The endothelial structure of the postcapillary venules of the lymph node and the passage of lymphocytes across the venule wall.
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Ultrastructure of venules in the cat brain.
Intracerebral venules of the cat were examined to establish criteria for a distinct separation between the venous and arterial system, and to characterize, in greater detail, the mural construction of individual venules. The intracerebral venules compared with those of other organs. Venules do not have a vascular wall composed clearly of endothelium, media, and adventitia, as is characteristic of arteries and arterioles. The venous endothlium has a similar structure to that of capillaries. The periendothelial cells of the venule differ in shape depending on the vascular diameter. The number of periendothelial cell processes in postcapillary venules increases progressively. Segments in which the basal lamina of the endothelium merges with that of the glia cover a smaller portion of the circumference than in venous capillary loops. In collecting venules, the endothelium is almost completely enveloped by periendothelial cells which have a larger number of filaments. There are no typical smooth muscle cells in the intracerebral venules. The perivascular space becomes wider in collecting venules, contains adventitial cells, phagocytes and a great number of collagen fibers.
Animals↗
The roles of catecholamines in responses evoked in arterioles and venules of rat skeletal muscle by systemic hypoxia.
1. Studies have been made in the anaesthetized rat of the roles played by alpha- and beta-adrenoreceptor stimulation in determining diameter changes induced in individual arterioles and venules of the spinotrapezius muscle during systemic hypoxia (breathing 6% O2 for 3 min). 2. Topical application to the spinotrapezius of phentolamine, the alpha-adrenoreceptor antagonist, or sotalol, the beta-adrenoreceptor antagonist, had no effect on the fall in systemic arterial pressure and tachycardia induced by hypoxia. 3. All arterioles and venules showed a decrease in diameter in response to topical application of noradrenaline (10(-6) g ml-1): these responses were abolished by topical application of phentolamine. Moreover, those arterioles and venules that showed a decrease in diameter during hypoxia before phentolamine, showed a significantly smaller decrease, or an increase in diameter after phentolamine. This effect was most marked in primary and secondary arterioles (13-50 microns diameter). 4. All arterioles and venules showed an increase in diameter in response to topical application of isoprenaline (10(-6) g ml-1); these responses were abolished by topical application of sotalol. Moreover, these arterioles and venules that showed an increase in diameter during hypoxia before sotalol, showed a significantly smaller increase or even a decrease in diameter after sotalol. 5. These results suggest that during hypoxia the arterioles of skeletal muscle, especially primary and secondary arterioles, are under the constrictor influence of a reflex increase in sympathetic nerve activity while the venules, which have no sympathetic innervation, are under the constrictor influence of circulating catecholamines. They also suggest that in individual arterioles and venules, these constrictor influences may be overcome by dilatation mediated by the beta-adrenoreceptor influence of circulating catecholamines. 6. Since some arterioles and venules still showed constriction during hypoxia after phentolamine and some still showed dilatation during hypoxia after sotalol, it seems that factors other than catecholamines contribute to the diameter changes. It is suggested that locally released metabolites exert a substantial dilator influence, particularly on terminal arterioles and collecting venules, those vessels nearest to the capillary bed.
Animals↗
Morphologic assessment of leukocyte-endothelial cell interactions in mesenteric venules subjected to ischemia and reperfusion.
Intravital microscopic studies of the mesenteric microcirculation have demonstrated that leukocyte adherence and emigration in postcapillary venules are a characteristic feature of tissues exposed to ischemia-reperfusion. The objectives of this study were to determine whether: (1) neutrophils are the predominant leukocytes that adhere and emigrate in postischemic mesenteric venules, and (2) leukocyte adherence and/or emigration are a prerequisite for reperfusion-induced increases in venular permeability. Leukocyte kinetics in cat mesenteric venules (25-35 microns diameter) were evaluated using both intravital microscopy and quantitative morphometry. The intestine and mesentery were exposed to 60 min of ischemia, followed by 60 min reperfusion. Some animals were pretreated with a monoclonal antibody (MoAb IB4) against the leukocyte adhesion glycoprotein, CD11/CD18. Vessels observed by intravital microscopy and adjacent venules of similar diameter were excised and processed for light (LM) and electron microscopy (EM). Horseradish peroxidase (HRP), administered intravenously, was used to assess vascular permeability by EM. By LM, the control (nonischemic) mesentery is sparsely populated by plasma cells, mast cells, and leukocytes; 30-50% of the resident population is neutrophils. Ischemia-reperfusion led to a significant increase in the number of extravascular cells, with neutrophils accounting for greater than 80% of the total cell population. Control and ischemic venules demonstrated no leakage of HRP into the interstitium. However, venules exposed to ischemia and reperfusion demonstrated HRP leakage between endothelial cells and into the surrounding interstitium; neutrophils were adherent to the luminal surface of the endothelium, transmigrating the vessel wall, and in the surrounding interstitium. Animals pretreated with MoAb IB4 presented the same cell profile as nonischemic controls, with no adherent or transmigrating neutrophils. However, some HRP leakage was noted following reperfusion in venules treated with MoAb IB4. The results of this study indicate that: (1) neutrophils are the predominate leukocytes that adhere and emigrate in postischemic venules, and (2) inhibition of leukocyte adhesion does not completely prevent the venular dysfunction associated with ischemia-reperfusion.
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Post-capillary venules in the lymphatic tissues of mice bearing experimental neoplasia.
The lymph nodes, thymus and Peyer's patches of DBA/2 mice bearing an experimental tumor, mastocytoma, were assessed histologically with special reference to the structure of the post-capillary venules. For each of the lymphoid organ studied, the post-capillary venule score (PCV-S) was determined on the three grades (grades 1, 2 and 3) of the venules classified according to the height of the endothelial cells. The highest scores were obtained in the lymph nodes and Peyer's patches of the control animals. The scores in these lymphoid organs of the tumor-bearing mice were statistically highly significantly lower than in the control series. The lowest scores, however, were obtained in the nodes and patches of mice bearing mastocytoma after the previous treatment with anti-theta-globulin. The scores in the thymuses did not deviate from each other in the three series of mice studied. The findings of the present work support the concept that the structural state of the post-capillary venules in the lymph nodes and Peyer's patches is an important regulator of the T-lymphocyte recirculation in these organs. On the other hand, the venules of the thymus seem to be unrelated both structurally and functionally to the post-capillary venules of the nodes and Peyer's patches, and a new name of "junctional venules" has been proposed for these low endothelium walled venules of the thymus.
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Role of CD11/CD18 in shear rate-dependent leukocyte-endothelial cell interactions in cat mesenteric venules.
In vivo microscopy was used to assess the relationships among shear rate (and shear stress), leukocyte rolling velocity, and leukocyte adherence in a cat mesentery preparation. Shear rate in individual venules and arterioles of 25-35 microns diameter were varied over a wide range by graded occlusion of an arterial loop. There was a linear decline in leukocyte rolling velocity (Vwbc) as red cell velocity (Vrbc) was reduced. The ratio Vwbc/Vrbc remained constant despite variations in shear stress from 5-25 dyn/cm2. A reduction in shear stress was associated with an increased leukocyte adherence, particularly when Vwbc was reduced below 50 microns/s. Reduction in wall shear rate below 500 s-1 in arterioles allowed 1-3 leukocytes to adhere per 100 microns length of vessel, while venules exposed to the same shear rates had 5-16 adherent leukocytes. In arterioles, leukocyte rolling was only observed at low shear rates. At shear rates less than 250 s-1 leukocyte rolling velocity was faster in arterioles than venules, and the ratio Vwbc/Vrbc for arterioles was 0.08 +/- 0.02, which was fourfold higher than the ratio obtained in venules at similar shear rates. Pretreatment with the CD18-specific antibody (mAb) IB4 increased leukocyte rolling velocity in venules by approximately 20 microns/s at red cell velocities below 2,000 microns/s. mAb IB4 largely prevented the leukocyte adherence to arterioles and venules, and increased the ratio Vwbc/Vrbc observed in venules at low shear elicit a CD18-dependent adhesive interaction between leukocytes and microvascular endothelium, and that differences in shear rates cannot explain the greater propensity for leukocyte rolling and adhesion in venules than arterioles.
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Endothelial, not hemodynamic, differences are responsible for preferential leukocyte rolling in rat mesenteric venules.
At the onset of the inflammatory process, leukocytes roll along venular but not arteriolar walls before they firmly attach and emigrate. To test whether differences in hydrodynamic flow conditions are responsible for the preferential occurrence of leukocyte rolling in venules, we varied wall shear rate, gamma w, between 30 and 2,000 sec-1 by selective micro-occlusion of side branches in venules and arterioles (diameter, 20-37 microns) of the exposed mesentery of anesthetized rats. In venules, 39% (range, 6-77%) of all passing leukocytes were found interacting with the endothelium (rolling), whereas this fraction was only 0.6% in arterioles. The fraction of rolling leukocytes in venules decreased from 49 +/- 13% at gamma w less than 100 sec-1 (N = 12) to 24 +/- 13% at gamma w greater than 400 sec-1 (N = 12). Mean leukocyte rolling velocity in venules increased with gamma w, but the most frequent rolling velocity class was 20-40 microns/sec at all shear rates. In arterioles, even prolonged (up to 90 minutes) conditions of reduced flow (gamma w less than 150 sec-1) did not induce leukocyte rolling. Radial distribution of freely flowing leukocytes not different in arterioles and venules. The data indicate that hemodynamic factors are not responsible for the difference of leukocyte adhesion between arterioles and venules. The venular endothelium appears to be specialized to support leukocyte adhesion during inflammation. This finding correlates with reports on preferential expression of various endothelial-leukocyte adhesion molecules on venular endothelial cells.
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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.
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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.
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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.
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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↗
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↗
Comparative vasodilator effects of magnesium salts on rat mesenteric arterioles and venules.
In vivo studies were undertaken to investigate the comparative effects of different magnesium (Mg) salts (i.e., MgCl2, MgSO4, Mg acetate, Mg aspartate HCl) on arterioles (10-20 microns i.d.) and venules (15-30 microns i.d.) of the mesenteric circulation of the pentobarbitone-anesthetized rat. Perivascular administration of these Mg salts (topical doses = 0.1-100 mumoles) produced dose-dependent vasodilatation (5-50% increases in lumen size) of arterioles and venules almost instantaneously. Arterioles were more sensitive than venules to topical MgCl2 and MgSO4 but not to either Mg aspartate HCl or Mg acetate. Intra-arterial infusion of the Mg salts (1-40 mumoles/min, i.e., 5-400 mumol/kg/min for 20 min) at each dose produced vasodilatation, i.e. 10-80% increases in lumen size of mesenteric arterioles; doses above 10 mumoles/min sometimes produced bleeding from venules. Systemic i.v. infusion (1-40 mumoles/min) of all 4 Mg salts lowered systolic and diastolic arterial blood pressure dose-dependently; however, the degree or presence of vasodilatation noted in the microvessels was not always correlated with the falls in arterial blood pressure. Intravenous administration of the Mg salts resulted in dose-dependent elevation in plasma Mg (0.3-4.7 mg/dl, over control levels); increments in plasma Mg were noted as soon as 1 min after the start of the infusion. Plasma Mg levels wre higher with inorganic salts and peaked more rapidly. Large i.v. doses of Mg salts (i.e., greater than 20 mumoles/min) induced some bleeding from the venules which varied with the anion. Administration of a variety of pharmacological receptor antagonists and a cyclo-oxygenase inhibitor did not interfere with vasodilatation of arterioles or venules induced by Mg salts. These results indicate that magnesium ions: 1) are vasodilators of intact microscopic mesenteric resistance and capacitance microvessels; and 2) bring about vasodilatation by direct actions on microvascular smooth muscle cells. In addition, our data indicate that the anion associated with Mg appears to exert significant influences on microvascular tone.
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Vascular smooth muscle structure and juvenile growth in rat intestinal venules.
The morphological structure of individual vascular smooth muscle cells from intestinal venules was evaluated with a combination of quantitative scanning (SEM) and transmission (TEM) electron microscopy techniques. In addition, growth of individual venular smooth muscle cells and of the overall vessel wall was compared from measurements of these variables during the rapid juvenile growth spurt from ages 4 to 6 and 10 to 12 weeks in Wistar-Kyoto rats. SEM revealed that smooth muscle cells of intestinal venules in weanling rats are very long (379 +/- 91 [SD] microns) and wide (6.0 +/- 1.3 microns) and very little further cell enlargement occurs during rapid juvenile growth. TEM studies indicated that passive inner vessel diameter and total muscle layer cross-sectional area of both the largest and intermediate diameter venules of young rats, as well as the percentage of the total wall area as muscle tissue in each venule type, did not significantly increase during body growth. These observations indicate that both the intestinal venules and their smooth muscle cells reach mature dimensions at a very early stage of life. Comparison of intestinal vascular smooth muscle cell dimensions indicates that venular smooth muscle cells are much larger in both cell length and volume than comparable arteriolar smooth muscle cells.
Aging↗
Differential effects of pentobarbital on intracerebral arterioles and venules of rats in vitro.
The vasoactive properties of pentobarbital (PB) were studied in intracerebral arterioles and venules (diameter, 30-90 microns). These vessels mediate changes in cerebrovascular resistance and capacitance, respectively. Mean control vessel diameters of arterioles and venules at pH 7.3 were 53.9 +/- 2.8 microns and 78.4 +/- 4.3 microns, respectively. Both arterioles and venules dilated when the pH of the extraluminal solution was lowered to 6.8 and constricted when the pH was raised to 7.6. PB, 10(-6) to 10(-2) mol/L, dilated intracerebral arterioles in a dose-dependent manner at pH 7.3, reaching a maximal dilation of 129.7 +/- 3.1% of control diameter at a dose of 10(-3) mol/L. In contrast, PB at 10(-6) to 10(-2) mol/L failed to produce significant changes in the diameter of intracerebral venules. In addition, PB at 10(-3) mol/L significantly inhibited arteriolar constriction induced by KCl (120 mmol/L), but not venular constriction. The present study suggests that intracerebral venules are relatively less responsive to PB than cerebral arterioles and peripheral veins. In addition to its effect on cerebral metabolism. PB may act to redistribute venous blood volume from cerebral veins to more responsive peripheral veins, thereby decreasing intracranial blood volume and intracranial pressure.
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Fluid dynamics and the thromboembolic reaction in mesenteric arterioles and venules.
In the mesentery of the anesthetized rabbit, the thromboembolic reaction after wall puncture lasts six times longer in arterioles than in venules, a difference that cannot be explained by fluid dynamic conditions before puncture. In the present study, it was investigated whether this difference in response between arterioles and venules results from a different degree of stenosis by the thrombus and/or a difference in velocity changes resulting in a different pressure drop over the thrombus. Arteriolar and venular mean red blood cell velocity and vessel diameter were measured before puncture and after this injury in the stenosed vessel segment and upstream. Thrombi with similar heights were formed in arterioles and venules and induced similar degrees of stenosis. A surface area reduction less than 55% induced only a small and similar decrease in volume flow (less than 10%) in arterioles and venules. Reduced velocity, a measure of wall shear rate, increased similarly in both vessel types for similar degrees of stenosis. In conclusion, changes in fluid dynamic factors, as induced by thrombus formation, cannot be held responsible for the difference in thromboembolic reaction between arterioles and venules.
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Effect of endothelial injury on the responses of isolated guinea pig pulmonary venules to reduced oxygen tension.
The influence of the endothelium on pulmonary venular responses to reduced oxygen tension has not been defined. To examine this question, endothelial injury was induced in small guinea pig pulmonary artery and venule segments (effective lumen radius, 174 +/- 5 and 122 +/- 2 microns, respectively) by perfusion with either a mixture of hypoxanthine (5 mM) and xanthine oxidase (0.05 U/ml) (HX/XO) or collagenase (2 mg/ml). HX/XO significantly (p less than 0.05) reduced the relaxation of precontracted pulmonary arteries by acetylcholine (ACH), bradykinin (BK), and A-23187, and the relaxations were restored by including superoxide dismutase (40 micrograms/ml) in the HX/XO solution. However, neither HX/XO nor collagenase affected vasodilation induced by ACH, BK, and A-23187 in precontracted pulmonary venules. In contrast, HX/XO significantly (p less than 0.05) augmented the sustained contraction of pulmonary venules to hypoxia (HX/XO, 3.2 +/- 1.0 mg/mm; control, 1.0 +/- 0.5 mg/mm) and anoxia (HX/XO, 35.1 +/- 6.6 mg/mm; control, 20.3 +/- 4.0 mg/mm). Collagenase also significantly (p less than 0.05) enhanced the anoxic contractions (collagenase, 36.0 +/- 3.7 mg/mm; control, 20.9 +/- 6.8 mg/mm). Superoxide dismutase (40 micrograms/ml) and catalase (323 micrograms/ml) abolished HX-XO-induced augmentation of the hypoxic and anoxic contractions of pulmonary venules. Collagenase removed 54 +/- 8% of the venular endothelium (control, 5 +/- 1%), whereas HX/XO-exposed endothelial cells contained numerous craters. Neither gossypol (5 microM) nor methylene blue (10 microM) affected pulmonary venular contractions to reduced PO2. Endothelial damage augments the PO2-dependent contractions of the pulmonary venule, and this augmentation does not appear to be due to decreased release of endothelium-derived relaxing factor.
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Dimensions of postcapillary venules sensitive to bradykinin and histamine-induced leakage of macromolecules.
Microvascular leakage of macromolecules was studied in the hamster cheek pouch preparation using fluorescein labelled dextran (FITC-dextran 145 Mw = 145,000) as a tracer. When the preparation is superfused with 10(-5) M histamine or 10(-7) M bradykinin the permeability to macromolecules increases exclusively at postcapillary venules. Microinjections of 30-200 picolitres (pl) of 0.1 M histamine and 10(-4) M bradykinin close to arterioles and capillaries caused extravasation from several postcapillary venules at a distance from site of injection but not from arterioles or capillaries. The minimal diameter of the postcapillary venules where leakage occurred was (n = 45) 8.6 +/- 2.6 (S.D.) microM and the maximal diameter was 14.0 +/- 5.3 microM. Histamine and bradykinin caused leakage of macromolecules in postcapillary venules but not in arterioles, capillaries or larger venules even when these were exposed to high local concentrations of these agents.
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