Cardiovascular Responses to Epinephrine During Acute Hypercapnia in Dogs: Effects of Autonomic Blocking Drugs

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Abstract
The reduction of cardiovascular responsiveness to epinephrine which develops during hypercapnia has been investigated in the pen-tobarbital-anesthetized dog. Parameters evaluated include arterial blood pH and pressor, chronotropic, and inotropic responses to epinephrine. Hypercapnia was induced by ventilation with either 15 or 30% carbon dioxide for a constant interval (either 2 or 10 minutes) before administration of epinephrine. In this species and under the conditions employed, it was shown that the chronotropic, pressor, and inotropic responses to epinephrine were reduced in that order by hypercapnia. These responses were found to be reduced both in amplitude and duration. Phentolamine enhances the cardiac blocking activity of carbon dioxide. The depressor response to epinephrine, following phentolamine, was found to be exquisitely sensitive to elimination by hypercapnia. Cardiac stimulatory responses elicited by acetylcholine in atropinized dogs were not reduced by the intensity of hypercapnia employed in this study. The degree of refractoriness to epinephrine produced by high concentrations of CO2 was less in those animals that had been exposed previously to high concentrations of carbon dioxide. Arterial blood pH determinations were found to be misleading when employed as an index of epinephrine responsiveness. Reduction of available catecholamine stores by reserpine, adrenalectomy, or P-286 reduced the pressor refractoriness. Ganglionic blockade was largely ineffective in this respect as was parasympathetic blockade with atropine.