Nakai T, Ichihara K
Department of Pharmacology, Hokkaido College of Pharmacy, Otaru, Japan.
Biol Pharm Bull. 1994 Oct;17(10):1341-4. doi: 10.1248/bpb.17.1341.
Effects of diazoxide on norepinephrine-induced vasocontraction in vitro and global ischemia-induced lactate accumulation in the myocardial tissue in vivo were studied in rats. Diazoxide produced relaxation of the isolated rat aorta contracted by norepinephrine in a dose dependent manner. The relaxation of the aorta was associated with reduction of intracellular Ca2+ concentration. This reduction may be due either to activation of KATP channels or Na(+)-K+ ATPase, or to both. Global ischemia induced by aorta constriction for 30 min in vivo increased the myocardial tissue level of lactate. Pretreatment with diazoxide (10 mg.kg-1, i.v.) significantly attenuated the accumulation of lactate due to global ischemia. The present study suggests that diazoxide reduces ischemic influence on the myocardium partly through its vasodilatory action.
在大鼠中研究了二氮嗪对去甲肾上腺素诱导的体外血管收缩以及体内全局缺血诱导的心肌组织乳酸积累的影响。二氮嗪以剂量依赖性方式使去甲肾上腺素收缩的离体大鼠主动脉舒张。主动脉的舒张与细胞内Ca2+浓度的降低有关。这种降低可能是由于KATP通道或Na(+)-K+ ATP酶的激活,或两者皆有。体内通过主动脉缩窄30分钟诱导的全局缺血增加了心肌组织中的乳酸水平。用二氮嗪(10mg.kg-1,静脉注射)预处理可显著减轻全局缺血导致的乳酸积累。本研究表明,二氮嗪部分通过其血管舒张作用减轻对心肌的缺血影响。