Capillary Flow and Capillary Transport in Dog Skeletal Muscle at Prolonged Low Perfusion Pressure

1972 ◽  
Vol 4 (3) ◽  
pp. 221-230 ◽  
Author(s):  
K.L. Appelgren
Keyword(s):  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Capillary Flow ◽  
Capillary Transport

Video microscopy of cerebrocortical capillary flow: response to hypotension and intracranial hypertension

1995 ◽  
Vol 268 (6) ◽  
pp. H2202-H2210 ◽  
Author(s):  
A. G. Hudetz ◽  
G. Feher ◽  
C. G. Weigle ◽  
D. E. Knuese ◽  
J. P. Kampine
Keyword(s):  
Cerebral Cortex ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Capillary Flow ◽  
Video Microscopy ◽  
Cell Counting ◽  
Correlation Technique ◽  
Cranial Window

Although autoregulation of cerebral blood flow is well established, the response of cerebral capillary circulation to reduced cerebral perfusion pressure (CPP) is unclear. The objective of this study was to determine whether red cell flow velocity in individual capillaries of the cerebral cortex is maintained during acute decreases in CPP. Microcirculation of the superficial parietal cerebral cortex of adult barbiturate-anesthetized artificially ventilated rats was visualized using a new design of closed-perfused cranial window and epifluorescent-intensified video microscopy. Fluorescein-isothiocyanate-labeled red blood cells (FRBC) injected intravenously were used as markers of capillary flow. CPP, defined as mean arterial pressure minus intracranial pressure, was reduced by controlled hemorrhage or by stepwise elevation of local intracranial pressure. The movement of FRBC in the parenchymal capillary network was video recorded at each pressure level, and FRBC velocity in each capillary was measured off-line with use of the dual-window digital cross-correlation technique. FRBC flux in the capillaries was measured by automated cell counting. FRBC velocity at normal perfusion pressure was 1.47 +/- 0.58 (SD) mm/s and changed little in the perfusion pressure range of 70-120 mmHg. The autoregulatory index in this pressure range was 0.0049 mm.s-1.mmHg-1. Opening of previously unperfused capillaries was not observed. FRBC flux correlated with FRBC velocity, but the latter was maintained in a narrower range than FRBC flux, suggesting a decrease in capillary diameter or hematocrit with decreasing perfusion pressure. The results suggest that flow autoregulation is associated with the maintenance of capillary flow velocity and that capillary recruitment does not contribute to flow autoregulation in the rat cerebral cortex.

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

Myogenic responses of isolated rat skeletal muscle venules: modulation by norepinephrine and endothelium

1996 ◽  
Vol 271 (1) ◽  
pp. H267-H272 ◽  
Author(s):  
G. Dornyei ◽  
E. Monos ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Perfusion Pressure ◽  
Receptor Activation ◽  
Intraluminal Pressure ◽  
Negative Slope ◽  
Internal Diameter ◽  
Myogenic Response ◽  
First Order ◽  
Diameter Curve

The pressure-induced myogenic response of large venules of skeletal muscle and its possible interactions with adrenergic receptor activation and endothelial factors have not yet been elucidated. Therefore, first-order venules of rat gracilis muscle were isolated, cannulated, and placed in an organ chamber. Changes in internal diameter of the vessels as a function of perfusion pressure (PP) were obtained. In response to increases in PP (0.5-17.5 mmHg), the diameter of venules increased from 197.1 +/- 23.96 to 369 +/- 14.1 microns. In passive conditions (in Ca(2+)-free solution), the pressure-diameter curve of venules shifted significantly upward. In the presence of norepinephrine (NE; 10(-6) M) in the bath solution, the pressure-diameter curve of active venules shifted significantly downward, and in the pressure-normalized diameter curve, a negative slope developed (-6.1 +/- 4.6). In both the absence and presence of NE, removal of endothelium significantly reduced venular diameters in the pressure ranges of 3-5 and 2-5 mmHg, respectively, but did not change significantly the characteristics of the pressure-diameter curves. These findings indicate that the smooth muscle of venules actively responds to changes in intraluminal pressure. This response is greatly facilitated by NE and modulated by the endothelium. The myogenic response of skeletal muscle venules, especially in the presence of NE, could have a role in the regulation of the resistance and capacitance of venules and, consequently, blood flow and tissue exchange in skeletal muscle.

Arteriole Vasospasm, Capillary Flow And Cell Death In Skeletal Muscle Ischemia-Reperfusion

2011 ◽  
Vol 165 (2) ◽  
pp. 183
Author(s):  
K.K. Kao ◽  
J.C. Jimenez ◽  
M.G. Stelzner ◽  
J.E. Thompson ◽  
D.J. Saltzman
Keyword(s):  
Skeletal Muscle ◽  
Cell Death ◽  
Capillary Flow ◽  
Ischemia Reperfusion ◽  
Muscle Ischemia

Vasodilation induced by endothelin: role of EDRF and prostanoids in rat hindquarters

1990 ◽  
Vol 259 (6) ◽  
pp. H1835-H1841 ◽  
Author(s):  
E. H. Ohlstein ◽  
L. Vickery ◽  
C. Sauermelch ◽  
R. N. Willette
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Microvascular Perfusion ◽  
Hemodynamic Effects ◽  
Hemodynamic Responses ◽  
Pithed Rats ◽  
Dose Dependent

Hemodynamic responses to endothelin (ET-1) were studied in hindquarters of anesthetized rats and also in isolated buffer-perfused hindquarters of pithed rats. ET-1 (10-100 pmol ia) produced brief dose-related increases in hindquarter blood flow. Acetylcholine (ACh. 0.3-1 micrograms ia) produced similar vasodilator responses. Hemodynamic responses elicited by either ET-1 or ACh were not significantly altered by pretreatment with indomethacin. ET-1 produced dose-dependent increases in skeletal muscle microvascular perfusion, whereas ET-1 had no effect on cutaneous microvascular perfusion, suggesting that vasodilation in the skeletal muscle of the hindlimb contributes to the increase in hindquarter blood flow induced by ET-1. Hemodynamic effects of ET-1 and ACh were studied in the isolated in situ buffer-perfused hindquarters of pithed rats. ET-1 (0.01-300 pmol ia) produced only dose-dependent increases in hindquarter perfusion pressure under basal conditions or when the vascular preparation was precontracted with methoxamine. ET-1 induced vasorelaxation was not observed. ACh (3 microgram ia) produced a 64% reduction in hindquarter perfusion pressure; indicative of endothelium-dependent relaxation. ET-3 (0.1-300 pmol) produced only dose-dependent increases in hindquarter perfusion pressure. When hemodynamic effects of ET-1 were studied under conditions of constant pressure, results were similar to those obtained under constant flow. This study demonstrates that in the rat hindquarters endothelium-derived relaxing factors and prostanoids do not appear to be mediators of endothelin-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

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