Cardiovascular responses to carbon dioxide before and after beta-adrenergic blockade.

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Abstract
Measurements of circulatory responses to breathing 10% CO2 were made on 30 dogs anesthetized with chloralose and urethan. Breathing CO2 for 10 min caused peripheral vasoconstriction, increased arterial pressure, and decreased cardiac output in the first group of 7 dogs. Observations were made in a second group of 14 dogs after treatment with hexamethonium to inhibit cardiovascular reflexes. In these, CO2 caused peripheral vasodilatation, decreased arterial pressure, and in-creased cardiac output. Observations were made in a third group of 9 dogs treated with hexamethonium after having administered propranolol (Inderal), a beta-adrenergic blocking agent. The dose of propranolol employed was sufficient to block the vascular and cardiac effects of large intravenous infusions of isoproterenol and the cardiac effects of electrical stimulation of the stellate ganglion. This dose of propranolol did not block the vasodilatation and increased cardiac output which occurred in response to carbon dioxide suggesting that these responses are not mediated through stimulation of beta adrenergic receptors.