Dopamine has been used for many years to treat patients with severe he
art failure. it is not clear whether improvements of cardiac function
may be due to a direct action on heart. This study was aimed to invest
igate the direct action of dopamine on failing heart. We chose male Wi
star rats which had undergone uninephrectomy under ether anaesthesia t
o induce hypertension to result in heart failure. After 5 weeks the he
arts were excised and perfused according to Langerdoff's technique. He
art rate, systolic and diastolic ventricular pressures, the derivative
of the intraventricular pressure lime ratio, and coronary flow were m
easured at baseline, at 2 and 5 min and then every 5 min during a 30-m
in period. Rat hearts were divided into 4 groups of 5 hearts: group 1,
perfused without drug; group 2, perfused with dopamine at 4 mu g/kg/m
in; group 3, perfused with dopamine at 8 mu g/kg/min; group 4, perfuse
d with dopamine al 8 mu g/kg/min and with 100 nM I. C.I. 118.551 (beta
2-ant: beta-2 receptors antagonist) at the same time. Our results sho
w that dopamine induced a negative inotropic effect and a reduction oi
coronary flow. Moreover, there was a significant chronotropic action
even when dopamine was administered at high concentrations. So we foun
d no positive dopamine effect on isolated failured hearts of rat. This
might be explained by both alpha-1-induced vasoconstriction and the s
timulation of alpha-1B receptors. We conclude that the favourable effe
cts or dopamine in heart failure could be due to DA1 vasodilation rath
er than to a direct inotropic action on the heart.