Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Venules”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

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.

Animals↗

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↗

Different effects of L-type and L+N-type calcium channel blockers on hamster cheek pouch venules.

Dihydropyridine calcium channel blockers are not uniform in terms of their action on calcium channel. L-type calcium channel blockers dilate the resistance arterioles. Cilnidipine is a dihydropyridine calcium channel blocker that also acts on N-type calcium channels, and may dilate venules through its effect on the sympathetic receptor. The influence of an L-type calcium channel blocker (nifedipine) or this L+N type blocker at 10(-7) mol to 10(-4) mol on venular diameter was examined by superfusion of male Syrian hamster cheek pouches. Nifedipine dose dependently dilated the arterioles alone, whereas cilnidipine dilated both arterioles and venules. Application of 10(-7) mol omega conotoxin, an inhibitor of N-type channels, after nifedipine led to significant dilation of venules, while it had no influence when administered after cilnidipine. These findings indicate that the effects of calcium channel blockers on the venules differ according to the action on N-type calcium channels, and that cilnidipine (an L+N type calcium channel blocker) dilates venules through its additional action on N-type channels.

Animals↗

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.

Animals↗

In vivo observations of the intramural arterioles and venules in beating canine hearts.

1. To evaluate the effects of cardiac contraction on intramyocardial (midwall) microvessels, we measured the phasic diameter change of left ventricular intramural arterioles and venules using a novel needle-probe videomicroscope with a CCD camera and compared it with the diameter change in subepicardial and subendocardial vessels. 2. The phasic diameter of the intramural arterioles decreased from 130 +/- 79 ìm in end-diastole to 118 +/- 72 micron (mean +/- S.D.) in end-systole by cardiac contraction (10 +/- 6 %, P < 0.001, n = 21). 3. The phasic diameter in the intramural venules was almost unchanged from end-diastole to end-systole (85 +/- 44 vs. 86 +/- 42 micron, respectively, 2 +/- 6 %, n. s., n = 14). 4. Compared with intramural vessels, the diameters of subendocardial arterioles and venules decreased by a similar extent (arterioles: 10 +/- 8 %, P < 0. 001; venules: 12 +/- 10 %, P < 0.001) from end-diastole to end-systole, respectively, whereas the diameter of the subepicardial arterioles changed little during the cardiac cycle, and subepicardial venule diameter increased by 9 +/- 8 % (P < 0.01) from end-diastole to end-systole. These findings are consistent with our previous report. 5. We suggest that the almost uniform distribution of the cardiac contractility effect and arteriolar transmural pressure between the subendocardium and the midmyocardium, which together constitute the systolic vascular compressive force, accounts for the similarity in the arteriolar diameter changes in both myocardial layers. The smaller intravascular pressure drop from deep to superficial myocardium relative to the larger intramyocardial pressure drop explains the difference in the phasic venular diameter changes across the myocardium.

Animals↗

Thrombin increases permeability only in venules exposed to inflammatory conditions.

Thrombin is widely used to stimulate a variety of responses in cultured endothelial cell monolayers as a model of acute vascular endothelial response to inflammatory mediators. However, preliminary results indicated that rat mesenteric venules did not respond acutely to thrombin. We tested the hypothesis that rat venules would respond to thrombin 24 h after prior injury by microperfusion. Vessel responsiveness was measured as hydraulic conductivity (Lp). When venules were exposed to rat thrombin (10 U/ml) within 2 h of initial perfusion with vehicle control, there was no increase in Lp of any vessel from a mean baseline of 1.2 +/- 0.2 x 10(-7) cm.s-1.cmH2O-1. In contrast, when perfused with thrombin at 25-27 h after initial perfusion, every venule responded to thrombin with a transient increase in Lp. The mean peak Lp on day 2 in response to thrombin was 24 +/- 4.2 x 10(-7) cm.s-1.cmH2O-1. Our results suggest that prior endothelial injury modifies the endothelial cell phenotype and alters the response of endothelial cells to thrombin after 24 h. Phenotypic plasticity of endothelial cells may play a key role in the regulation of permeability of some endothelial cells in culture and in intact venules, where localized leaky sites may form where there had been a previous inflammatory response.

Animals↗

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.

Animals↗

Endothelial gaps and permeability of venules in rat tracheas exposed to inflammatory stimuli.

This study determined the number of endothelial gaps in venules of the rat trachea and related these values to the amount of plasma extravasation after an inflammatory stimulus (neurogenic inflammation). From 1 to 30 min after the stimulus, vessels were fixed by vascular perfusion, and endothelial cell borders were stained with silver nitrate, which made it possible to quantify the number and distribution of endothelial gaps. It also was possible to quantify the leukocyte attachment sites, to measure the size, shape, and number of endothelial cells, and to delineate the architecture of the tracheal vasculature. Sites of increased vascular permeability were localized with Monastral blue B, india ink, or fluorescent microspheres. After the stimulus, the silver lines around endothelial cells of postcapillary venules and collecting venules were interrupted by stereotyped silver dots (diam, 1.4 +/- 0.03 microns; +/- SE), which were found by electron microscopy to be silver deposits at endothelial gaps. The dots were most abundant in the smallest postcapillary venules (diam, 7-20 microns) where Monastral blue extravasation was greatest. The number of silver dots (14.4 +/- 0.7 dots/endothelial cell) and the amount of extravasation were maximal 1 min after the stimulus. However, the dots disappeared more slowly (half-life, 3.2 min) than did the extravasation (half-life, 1.3 min). In addition to the silver dots, 64% of the sites at which leukocytes were attached to the endothelium were stained with silver. These sites were marked by silver rings (diam, 3.4 +/- 0.2 microns) and were most numerous in the largest postcapillary venules (diam, 20-40 microns). Most (95%) of the silver rings were located at intercellular junctions but usually were not sites of Monastral blue extravasation. The results indicate that endothelial gaps at intercellular junctions are focal openings, which occupy < 3% of the luminal surface and are distinct from sites of leukocyte attachment. The reduction in Monastral blue extravasation that precedes the closure of the gaps could result from a decrease in the driving force for the convective movement of the tracer or from a decrease in the conductance of the gaps, perhaps due to the accumulation of sievelike substances within the gaps.

Animals↗

Dilatory effect of furosemide on rat tracheal arterioles and venules.

Furosemide pretreatment greatly reduces the severity of an asthmatic response to several types of bronchoconstrictor challenge. Indirect evidence suggests that furosemide exerts its protective effects by dilating the airway vasculature during thermal stress. To test the hypothesis that furosemide dilates airway microvessels, the tracheas of anesthetized rats were surgically exposed and continuously suffused with Krebs Ringer bicarbonate warmed to 37 degrees C. Tracheal adventitial arterioles (13.0 to 41.0 microns initial diameter, n = 47) and venules (50.0 to 99.0 microns initial diameter, n = 46) were visualized with a videomicroscope, and vessel diameters were measured using videocalipers. When vessels were preconstricted with 10(-4) M phenylephrine, a selective alpha 1-adrenergic agonist, and then treated with 10(-4) M furosemide, significant (p < 0.05) dilation was observed in both arterioles (from 64.6 to 79.5% of their initial diameter) and venules (from 52.1 to 65.4% of their initial diameter). When vessels were preconstricted with 10(-4) phenylephrine, after pretreatment with the cyclooxygenase inhibitor indomethacin (5.0 mg/kg), 10(-4) M furosemide significantly dilated arterioles (from 77.5 to 93.0% of their initial diameter) and venules (from 58.5 to 80.1% of their initial diameter). In vessels preconstricted with 10(-3) M L-NAME, an inhibitor of nitric oxide synthesis, addition of 10(-4) M furosemide to the suffusion still caused significant dilation in arterioles, from 77.4 to 88.8% of their initial diameter, and in venules from 79.5 to 86.7% of their initial diameter. These data confirm that furosemide, when applied topically, dilates tracheal arterioles and venules by cyclooxygenase- and nitric oxide-independent mechanisms.

Animals↗

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.

Animals↗

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.

Animals↗

Arteriolar dilation produced by venule endothelium-derived nitric oxide.

OBJECTIVE: We conducted bioassay experiments to determine whether nitric oxide produced by endothelial cells (endothelial-derived nitric oxide, or EDNO) within large venules could act to dilate arterioles. METHODS: In these experiments parallel segments of first-order arterioles and venules were isolated from skeletal muscle and were cannulated in series with a glass connecting tube (length: 300-500 microns). Arterioles were mechanically denuded of endothelium by a delicate yet abrasive rubbing technique. Venular endothelium remained intact. Endothelial denudation of arterioles was confirmed by the absence of dilation during exposure to acetylcholine (10(-6) mol/L). The cannulated vessels were pressurized to 30 cm H2O and the arterioles pre-constricted by approximately 50% with norepinephrine (10(-10) mol/L). RESULTS: Topical applications of acetylcholine (10(-6) mol/L) or bradykinin (10(-9) mol/L) during luminal perfusion from venule to arteriole produced significant arteriolar dilation. In contrast, a slight arteriolar constriction was observed when the direction of flow was reversed (i.e., arteriole to venule) in the presence of either acetylcholine (10(-6) mol/L) or bradykinin (10(-9) mol/L). Inhibition of venular EDNO with NG-monomethyl-L-arginine (L-NMMA; 10(-5) mol/L; 1 hour) completely abolished the arteriolar dilation observed in response to acetylcholine or bradykinin during venule to arteriole perfusion. CONCLUSIONS: These results demonstrate that venular-derived EDNO can relax arteriolar vascular smooth muscle.

Adenosine↗

Pathways of macromolecular tracer transport across venules and small veins. Structural basis for the hyperpermeability of tumor blood vessels.

BACKGROUND: Blood vessels supplying tumors are hyperpermeable to macromolecules, but the mechanisms responsible are poorly understood. EXPERIMENTAL DESIGN: To investigate the structural basis for the leakiness of tumor blood vessels, we performed a transmission electron microscopic study of three syngeneic transplantable carcinomas (mouse ovarian carcinoma and the line 1 and line 10 bile duct guinea pig carcinomas) at early intervals after intravenous injection of several macromolecular tracers. Tracers with widely differing physical properties were studied: horseradish peroxidase, ferritin, 150 kilodalton fluorescein isothiocyanate-dextran and gold-bovine serum albumin. RESULTS: All tracers leaked primarily from venules and small veins at the tumor-host interface, for the most part vessels lined by a continuous endothelium. The predominant pathway by which all four tracers exited venules in all three tumors was by way of a system of smooth membrane-bound, interconnecting vesicles and vacuoles; these tended to cluster together at irregular intervals in the endothelial cell cytoplasm to form organelle-like structures, vesiculo-vacuolar organelles (VVO). In favorable sections, VVO interfaced with both the luminal and abluminal surfaces of endothelial cells. HRP alone crossed venules and small veins through apposed inter-endothelial cell junctions. Tracers also exited vessels by way of endothelial fenestrae where these occurred (rarely) in mouse ovarian tumor-associated venules. VVO occurred with similar frequency and complexity in the continuous endothelium-lined venules and small veins that supplied the normal subcutis of either tumor-bearing or control animals. As in tumor-associated vessels, VVO provided the predominant pathway by which all four tracers exited normal vessels, but VVO labeling and extravasation were both much greater in tumor than in control vessels (p < 0.001 for ferritin). CONCLUSIONS: VVO are prominent structures in both tumor-supplying and control vessel endothelial cells and provide the primary pathway for macromolecular extravasation. The large increase in permeability characteristic of tumor vessels is likely attributable to upregulation of VVO function.

Animals↗

Lectin-like cell adhesion molecule 1 mediates leukocyte rolling in mesenteric venules in vivo.

During the inflammatory response, granulocytes and other leukocytes adhere to and emigrate from small venules. Before firm attachment, leukocytes are observed rolling slowly along the endothelium in venules of most tissues accessible to intravital microscopy. The molecular mechanism underlying this early type of leukocyte-endothelial interaction is unknown. Leukocyte rolling was investigated in venules (diameter, 40 microns) of the exposed rat mesentery. Micro-infusion of a recombinant soluble chimera (LEC-IgG) of the murine homing receptor lectin-like cell adhesion molecule 1 (LEC-CAM 1; gp90MEL) into individual venules reduced the number of rolling leukocytes by 89% +/- 2% (mean +/- SEM, n = 20 venules), while a similar CD4 chimera (CD4-IgG) had no effect (inhibition 14% +/- 7%, n = 25). Rolling was also greatly reduced by a polyclonal serum against LEC-CAM 1 (inhibition 84% +/- 3%, n = 35); preimmune serum was ineffective (11% +/- 13% inhibition, n = 28). These findings indicate that LEC-CAM 1 mediates the adhesive interaction underlying leukocyte rolling and thus may play an important role in inflammation and in pathologic conditions involving leukocytes.

Animals↗

Thromboembolic reaction following wall puncture in arterioles and venules of the rabbit mesentery.

The walls of rabbit mesenteric arterioles and venules (diameter 20 to 40 microns) were punctured with glass micropipets (tip diameter 6 to 8 microns). Thromboembolic reactions resulting from this standardized, small mechanical vessel wall injury could be quantified in vivo with the use of intravital video-microscopy. Following induction of the injury thrombus growth started immediately (less than 0.1 s). Bleeding times were short, on the average less than 2 s, and did not differ between arterioles and venules. The duration of the embolization process was significantly longer in arterioles than in venules (median 101 and 17 s, respectively), and more emboli were produced in arterioles than in venules (median 6 and 1, respectively). Arteriolar thrombi were more effective in plugging the punctured holes than venular thrombi. The differences in thromboembolic reaction between arterioles and venules, as found in the present study, can probably not be explained by fluid dynamic factors.

Animals↗

Endothelin-1-induced vasoconstriction causes a significant increase in portal pressure of rat liver: localized constrictive effect on the distal segment of preterminal portal venules as revealed by light and electron microscopy and serial reconstruction.

Intraportal infusion of endothelin-1 (ET-1), a potent vasoconstrictor, significantly elevates portal venous pressure. To determine the major site of vascular constriction in the intrahepatic porto-sinusoidal system, we performed an in situ perfusion of rat livers with 1 nmol/L ET-1 at a flow rate of 20 mL/min. Portal pressure rose from 22 cm H2O to 54 cm H2O within 25 minutes. Specimens were prepared for light-microscopic serial reconstruction and electron microscopy. The distal segment of preterminal portal venules (DS/PPV) with an inner diameter of 40 to 80 microm showed complete obliteration of the lumen over a 300-microm distance caused by the intense contraction of perivascular smooth muscle cells and protruding of endothelial cells into the lumen. The proximal segment of preterminal portal venules (PS/PPV) with a larger diameter up to 150 microm also underwent strong constriction, but still had luminal space for the flow, while the PS/PPV with a diameter of 150 to 400 microm showed moderate or mild constriction and retained a wide lumen. Neither terminal portal venules, inlet venules, sinusoids, nor central veins, however, exhibited demonstrable constriction. Liver parenchyma fed by the inlet venules that emerged from the PS/PPV exhibited a wide sinusoidal lumen and vacuolated hepatocytes caused by the influx of excess portal perfusate that escaped from the occlusive areas. The present study has revealed that the DS/PPV functions as a presinusoidal quasi-sphincter mechanism and is involved in the redistribution of intrahepatic portal flow under increased portal pressure.

Animals↗

The role of adenosine in dilator responses induced in arterioles and venules of rat skeletal muscle by systemic hypoxia.

1. In experiments on anaesthetized rats, we have studied the role of adenosine in mediating responses induced in individual arterioles and venules of the spinotrapezius muscle by systemic hypoxia. 2. During systemic hypoxia induced by breathing 6% O2 for 3 min, some arterioles and venules dilated while others constricted. Topical application of the adenosine receptor antagonist, 8 phenyl-theophylline (8-PT), to the spinotrapezius had no effect on the constrictor responses but greatly reduced the dilator responses. The vessels nearest to the capillary bed-terminal arterioles and collecting venules--were most affected; their mean changes in diameter were reduced from 39 and 8% to 11 and -1.6% respectively. 3. In accord with these results, topical application of adenosine (2 x 10(-7)-2 x 10(-3) M) produced graded dilation of all sections of the arterial and venous trees; the terminal arterioles and collecting venules were most responsive, being dilated at maximum by 31 and 15% respectively. The dilator responses induced in those vessels that constricted during hypoxia were fully comparable with those that dilated during hypoxia. 4. Histochemical analysis of the spinotrapezius revealed that oxidative fibres that most readily release adenosine, glycolytic and mixed fibres were all evenly distributed throughout the muscle. There is no reason to suppose that some vessels are preferentially influenced by oxidative fibres. 5. These results indicate that adenosine plays a major role in dilating both arterioles and venules of muscle during systemic hypoxia. But, they are consistent with the idea that the adenosine that is important is not released from muscle fibres, but synthesized by 5'-nucleotidase localized to the blood vessels; its activity may decrease proximally along the vascular tree and may vary from one vessel to another depending on the local O2 tension.

Adenosine↗

An electron microscope study on permeability in cerebral venules in the rats with hypertensive encephalopathy.

Hypertensive encephalopathy was induced in the rat by clipping one renal artery and contralateral nephrectomy. The possible changes of vascular permeability of the cerebral blood capillaries and venules were investigated by using ferritin as a tracer. The uninephrectomized rats served as controls. In controls, ferritin was never seen in the basement membranes, within plasmalemmal vesicles on the basal surface of the endothelium, or in endothelial cell junctions of cerebral capillaries and venules up to 180 min after the injection. In venules of the brain in rats with hypertensive encephalopathy, a number of ferritin particles appeared in the basement membrane in 60 min after the injection. Many plasmalemmal vesicles in the endothelial cells of venules were labeled with ferritin. However, ferritin particles were never found in the endothelial cell junctions. The results suggested that leakage of macromolecules, such as serum proteins, occurred in venules mainly by increased vesicular transport.

Animals↗