beta-Adrenergic activity and cardiovascular response to severe respiratory acidosis

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Abstract
The mechanism responsible for the depressive myocardial effects of severe respiratory acidosis is unclear, but sympathetic stimulation and catecholamines are involved. The influence of .beta.-adrenergic receptor activity on the myocardial response to severe respiratory acidosis was studied in 18 anesthetized, mechanically ventilated dogs. Arterial CO2 tension (PaCO2) was raised by increasing the inspired CO2 fractions in O2. In control animals, as PaCO2 increased, heart rate (HR) decreased (PaCO2 .apprx. 110 mm Hg), then returned to control (PaCO2 .apprx. 220 mm Hg); arterial blood pressure (.hivin.Pa) and cardiac output (.ovrhdot.Q) remained unchanged from prehypercapnia levels. At PaCO2 > 350 mm Hg, .hivin.Pa, HR and .ovrhdot.Q decreased and left ventricular function (LVF) curves were depressed. Death occurred at a PaCO2 of 404 .+-. 25 mm Hg (pH 6.48 .+-. 0.02). In a 2nd group of animals, administration of isoproterenol during the increase in PaCO2 did not result in depression of myocardial function and death did not occur even at a significantly higher PaCO2 (PaCO2 496 .+-. 12 mm Hg; pH 6.39 .+-. 0.02) than in the control group. Administration of propranolol to a 3rd group of animals as PaCO2 increased did not change .hivin.Pa, HR and .ovrhdot.Q; LVF curves indicated a more rapid and severe depression of myocardial performance than in control, and death occurred at a significantly lower PaCO2 (PaCO2 220 .+-. 25 mm Hg; pH 6.65 .+-. 0.02). .beta.-Adrenergic receptor stimulation can prevent hypercapnic heart failure. .beta.-Adrenergic receptor activity is involved in the mechanism responsible for this failure.