Abstract
In the anesthetized dog, experimentally induced ventricular tachycardia resulted initially in a very marked decrease in mean arterial blood pressure and cardiac output, then blood pressure and cardiac output rose and stabilized slightly below or markedly below their control levels. Such tachycardia resulted in a rise in the catecholamines blood level. Acute arteriovenous fistula resulting in a definite decrease in mean arterial blood pressure followed by complete or partial recovery of the blood pressure also resulted in an increase in the catecholamines blood level. The mechanisms, origin and role of this increase in catecholamines blood level are discussed.
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