Effect of Pentobarbital and Atropine on Arterial Pressure Response to Ganglion Blocking Agents

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Abstract
Pentobarbital anesthesia produces an important change in the dog's arterial pressure response to TEAC. Without anesthesia, the response, instead of being sharply depressor, is characteristically pressor, or biphasic and mainly pressor. Only occasionally is it depressor. Small doses of TEAC more often elicited depressor responses than did large ones. Mecamylamine, hexamethonium and chlorisondamine usually also failed to cause appreciable lowering of arterial pressure in unanesthetized dogs, but did not show as much pressor activity as did TEAC. Responses to TEAC in hypertensive conscious man showed considerable variability, but the overall pattern of response tended more to resemble that of anesthetized than that of unanesthetized dogs. Atropine caused narrowing of pulse pressure, tachycardia, little change in mean pressure, and the response to TEAC to become mainly depressor—though not to the same degree as did pentobarbital. The greatly augmented depressor activity of ganglion blocking agents after pentobarbital anesthesia probably depends in large part upon nearly complete inhibition of parasympathetic cardioinhibitory activity by the anesthetic agent, and upon partial suppression of sympathetic compensatory reflexes by the ganglion blocking action of pentobarbital. Cardiovascular reactivity measurements are closely dependent on the conditions of the experiment and anesthesia is one of the most important of these conditions.