Angiotensin II-induced myocardial damage with a special reference to low cardiac output syndrome.

The effects of large doses of angiotensin II on the rabbit kidney and heart and or the ability of perfused canine kidney to inactivate angiotensin II were examined to clarify the role of angiotensin II in the low cardiac output syndrome after open-heart surgery. Intravenous infusion of angiotensin II at a rate of 1.1 to 1.4 microgram/Kg/min for 48 hours caused multifocal myocardial necrosis and renal mononuclear cell infiltration and necrosis. Isolated canine kidney preparations inactivated 76% of angiotensin I and 79% of angiotensin II. The results indicates that the kidney can inactivate angiotensin and that high doses of angiotensin II can produce myocardial and renal lesions. It is suggested that an increased concentration of angiotensin II may result in the low cardiac output syndrome through myocardial damage, and that decreased inactivation of angiotensin II by the kidney accelerates the myocardial damage.