Abstract
The purpose of this investigation was to determine the role of increased beta-adrenergic activity in regulating the increase in myocardial oxygen consumption that occurs during hypoxemia in unanesthetized newborn lambs. Through a left thoracotomy, fluid-filled catheters were placed in the ascending aorta, coronary sinus and left atrium, a pressure transducer was introduced into the left ventricle, and pacing wires were sutured onto the left atrium. The lambs were studied 3 d later by making intermittent measurements of aortic and coronary sinus blood oxygen saturations and Hb concentrations, left ventricular myocardial blood flow, cardiac output, heart rate, left atrial and aortic blood pressures, the maximal first derivative of left ventricular pressure, aortic and coronary sinus blood oxygen contents, the arteriovenous difference of oxygen across the left ventricular myocardium, myocardial oxygen consumption, and external cardiac work (aortic mean blood pressure times cardiac output). In nine lambs with an intact beta-adrenergic nervous system (group 1), the above measurements were made during a control period and during hypoxemia (FiO2 = 0.08-0.10) with spontaneous tachycardia. In another group of 12 lambs (group 2), the measurements were made during a control period, after beta-blockade (1.5 mg/kg intravenous propranolol) with pacing at the control heart rate, during hypoxemia with pacing at the control heart rate, and during hypoxemia with pacing-induced tachycardia. In the group 2 lambs, beta-blockade completely inhibited the increase in heart rate, maximal first derivative of left ventricular pressure, cardiac output and cardiac work that occurred during hypoxemia in the group 1 lambs that had an intact beta-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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