Key result
Vasopressin infusion raises fetal MAP by ~9 mmHg while slowing heart rate and redistributing cardiac output.
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The effects of intravenous infusion of vasopressin on the circulation of the fetus were studied in lambs in utero with chronically maintained intravascular catheters. Vasopressin infused in doses of 0.91-2.26 mU/min per kg fetal weight resulted in plasma levels of arginine vasopressin of 6.8-36.4 /iU/ml; these levels are similar to those achieved during fetal hypoxia. Petal mean arterial blood pressure increased from control levels of 47 1.7 to 56 1.9 nun Hg, and heart rate fell from 174 4.1 to 144 4.4 beats/min. Fetal cardiac output and its distribution and actual organ blood flows were measured before and during vasopressin infusion by the radionuclide-labeled microsphere technique. Combined ventricular output did not change significantly, but there was a redistribution of flow, with a marked reduction of the proportion of cardiac output to the gastrointestinal and peripheral circulations and an increase in the percent of cardiac output to the umbilical-placental, myocardial, and cerebral circulations. This redistribution was associated with a significant increase in fetal arterial Po from 22 to 24 torr. Changes in heart rate, cardiac output, and distribution of cardiac output to various fetal organs are similar to those seen during fetal hypoxia and suggest that vasopressin release may play an important role in the fetal cardiovascular response to stress.
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Iwamoto et al. (1979) studied Fetal hemodynamic response to vasopressin/hypoxia. Intravenous vasopressin infusion vs. Pre-infusion control baseline was evaluated on Fetal mean arterial blood pressure (mmHg). Intravenous vasopressin infusion in fetal lambs increased mean arterial pressure from 47 to 56 mmHg, decreased heart rate from 174 to 144 beats/min, and redistributed cardiac output.
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