MYOCARDIAL CONTRACTILE FUNCTION AND MYOFIBRILLAR ADENOSINE-TRIPHOSPHATASE ACTIVITY IN CHEMICALLY SYMPATHECTOMIZED RATS

The contractile properties and contractile protein enzymatic activity of skeletal muscle can be altered by neural influences. To determine whether similar influences apply to cardiac muscle, adult rats were chemically sympathectomized by i.v. injection of 6-hydroxydopamine (6-OHDA). After 2 wk of treatment rats were anesthetized and an index of myocardial contractility (max dP/dt) was measured in situ. Max dP/dt was depressed in 6-OHDA-treated rats [4560 .+-. 420 (mean .+-. SE) mm Hg/s] compared to controls (6710 .+-. 580 mm Hg/s). Sympathectomy was verified by reduced hemodynamic responsiveness to tyramine injections. After functional measurements were completed, the heart was excised. Myofibrils were prepared from left ventricular tissue and analyzed for ATPase activity. Myofibrillar protein yield averaged 38 .+-. 2 mg/g in controls and was not significantly different in 6-OHDA rats. Myofibrillar ATPase activity was 0.314 .+-. 0.014 .mu.mol Pi/mg per min in controls. Enzyme activity was significantly reduced to 0.230 .+-. 0.020 .mu.mol Pi/mg per min in 6-OHDA rats. A chronic reduction in sympathetic stimulation to the heart may result in depression of myocardial contractile function accompanied by reduced myofibrillar ATPase activity. Acute (16-18 h) chemical sympathectomy depressed the contractile function index without altering ATPase activity. Bilateral adrenalectomy produced no further decrement in myofibrillar ATPase activity in chronically (2 wk) sympathectomized rats. Changes in contractile protein enzymatic properties may be mediated by sympathetic neural influences and involve synthesis of new contractile protein(s) with altered enzymatic properties.