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Although metabolic acidemia reduces the contractility of cardiac muscle in isolated preparations, it does not do so to the same extent in intact animals or those with a functioning sympathoadrenal system. The present study was designed to determine if the resistance of the heart to acidemia is the consequence of concurrent adrenergic influences on the myocardium. The function of the cat's left ventricle was examined in a preparation that allowed control of aortic pressure, cardiac output, heart rate and temperature. The arterial blood pH, Po2, Pco2, and temperature were continuously measured. Acidemia was produced either endogenously by temporarily diminishing perfusion of peripheral tissues, or by infusion of 0.5N lactic acid. Studies were made before and after beta-receptor blockade with propranolol, 0.25 to 0.5 mg/kg iv or im. In eight control animals, reduction of pH from 7.34 to 7.08 failed to diminish contractility. In 14 animals with beta-receptor blockade, reduction of pH to 7.02 reduced contractility by about 25% (P<.001). Correction of the acidemia by infusion of tris(hydroxymethyl)aminomethane returned contractility to approximately 95% of control. Rapid reduction of pH transiently diminished contractility in control animals and severely depressed those with beta-receptor blockade. These data support the position that sympathoadrenal activity is necessary to preserve ventricular function in the presence of severe metabolic acidemia.

Preservation of Ventricular Function by Adrenergic Influences during Metabolic Acidosis in the Cat