The effect of beta-adrenergic stimulation on fetal cardiovascular function during hypoxemia.
The effect of beta-adrenergic stimulation on fetal cardiovascular function during hypoxemia was studied in six lamb fetuses with gestational ages of 119 to 140 days. In chronic preparations, we determined fetal heart rate, umbilical blood flow (by electromagnetic flowmeter), PO2, PCO2, and pH and calculated fetal cardiac output and organ blood flows (using 15 mu nuclide-labeled microspheres). Observations were made during control periods and periods of hypoxemia, beta-adrenergic blockade by propranolol, and hypoxemia superimposed upon the beta-adrenergic blockade. Beta blockade effected a decrease in fetal heart rate both at rest and with hypoxemic stress. Propranolol produced a fall in cardiac output with hypoxemia, but the meaning of this in regard to beta-adrenergic effects is unclear. Beta blockade did not alter fetal arterial pressure or general blood flow distribution. However, we observed a decrease in umbilical blood flow in response to propranolol under both normoxic and hypoxemic conditions.
D000818:Animals; D001783:Blood Flow Velocity; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D005260:Female; D005312:Fetal Blood / Q000187:drug effects; D005318:Fetal Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000150:complications*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011247:Pregnancy; D011433:Propranolol / Q000494:pharmacology*
D002245:Carbon Dioxide; D011433:Propranolol; D010100:Oxygen