Hemodynamic effects of peripheral vasoconstriction in normal and thyrotoxic subjects.

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Abstract
These studies were done to determine whether the high cardiac output of thyrotoxicosis might be in part a reflex phenomenon secondary to peripheral vasodilatation. Phenylephrine infusions were given to 7 normal subjects and 7 thyrotoxic patients. Phenylephrine was chosen for its alpha-adrenergic stimulating properties and minimal positive inotropic effects. All subjects were atropinized to attenuate the bradycardia from phenylephrine. Measurements of mean arterial pressure, mean right atrial pressure, heart rate, and cardiac index were not significantly different in the 2 groups after atropine. During phenylephrine infusions the increases in mean arterial and mean right atrial pressures in the thyrotoxic patients did not differ appreciably fromthose of the normal subjects. Reductions in heart rate were small and not significantly different in the 2 groups. Significant dose-related decreases in cardiac output occurred in the thyrotoxic patients during phenylephrine infusions but not in the normal subjects. The decreased cardiac output in the thyrotoxic patients was probably due in part to vasoconstriction, suggesting that the increased cardiac output in thyrotoxicosis is in part secondary to peripheral vasodilatation.