Holt G W, Norris R L, Ravenscroft P J, Bett J H, Dryburgh L G, Boyle C M
J Cardiovasc Pharmacol. 1983 Jan-Feb;5(1):51-4.
We used M-mode echocardiography and recordings of systolic time intervals to follow changes in left ventricular systolic function of 10 normal subjects during administration of 200 mg oral disopyramide every 8 h. Left ventricular function was significantly depressed (peak rate of change of dimension - 17%, p less than 0.001; mean velocity of circumferential fiber shortening - 15%, p less than 0.01; percent fractional shortening - 16%, p less than 0.05) for as long as 7 h after a dose. These changes could be correlated with those in plasma concentrations of free and total disopyramide, and of its mono-N-dealkylated metabolite (change in peak rate of change of dimension versus levels of disopyramide plus metabolite, r = -0.41, p less than 0.03; changes in ratio preejection time/ejection time versus levels of disopyramide and metabolite, r = 0.62, p less than 0.002).
我们采用M型超声心动图和收缩期时间间期记录法,对10名正常受试者每8小时口服200毫克双异丙吡胺期间左心室收缩功能的变化进行了跟踪研究。给药后长达7小时,左心室功能显著降低(内径变化峰值速率降低17%,p<0.001;圆周纤维缩短平均速度降低15%,p<0.01;缩短分数百分比降低16%,p<0.05)。这些变化与游离和总双异丙吡胺及其单-N-去烷基代谢产物的血浆浓度变化相关(内径变化峰值速率变化与双异丙吡胺加代谢产物水平的关系,r = -0.41,p<0.03;射血前期时间/射血时间比值变化与双异丙吡胺和代谢产物水平的关系,r = 0.62,p<0.002)。