|Budget Amount *help
¥2,200,000 (Direct Cost : ¥2,200,000)
Fiscal Year 1996 : ¥200,000 (Direct Cost : ¥200,000)
Fiscal Year 1995 : ¥2,000,000 (Direct Cost : ¥2,000,000)
Introduction : (1) Recently, it has been sugested that halogenated anesthetics inhibit endothelium-dependent relaxation in vitro study. However, in vivo data, the interaction between volatile anesthetics, especially sevoflurane, and nitric oxide are less clear. Therefore, we examined the hypothesis that there was a dose-response relationship between sevoflurane concentrations and inhibition of EDNO-induced vasodilation in a canine model. Regional blood flow was measured with radiolabeled micropheres. (2) The mechanisms of vasodilation induced by hypercapnia are less clear. We examined whether vasodilation induced by hypercapnia was mediated by nitric oxide under sevoflurane anesthesia.
Method : (1) Dose were divided into three groups (0.75,1.0 and 1.25 MAC of sevoflurane : group L,M and H), FIO_2=0.4 and mechanically ventilated. Radioactive microspheres were injected into left ventricle, before and 10 minutes after L-NAME (10mg/kg) injection. We calculated the rate of regional vascular
resistance change. (2) Under 1.25 MAC sevoflurane anesthesia, dogs were divided into two groups (55mmHg <PaCO2 <65 mmHg : group H,35 mmHg<PaCO2 <45mmHg : group N). We calculated the rate of regional vascular resistance change using the same method.
Results : (1) At coronary, lung, pancreas, stomach and muscle vessels, the rate of vascular resistance increase caused by L-NAME in group H,was significantly smaller than that in group L.At cerebral, liver, kidney, adrenal grand, spleen, minor and major intestine and skin vessels, the rate of vascular resistance increase were significant in all groups, but there was no siginificant change between group H and group L.(2) Vascular resistances at cerebral, coronary, digestive organs were siginificantly smaller in group H than that in group N,before and after L-NAME.The rate of vascular resistance increase caused by L-NAME was siginificantly less in group H than that in group N at cerebral, but there were no change at coronary and digestive organs.
Conclusions : (1) These data indicate that sovoflurane anesthesia inhibits endothelium-dependent relaxation caused by nitric oxide at coronary, lung, pancreas, stomach and muscle vessels in dose dependent manner, in vivo study. It is coincided with provious data in vitro study.
(2) Our results suggest that NO does not mediate the hypercapnic vasodilation at cerebral, coronary and digestive organs. Less