Kissin I, Kilpatrick J V
J Cardiovasc Pharmacol. 1982 Jan-Feb;4(1):111-5. doi: 10.1097/00005344-198201000-00018.
The effect of nifedipine on the myocardial energy demand--supply imbalance caused by vasopressin-induced vasoconstriction, coronary occlusion, and their combined action was studied in isolated perfused rabbit hearts using the method of NADH fluorometry. Nifedipine (0.015 microgram/ml) completely prevented the development of NAD/NADH imbalance caused by coronary vasospasm. The role of vasoconstriction as an addition to coronary occlusion was very small in the development of regional energy imbalance and the vasopressin-induced detrimental effect was prevented by nifedipine. Energy imbalance caused by the occlusion alone was only partially improved by the drug. There was a delay in the development of energy imbalance and reduction in the final degree of NADH fluorescence response to the occlusion (97 +/- 8% vs. 66 +/- 9%, p less than 0.05).
采用NADH荧光测定法,在离体灌注兔心脏中研究了硝苯地平对由血管加压素诱导的血管收缩、冠状动脉闭塞及其联合作用所引起的心肌能量供需失衡的影响。硝苯地平(0.015微克/毫升)完全阻止了由冠状动脉痉挛引起的NAD/NADH失衡的发展。在局部能量失衡的发展过程中,血管收缩作为冠状动脉闭塞的附加因素,其作用非常小,且硝苯地平可预防血管加压素诱导的有害作用。仅由闭塞引起的能量失衡仅被该药物部分改善。能量失衡的发展出现延迟,并且对闭塞的NADH荧光反应的最终程度降低(97±8%对66±9%,p<0.05)。