Vascular smooth muscle dysfunction following acute aortic ischemia-reperfusion

A hyperemic response manifested by increased blood flow is seen following extremity ischemia and reperfusion. We examined whether impairment of vascular smooth muscle relaxation or contraction could contribute to this effect. Methods Sprague-Dawley male rats (n=15) underwent four hours of infrarenal aortic clamping ischemia and one hour of reperfusion. A control group (n=11) had a sham operation. The aorta was subsequently excised, cut into rings, and suspended in a bath chamber Maximal isometric force and dose-response contraction/relaxation to KCl, norepinephrine (NE), acetylcholine (ACh), and nitroprusside (NTP) were measured and compared. Results There were no differences in ACh-induced relaxation between the two groups in the dose range from 10^-8 to 10^-5M. There was, however, a significant decrease in contractile response to KCL and righrward shift following ischemia-reperfusion [p < 0.0005] with a large decrease in the maximal induced isometric force [44 ± 3 vs 27 ± 4 nM/mm²; p < 0.005]. No changes in NE-induced contraction or NTP-relaxation were seen. Conclusions Acute aortic ischemia and reperfusion induces diminished smooth muscle contraction (KCl) which is not adrenergic-mediated (NE) and occurs before significant endothelial cell dysfunction (ACh). Such decreased smooth muscle constriction may contribute to vessel dilation and increased blood flow with reperfusion following ischemia.