Studies of hypotension and cardiac flow in lsoproterenol-induced myocardial necrosis

The role of hypotension in isoproterenol-induced myocardial necrosis was evaluated using suprarenal aortic ligation as a means of mechanically reversing the severe hypotension caused by isoproterenol. Total myocardial metal content was measured as a sensitive indicator of myocardial damage at 3 and 6 hr after subcutaneous isoproterenol administration (100 mg/kg). A marked increase in Ca²⁺ content indicative of severe myocardial necrosis occurred in spite of aortic ligation. The magnitude of the Ca²⁺ increase was diminished in ligated animals, however, probably due to hyperkalemia, increased myocardial K⁺ content, and decreased myocardial Na⁺ induced by the ligation procedure. Fractional blood flow was also examined by a ⁸⁶Rb technique following isoproterenol alone and isoproterenol with aortic ligation. Isoproterenol increased flow to the entire heart-preferentially to the epicardium-and decreased flow to kidney and liver. Aortic ligation with isoproterenol markedly increased flow to both the epicardium and endocardium of the heart, and increased flow to the liver. These findings seriously question the importance of hypotension and decreased cardiac flow in the etiology of isoproterenol-induced myocardial necrosis.