Coronary venular responses to flow and pressure.

Abstract

In previous studies, we demonstrated that both endothelium-dependent flow-induced vasodilation and endothelium-independent myogenic responses occur in porcine coronary arterioles. However, it was not established whether these responses are present in the coronary venular microcirculation. The aim of this study was to test the hypotheses that 1) coronary venules, like arterioles, exhibit flow-induced dilation and myogenic responsiveness, and 2) venular flow-induced dilation is endothelium-dependent and is mediated by the release of a nitrovasodilator. Experiments were performed in porcine subepicardial coronary venules, 80-120 microns in diameter, by using cannulated isolated vessel techniques to allow intraluminal pressure and flow to be independently controlled. Flow was initiated by simultaneously moving two perfusion reservoirs connected to the cannulating pipettes in equal amounts but in opposite directions. In the absence of flow, i.e., zero pressure gradient (delta P) between the two reservoirs, venules developed spontaneous tone to 75-80% of maximum diameter at 10 cm H2O intraluminal pressure. Venules gradually dilated in response to stepwise increases in flow (i.e., delta P). The threshold for the flow-induced dilation occurred at delta P = 1 cm H2O (flow = 3.5 nl/sec), and the maximal response (dilation to 93 +/- 2% of maximum diameter) occurred when delta P was elevated to > or = 6 cm H2O (flow = 21 nl/sec at delta P = 6 cm H2O). Flow-induced dilation was abolished after the endothelium was damaged by perfusion of an air bolus through the lumen. Vasoconstriction was observed when denuded venules were subjected to relatively high luminal flows (> or = 21 nl/sec).(ABSTRACT TRUNCATED AT 250 WORDS)

Protein kinase G regulates the basal tension and plays a major role in nitrovasodilator‐induced relaxation of porcine coronary veins

“…Hence, under some circumstances, coronary veins may play a greater role than the arteries in regulating coronary blood flow. With regard to the role of EDNO in the coronary venous system, there is a study showing that flow-induced dilation of porcine coronary venules is mediated in an EDNO-dependent manner and that the venular dilation induced by flow is converted to constriction when the endothelium is denuded (Kuo et al, 1993). This suggests that EDNO may play an important role in ensuring adequate blood flow and oxygen transport to the heart during intense metabolic demands (Kuo et al, 1993).…”

“…With regard to the role of EDNO in the coronary venous system, there is a study showing that flow-induced dilation of porcine coronary venules is mediated in an EDNO-dependent manner and that the venular dilation induced by flow is converted to constriction when the endothelium is denuded (Kuo et al, 1993). This suggests that EDNO may play an important role in ensuring adequate blood flow and oxygen transport to the heart during intense metabolic demands (Kuo et al, 1993). In this study, nitroglycerin and nitric oxide caused a marked relaxation of porcine coronary veins, which is comparable to that of coronary arteries (Qin et al, 2007).…”

“…Such a phenomenon may contribute to the adjustment of postcapillary resistance to maintain optimal myocardial perfusion and fluid filtration across the capillary wall during cardiovascular stress, such as physical exercise. However, when the veins are denuded of endothelium, the dilation induced by flow is converted to constriction, suggesting that when the vascular endothelium is damaged, blood flow and oxygen transport to the heart may be compromised during intense metabolic demands (Kuo et al, 1993).…”

“…Such a phenomenon may contribute to the adjustment of postcapillary resistance to maintain optimal myocardial perfusion and fluid filtration across the capillary wall during cardiovascular stress, such as physical exercise. However, when the veins are denuded of endothelium, the dilation induced by flow is converted to constriction, suggesting that when the vascular endothelium is damaged, blood flow and oxygen transport to the heart may be compromised during intense metabolic demands (Kuo et al, 1993).In various vessel types including coronary arteries, EDNO and nitric oxide-releasing agents may relax the vessels through activation of soluble guanylyl cyclase, followed by elevation of cGMP and activation of cGMP-dependent protein kinase (PKG) (Francis and Corbin, 1994;Walsh et al 1995;Lohmann et al, 1997;Gao et al, 1999;Lincoln et al, 2001;Qin et al, 2007). However, nitric oxide may also cause relaxation through cGMP-independent as well as PKG-independent mechanisms (Abderrahmane et al, 1998;Janssen et al, 2000;Francis et al, 2005).…”

Vázizomkisvénák vazomotortónusának intrinszik szabályozómechanizmusai

“…A vá-lasz lényege, hogy az intraluminalis nyomás növekedése-kor az erek átmérője csökken, a nyomás csökkenésekor viszont az átmérő növekszik. A miogén vazomotorvá-laszt először 1902-ben Bayliss írta le kutya arteria carotisával végzett kísérletei alapján [5], amelynek meglétét később különböző állatfajok számos szerveiben, számos artériás érterületein is igazolták [6][7][8][9][10][11][12][13][14][15], és jelenlétét emberi erekben kimutatták [2][3][4].…”