THE LEFT-VENTRICULAR CONTRACTILITY OF THE RAT-HEART IS MODULATED BY CHANGES IN FLOW AND ALPHA(1)-ADRENOCEPTOR STIMULATION

Myocardial contractility depends on several mechanisms such as coronar y perfusion pressure (CPP) and flow as well as on alpha(1)-adrenocepto r stimulation. Both effects occur during the sympathetic stimulation m ediated by norepinephrine. Norepinephrine increases force development in the heart and produces vasoconstriction increasing arterial pressur e and, in turn, CPP. The contribution of each of these factors to the increase in myocardial performance needs to be clarified. Thus, in the present study we used two protocols: in the first we measured mean ar terial pressure, left ventricular pressure and rate of rise of left ve ntricular pressure development in anesthetized rats (N = 10) submitted to phenylephrine (PE) stimulation before and after propranolol plus a tropine treatment. These observations showed that in vivo alpha(1)-adr energic stimulation increases left ventricular-developed pressure (P<0 .05) together with arterial blood pressure (P<0.05). In the second pro tocol, we measured left ventricular isovolumic systolic pressure (ISP) and CPP in Langendorff constant flow-perfused hearts. The hearts (N = 7) were perfused with increasing flow rates under control conditions and PE or PE + nitroprusside (NP). Both CPP and ISP increased (P<0.01) as a function of now. CPP changes were not affected by drug treatment but ISP increased (P<0.01). The largest ISP increase was obtained wit h PE + NP treatment (P<0.01). The results suggest that both mechanisms , i.e., direct stimulation of myocardial alpha(1)-adrenoceptors and in creased flow, increased cardiac performance acting simultaneously and synergistically.