342. Labeled cells were infused intravenously back into donors, and sheep were killed at various intervals after infusion. Frozen sections of lymph nodes were examined microscopically for the location of labeled cells. Ten minutes after infusion, labeled cells were seen in the lumen of venules located in the paracortical region of the nodes. At later time points, cells were seen apparently migrating through the venule walls and in the adjacent paracortical tissue. Similar experiments were performed in which H33342-labeled murine lymphocytes were infused into syngeneic mice. When equivalent cell numbers (based on animal size) were infused, no obvious differences were seen between location and kinetics of appearance of labeled cells in lymph nodes of sheep compared to those of mice. These results indicate that lymphocyte extravasation in sheep proceeds via paracortical venules in lymph nodes. The function of these venules appears to be analogous to HEV in nonruminant species.

Animals↗
PubMed2006

Mediators of CD18/P-selectin-dependent constriction of venule-paired arterioles in hypercholesterolemia.

This study addresses the role of venule-derived mediators in the arteriolar constriction that accompanies hypercholesterolemia. Constriction was assessed by measuring the tone of small arterioles closely paired with venules in the mesentery of normal cholesterol rats (NC), high cholesterol rats (HC), HC rats injected with antibodies against CD18 and P-selectin (HC/mAbs), HC rats treated with the thromboxane synthase inhibitor, ozagrel (HC/ozagrel), and HC rats pretreated with anti-platelet serum (HC/APS). Venule-paired arterioles in the untreated HC group demonstrated enhanced tone compared with arterioles in the NC group, while no difference was found between unpaired arterioles of the two groups. Perivascular nitric oxide (NO) concentrations were found to be significantly decreased in venule-paired arterioles of HC rats (238+/-14 nM) compared with those of NC rats (426+/-42 nM). The injection of anti-adhesion antibodies successfully attenuated the enhanced arteriolar tone and venular leukocyte adherence in the HC group, and tended to increase levels of NO in venule-paired arterioles by 33% (to 326+/-19 nM; still lower than that of the NC group). Ozagrel and platelet depletion attenuated the enhanced arteriolar tone by 53% and 33%, respectively, without affecting NO concentrations. These findings indicate that the mechanism of blood cell-dependent arteriolar constriction during hypercholesterolemia may be dependent on thromboxane, a decrease in NO, and the proximity of the arterioles to postcapillary venules.

Animals↗
PubMed2002

Experimental macular edema induced by macular venule occlusion in monkey.

PURPOSE: Visual prognosis after retinal vein occlusion varies, because it may be affected by macular edema or an avascular area. The mechanism describing how macular edema and avascular areas occur, however, has not been clearly understood. We induced macular edema in cynomolgus monkeys by occluding macular venules to evaluate the retinal microcirculation. METHODS: We produced venous occlusion by applying dye laser in three cynomolgus monkeys. Macular edema was examined by slit lamp biomicroscopy and optical coherence tomography. Acridine orange leukocyte fluorography (AOLF) and fluorescein angiography were performed to study blood flow and vascular leakage before and after laser application. RESULTS: We observed three types of retinal changes in the macular area: (1) macular edema did not develop; (2) macular edema developed, but improved with avascular area formation; (3) macular edema developed, but disappeared without avascular area formation. Under physiological conditions, observation revealed that leukocytes flowed from arterioles into either superior or inferior venules. When macular edema did not develop, most leukocytes from arterioles escaped into the adjacent non-occluded venules. In contrast, when macular edema occurred, leukocyte flow became stagnated. Macular edema developed when capillary leakage was observed from venules and subsequently arterioles, but disappeared when an avascular area was formed by arteriole occlusion. CONCLUSIONS: We demonstrated that experimental macular edema could be induced by macular venule occlusion in monkeys. According to our observation by AOLF, whether macular edema is induced or not depends on the function of collateral routes of the remaining non-occluded venules. We could consider that a gradual increase in intravascular pressure was associated with the avascular area formation.

Acridine Orange↗
PubMed2005

Preferential binding of leukocytes to the endothelial junction region in venules in situ.

OBJECTIVE: To determine whether leukocytes show a preference to firmly adhere to the endothelium near the endothelial cell (EC) junction in their native environment, i.e., blood-perfused venules in situ. METHODS: Intravital confocal microscopy was used to determine the positions of firmly adherent leukocytes with respect to EC junctions in cremaster muscle venules in anesthetized mice. EC area and EC junction locations were identified using immunofluorescent labeling of platelet-endothelial cell adhesion molecule-1 (PECAM-1), an endothelial junction protein. Leukocytes were identified using transillumination through the same optical path. RESULTS: Seventy-five percent of firmly adherent leukocytes overlapped an EC junction (the average distance to the nearest EC junction was 2.4 +/- 0.1 micro m, n = 263). This distance was less in smaller diameter venules, hence the percentage of adherent leukocytes that overlapped an endothelial junction was larger. EC shape and size varied with venular diameter: in smaller venules (30-49 micro m diameter), ECs had significantly less area (316 +/- 19 micro m(2)) and were narrower (12.5 +/- 0.4 micro m) than in larger (70-89 micro m diameter) venules, which had 614 +/- 28 micro m(2) area and 17.8 +/- 0.5 micro m width, respectively (p < .001). Furthermore, the majority (73.0%) of firmly adherent leukocytes crawled an average distance of 29.4 +/- 2.8 micro m at a mean intralumenal migration velocity of 7.6 +/- 0.4 micro m/min before undergoing transmigration or detaching and reentering the free fluid stream. CONCLUSIONS: Most adherent leukocytes in blood-perfused venules are located at or near EC junctions. This is primarily due to the size and shape of venular ECs. Further, most leukocytes that appear to be adherent are in fact motile, and migrate a significant distance along the lumenal wall. The authors speculate that this reflects movement to those EC junctional regions that support transendothelial migration.

Animals↗
PubMed2004

Role of shear forces and adhesion molecule distribution on P-selectin-mediated leukocyte rolling in postcapillary venules.

Rolling on the venular endothelium is a critical step in the recruitment of leukocytes during the inflammatory response. P-selectin is a key mediator of leukocyte rolling, which is an early event in the inflammatory cascade; this rolling is likely to be directly regulated by both local fluid shear forces and P-selectin site densities in the microvasculature. However, neither the spatial pattern of P-selectin expression in postcapillary venules nor the effect of local expression patterns on rolling behavior in intact functional venules is known. We investigated the influence of local shear forces and the spatial distribution of endothelial P-selectin in intact blood perfused post capillary venules in anesthetized mice using intravital confocal microscopy, high temporal resolution particle tracking, and immunofluorescent labeling. We demonstrated a shear-dependent increase in average leukocyte rolling velocity that was attributable to a shear-dependent increase in the occurrence of transient leukocyte detachments from the endothelial surface: translational velocity during leukocyte contact with the vessel wall remained constant. P-selectin expression was not different in venules with characteristically different shear rates or diameters but varied significantly within individual venules. In postcapillary venules, regions of high P-selectin expression correlated with regions of slow leukocyte rolling. Thus the characteristically variable leukocyte rolling in vivo is a function of the spatial heterogeneity in P-selectin expression. The study shows how the local hydrodynamic forces and the nonuniform pattern of P-selectin expression affect the behavior of interacting leukocytes, providing direct evidence for the local variation of adhesion molecule expression as a mechanism for the regulation of leukocyte recruitment.

Animals↗
PubMed1990

EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles.

Communication from venules to arterioles through the release of endothelial-derived relaxing factor (EDRF) was evaluated. To demonstrate that the rat intestinal and the spinotrapezius muscle arterioles can respond to EDRF, the vessels were dilated by iontophoretically applied acetylcholine (ACh), and this dilation was greatly attenuated by the inhibitors of EDRF actions, methylene blue (100 microM) and dithiothreitol (50 microM). The EDRF inhibitors did not suppress arteriolar dilation to typically applied adenosine (10(-4) M), an endothelium-independent dilator. Although ACh release onto the venular wall had minimal effects on the diameter of the venule, the paired arteriole would dilate 20-30% in the intestine and 50-60% in the spinotrapezius muscle. After EDRF inhibition, venular ACh exposure did not cause arteriolar dilation. ACh diffusion from venules to arterioles was not the cause of arteriolar dilation, because release of ACh into the tissue at the same distance as from the arteriole to the venular ACh release site caused minimal arteriolar dilation. Neither blockade of neural reflexes with tetrodotoxin (3 X 10(-6) M) nor suppression of prostaglandin formation with indomethacin (10(-5) M) prevented the arteriolar dilation during release of ACh onto the venular wall. The overall study indicated that communication from venules to arterioles through the release of EDRF from the venule did occur and caused substantial arteriolar vasodilation. Therefore circumstances within and around venules may influence regulation of nearby arterioles through an EDRF-mediated mechanism.

Acetylcholine↗
PubMed1992

Leukocyte rolling: a prominent feature of venules in intact skin of anesthetized hairless mice.

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.

Acridine Orange↗
PubMed1993

Spontaneous contractions of isolated bat wing venules are inhibited by luminal flow.

The hypothesis that spontaneous contractions of bat wing venules could be modulated by luminal flow was tested. Single venules (114 +/- 5 microns diam) from the wings of anesthetized pallid bats were dissected, cannulated, and pressurized in vitro. A dual reservoir system was used to independently control luminal pressure and flow. In the absence of flow, and with pressure set to 10 cmH2O, all venules contracted spontaneously at rates between 20 and 40 cycles/min. Pressure elevation over the range of 3-10 cmH2O caused a rapid increase in contraction frequency and decrease in amplitude; pressure reduction caused a rapid decrease in contraction frequency and increase in amplitude. In contrast, initiation of flow resulted in a delayed and gradual reduction of contraction amplitude and/or frequency (sometimes to zero). The net effect of flow was to increase mean diameter and decrease the product of frequency x cross-sectional area. Flow-induced inhibition of venular contraction was eliminated by endothelial denudation but persisted in the presence of NG-monomethyl-L-arginine (10(-4) M) or indomethacin (10(-5) M) in concentrations that blocked the effects of exogenously applied ATP or arachidonic acid, respectively. The flow-induced venular response also persisted in the presence of superoxide dismutase (55 U/ml). Denuded venules responded to flow when placed downstream (i.e., perfused in series) from venules with intact endothelium. These results indicate that luminal flow can modulate the contractile function of bat wing venules via release of a transferable substance from the endothelium. The exact nature of the substance is not yet known but it does not appear to be classical endothelium-derived relaxing factor, a prostaglandin, or an oxygen radical.

Adenosine Triphosphate↗
PubMed1995

Interaction of neutrophils and endothelium in isolated coronary venules and arterioles.

This study reports measurements of porcine neutrophil dynamics in isolated microvessels. Porcine coronary venules and arterioles were isolated, cannulated, and perfused with fluorescently labeled neutrophils at a series of flow velocities. In venules (62.50 +/- 5.41 microns diam) under control conditions, rolling neutrophils were often observed at intraluminal flow velocities ranging from 600 to 6,000 microns/s, and the rolling fraction varied inversely as a function of flow velocity. There was no significant adherence under the control conditions at any of the various flow velocities. Pretreatment of the neutrophils with human recombinant complement 5a (C5a, 10(-8) M) increased adherence at low flow velocities but did not alter the rolling fraction. In contrast to venules, rolling neutrophils were not observed in arterioles (58.80 +/- 5.6 microns diam). Furthermore, neutrophils that were pretreated with C5a did not adhere to the arteriolar endothelium even at low flow velocities. We suggest that 1) isolated microvessels perfused with fluorescently labeled neutrophils are suitable models for the study of the interaction between neutrophils and the microvascular endothelium, 2) shear force plays an important role in neutrophil rolling in coronary venules but is not the major factor that prevents neutrophil rolling and adherence in arterioles, and 3) C5a causes neutrophil adherence in venules but not in arterioles, indicating that different mechanisms underlie the interaction between neutrophils and endothelium in venules and arterioles.

Animals↗
PubMed1998

Flow-induced responses in skeletal muscle venules: modulation by nitric oxide and prostaglandins.

Skeletal muscle arterioles dilate in response to increases in flow velocity/wall shear stress (WSS). The effect of flow/WSS on the diameter of skeletal muscle venules and the possible endothelial mediation of the response, however, have not yet been characterized. Thus changes in diameter of pressurized (10 mmHg) and norepinephrine-preconstricted venules (179 +/- 8 micron in diameter) to increases in perfusate flow before and after endothelium removal or application of inhibitors of NO and prostaglandin (PG) synthesis, Nomega-nitro-L-arginine (L-NNA, 10(4) M) and indomethacin (Indo, 2.8 x 10(5) M), respectively, were measured. Increases in perfusate flow [elicited by increases in the pressure difference (Pdiff) between proximal and distal cannulas] evoked with a delay of 17 +/- 2 s dilations, up to 36 +/- 9 micron at the highest flow, a response that was completely eliminated by removal/disruption of the venular endothelium. Calculation of WSS indicated that in endothelium-intact venules, the midpoint of the shear stress-diameter curve was at approximately 8 dyn/cm2, whereas in endothelium-denuded vessels, shear stress increased in a linear fashion with increases in flow, up to 40 dyn/cm2. L-NNA significantly reduced flow-induced dilations (from 38 +/- 11 to 17 +/- 9 micron at 14 mmHg Pdiff), whereas in the additional presence of Indo, flow elicited constriction of venules decreasing basal diameter (by 21 +/- 8 micron at Pdiff 12 mmHg). Thus in skeletal muscle venules an increase in shear stress due to increases in perfusate flow stimulates the release of endothelium-derived NO and PGs eliciting dilation, which in turn, regulates WSS, albeit at a lower value than what is observed in arterioles. In the absence of NO and PGs, flow-induced constriction is revealed, the cause of which remains obscure. From these data, we propose that shear stress-related responses of venules are involved in the regulation of venular resistance, especially during high flow conditions, such as reactive and exercise hyperemia.

Animals↗
PubMed2002

Hypercholesterolemia enhances thromboembolism in arterioles but not venules: complete reversal by L-arginine.

We investigated in vivo the effect of cholesterol diet-induced hypercholesterolemia (HC) on thromboembolism in nonatherosclerotic rabbit mesenteric arterioles and venules (diameter 21 to 45 micrometer). After mechanical vessel wall injury, the ensuing thromboembolic reaction was studied by intravital videomicroscopy. A dramatic prolongation of embolization duration (median >600 seconds) was observed in the arterioles of the HC group compared with the arterioles of a normal chow-fed (NC) control group (142 seconds, P<0.0001); concomitantly, relative thrombus height increased (thrombus height/vessel diameter was 68% for the HC group and 58% for the NC group; P<0.05). By contrast, in venules, cholesterol did not affect embolization duration (42 seconds for HC group, 34 seconds for NC group) and thrombus height (66% for HC group, 64% for NC group). Furthermore, the role of endothelial NO synthesis was studied. In arterioles, stimulation of endogenous NO synthesis through mesenteric superfusion of L-arginine (1 mmol/L) completely reversed cholesterol-enhanced embolization (152 seconds) but did not influence thrombus height (63%). L-Arginine had no effect in venules of the HC group (51 seconds) and nor in the arterioles and venules of the NC group (177 seconds for arterioles, 43 seconds for venules). This study indicates that hypercholesterolemia selectively enhances thrombus formation and embolization in arterioles but not in venules and that stimulation of endogenous NO production antagonizes this enhancement of arteriolar thromboembolism.

Animals↗
PubMed1998

Endogenous nitric oxide protects against thromboembolism in venules but not in arterioles.

Because nitric oxide (NO) inhibits aggregation and adhesion of blood platelets, NO may play a role in platelet-vessel wall interactions. Therefore, the purpose of this study was to investigate the involvement of endogenous NO in thromboembolic processes, as induced by wall puncture, in rabbit mesenteric arterioles and venules (diameters 20 to 43 microm). In venules, inhibition of NO synthase by superfusion of the mesentery with N omega-nitro-L-arginine (L-NA; 0.1 mmol/L) significantly increased the duration of embolization (from 50 seconds to 511 seconds) and the number of emboli produced (from 2 to 11 emboli per vessel), while the median period of time needed to produce an embolus was not influenced. On the contrary, in arterioles, L-NA had no significant effect on embolization (duration of embolization: 426 seconds in the control and 382 seconds in the L-NA group, with 20 and 12 emboli per vessel, respectively). Addition to the L-NA superfusate of L-arginine (L-ARG; 1 mmol/L), the active precursor for endogenous NO synthesis, resulted in a complete reversal of the L-NA effects in venules, while addition of the inactive D-arginine (D-ARG; 1 mmol/L) had no effect. Addition of L-ARG and D-ARG had no significant effect in arterioles. Addition to the L-NA superfusate of the exogenous NO donor sodium nitroprusside (0.1 micromol/L) also resulted in reversal of the L-NA effects in venules, while in arterioles, it slightly but significantly decreased embolization duration. The differences in effect of L-NA on embolization between arterioles and venules were not caused by differences in fluid dynamic conditions. It is concluded that the role of endogenous NO in inhibiting thromboembolic processes is more important in venules than in arterioles.

Animals↗
PubMed2002

[Oxygen diffusion through the venule walls in the rat cerebral cortex during breathing with pure oxygen].

Using oxygen microelectrodes, distribution of oxygen tension (pO2) has been studied in venules of the rat brain cortex at normobaric hyperoxia (spontaneous breathing with pure oxygen). It has been shown that inhalation of oxygen results in sharp increase of pO2 in majority of the venules under study. The pO2 distribution along the length of venous microvessels of 7-280 microns in diameter is best approximated by equation: pO2 = 76.44 e-0.0008D, n = 407. The pO2 distribution was characterised by extremely high pO2 values (180-240 mm Hg) in some minute venules. Heterogeneity of pO2 distribution in venous microvessels at hyperoxia was shown to be significantly increased. Profiles of pO2 between neighbouring arterioles and venules were for the first time measured. The data clearly evidenced that O2 diffusional shunting took place between cortical arterioles and venules, provided they were distanced from each other for not over 80-100 microns. Distribution of pO2 in venules has been shown to be dependent on the blood flow in the brain cortical microvessels.

Animals↗
PubMed1995

Desmopressin induces endothelial P-selectin expression and leukocyte rolling in postcapillary venules.

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.

Animals↗
PubMed2002

Similar permeability responses to nitric oxide synthase inhibitors of venules from three animal species.

The influence of nitric oxide (NO) on microvascular permeability remains unclear. NO synthase (NOS) inhibitors have been reported to increase as well as to decrease permeability in different experimental models and animal species. We tested the hypothesis that NOS inhibitors influence venular permeability differently in amphibians and mammals. Permeability coefficients to albumin (P(alb)(s)) were measured on in situ mesenteric venules of the frog and rat and excised pig coronary venules before and after exposure to NOS inhibitors. Despite individual variability in magnitude of responses, NOS inhibitors resulted in a reduction in P(alb)(s) in each species. Superfusion with 10(-5) M N(G)-monomethyl-l-arginine (l-NMMA) reduced P(alb)(s) of frog mesenteric venules by 42% (from a median of 11.4 x 10(-7) cm s(-1), n = 12, P < 0.01) and by 67% in porcine coronary venules (from 12.5 x 10(-7) cm s(-1), n = 5, P < 0.05). The response was attenuated in rat mesenteric venules; 10(-4) M N(G)-nitro-l-arginine methyl ester (l-NAME) reduced P(alb)(s) by 23% (from 7.6 x 10(-7) cm s(-1), n = 9, P = 0.01). The inactive d-enantiomers of the NOS inhibitors were without effect on P(alb)(s) in each model. In pig venules, perfusion with blood modified the permeability responses to l-NMMA, suggesting that effects of NO on permeability are modified by one or more elements of blood. These data support a role of nitric oxide release on venular permeability to albumin that is conserved among the three animal species.

Albumins↗
PubMed1973

Relationship between the velocity of rolling granulocytes and that of the blood flow in venules.

1. The mean velocities at which granulocytes roll along the walls of small venules have been related to their mean blood flow velocities in preparations of hamster cheek pouch and mouse mesentery. In animals anaesthetized with Nembutal, 30-200 mum venules were observed microscopically and the movement of rolling granulocytes quantitated on films. Apparent mean blood flow velocity was determined from films of embolizing platelet thrombi.2. In four venules the velocity distribution of about 100 rolling cells was almost symmetrical about the mode, with a small proportion moving at up to three times the mode velocity. Therefore, the mean and mode velocities were very similar.3. In two mesenteric and two cheek-pouch venules, blood flow velocity was temporarily altered during and after gentle compression with a fine glass fibre; this was associated with proportional changes in mean cell velocities.4. In four different venules of a hamster cheek pouch, the mean velocity of rolling granulocytes increased in proportion to the mean blood flow velocity (r = 0.963).5. In thirty-six venules of ten mouse mesenteries, the velocities were proportional (r = 0.915) between blood velocities of about 300 and 1000 mum/sec. Above this the velocity of the cells did not increase further.6. The rolling of granulocytes is presumably governed by two forces, the shear force of the flowing blood and an adhesive force between the surfaces of granulocytes and vascular endothelium. Our results suggest that, within limits, the proportionality between the velocities of blood flow and rolling cells is due to shear force, the adhesive force being similar for all the cells. The results suggest that this adhesion force per granulocyte is of the order of 10(-5) dynes.

Adhesiveness↗