Effect of chemical sympathectomy on cardiac hypertrophy and hemodynamics following myocardial infarction in the rat.

The effects of sympathectomy on cardiac structure and function were studied in an animal model of myocardial infarction. Ninety-six rats were double randomized to control or infarction disease state and to placebo or chemical sympathectomy (guanethidine, 30 mg/kg daily, intraperitoneal). Five weeks after anterior infarction, there was hypertrophy in placebo-treated animals in myocardial fibers remote from the infarct (9.8 +/- 1.8 microns in infarction vs 8.1 +/- 1.0 microns in control, p less than 0.05). However, myocardial hypertrophy was not present in guanethidine-treated animals (8.6 + 1.6 microns in infarction vs 8.0 + 0.6 microns in control, p = N.S.). Guanethidine treatment caused significant reductions in systolic arterial blood pressure and indices of left ventricular contractility and relaxation (p less than 0.05), but these effects were not different between infarct and control treatments (p = N.S.). Although both effects of guanethidine treatment (sympathectomy and hemodynamic) were correlated with myocardial fiber diameter by univariate analysis, only sympathectomy was significant by stepwise regression analysis (p less than 0.05). Therefore, the cardiac sympathetic nerves have important effects on the development of hypertrophy after myocardial infarction, and sympathectomy alters this process in the rat model.