BACKGROUND:Acute administration of cocaine leads to left ventricular dysfunction and a decrease in coronary blood flow. This experiment studied the relationship between function and flow over time in cocaine heart disease and examined the effects of captopril on this relationship. METHODS:Dogs anesthetized with pentobarbital (n = 13) were given a 3 mg/kg body weight intravenous bolus of cocaine followed by a 7 mg/kg infusion over 10 minutes. Animals were then randomly assigned to receive either captopril (0.5 mg/kg infused over 5 minutes, followed by 0.5 mg/kg/h) or an equivalent volume of saline beginning 15 minutes after cocaine administration. Coronary blood flow (radioactive microspheres and Doppler flow probes) and left ventricular function (two-dimensional echocardiogram and dP/dt) were monitored for 2 hours. RESULTS:Within 15 minutes, cocaine caused a drop in dP/dt by 39% to 42% and in coronary blood flow by 35%. Cocaine also caused an increase in left ventricular end-diastolic pressures in both groups. Cocaine resulted in prolongation of an index of end-diastolic isovolumic relaxation time (tau) from a baseline of 34 milliseconds to 56 milliseconds at 15 minutes after cocaine administration in the control group and from a baseline of 35 milliseconds to 49 milliseconds in the captopril group (P < 0.05). By 2 hours after therapy, the tau in the control group remained elevated, whereas in the captopril group it returned toward baseline. At 2 hours of observation, systolic function recovered while coronary flow remained depressed. There was no difference between the captopril and control groups in coronary blood flow or systolic cardiac function at any time during the study. CONCLUSIONS:Cocaine caused left ventricular systolic and diastolic dysfunction as well as reduced coronary blood flow. At 2 hours there is a dissociation of systolic function, which recovers, and of coronary blood flow, which does not. Captopril had no effect on coronary blood flow or systolic left ventricular function following cocaine administration.

译文

背景:可卡因的急性给药导致左心功能不全和冠状动脉血流减少。该实验研究了可卡因心脏病患者的功能和血流随时间的关系,并研究了卡托普利对这种关系的影响。
方法:对戊巴比妥麻醉的狗(n = 13)给予3 mg / kg体重的可卡因静脉推注,然后在10分钟内输注7 mg / kg。然后将动物随机分配为在服用可卡因后15分钟开始接受卡托普利(0.5 mg / kg输注5分钟,然后输注0.5 mg / kg / h)或等体积的盐水。监测冠状动脉血流量(放射性微球和多普勒血流探头)和左心室功能(二维超声心动图和dP / dt)持续2小时。
结果:在15分钟内,可卡因使dP / dt下降了39%至42%,冠状动脉血流量下降了35%。可卡因还引起两组左心室舒张末期压力的升高。可卡因导致对照组的可卡因给药后舒张末期等容舒张时间指数从34毫秒延长至56毫秒,卡托普利组从35毫秒延长至49毫秒(P <0.05)。到治疗后2小时,对照组的tau仍然升高,而卡托普利组的tau恢复到基线。观察2小时后,收缩功能恢复,而冠状动脉血流却保持下降。在研究过程中的任何时候,卡托普利和对照组之间的冠状动脉血流量或心脏收缩功能均无差异。
结论:可卡因引起左心室收缩和舒张功能障碍以及冠状动脉血流量减少。在2小时时,收缩功能恢复正常,而冠状动脉血流没有恢复。可卡因给药后,卡托普利对冠状动脉血流或收缩期左心室功能无影响。

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