Angiotensin II-induced myocardial damage with a special reference to low cardiac output syndrome
T Kuroda, H Shida - Japanese Heart Journal, 1983 - jstage.jst.go.jp
T Kuroda, H Shida
Japanese Heart Journal, 1983•jstage.jst.go.jpThe 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 ƒÊg/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
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 ƒÊg/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
Summary
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 ƒÊg/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
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