The effect of fetal heart rate on cardiovascular function during hypoxemia.
The effect of heart rate changes on cardiovascular function during hypoxemia was studied in lamb fetuses. In chronic preparations, we determined fetal heart rate, descending aortic blood flow (by electromagnetic flowmeter), PO2, PCO2, and pH and calculated fetal cardiac output (CO) and organ blood flows (with the use of 15 mu nuclide-labeled microspheres). Observations were made during control and hypoxemic states either alone or in the presence of parasympathetic blockade by atropine. Fetuses exposed to moderate hypoxemia (ewe breathing 10% oxygen) developed a significant bradycardia which was prevented by atropine pretreatment; no significant change in CO occurred in either case. Fetuses exposed to severe hypoxemia (8% oxygen) developed bradycardia and a significant decrease in CO; atropine pretreatment prevented the bradycardia but failed to prevent the decrease in CO. Atropine administered to the already severely hypoxemic fetus increased the heart rate but did not restore the depressed CO. The redistribution of blood flow from low-priority (e.g., viscera) to high-priority (e.g., myocardium) tissues correlated with the degree of hypoxemia. Myocardial blood flow was greater during hypoxemia when bradycardia was prevented by atropine than during hypoxemia alone; otherwise, blood flow distribution in response to hypoxemia was unaffected by atropine blockade.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001783:Blood Flow Velocity; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D005260:Female; D005318:Fetal Heart / Q000187:drug effects / Q000503:physiopathology*; D006339:Heart Rate; D000860:Hypoxia / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D011247:Pregnancy; D012039:Regional Blood Flow; D012756:Sheep
D002245:Carbon Dioxide; D001285:Atropine; D000109:Acetylcholine; D010100:Oxygen