THE CORONARY CIRCULATION IN THE DOG

Abstract

In heparinized dogs, anesthetized with nem-butal or morphine-chloralose, blood was circulated from a carotid artery through a bubble flowmeter into a cannulated left descending or circumflex coronary artery. The chest was then closed and spontaneous respiration resumed. Under such "normal" conditions the volume of blood passing through the coronary arteries averaged 65 ml./100 g. of heart/min. Coronary flow was found to bear a close relationship to blood pressure; a given percentile drop in blood pressure led to a similar drop in flow. An acceleration of heart rate led to an increase in coronary flow. Parasympathetic stimulation (stimulation of the peripheral end of the cut vagus before and after atropine, increased tension in the gall bladder, and occluding one coronary artery while flow was being measured in another coronary artery) led to no significant alteration in coronary flow. Likewise, sympathetic (accelerator) stimulation led to only minimal increases in flow. Acetyl-choline and epinephrine injected in minute quantities intra-arterially resulted in marked transient acceleration in coronary flow independent of changes in heart rate or blood pressure. The fraction of the cardiac output flowing through the coronary arteries varied inversely with the cardiac output. The heart of these animals under "normal" conditions received 4-5% of the total cardiac output but this proportion was considerably higher when the circulation was depressed. Cardiac anoxia produced by brief occlusion of the coronary arterial inflow led to marked and transient increases in coronary flow. Likewise, decreasing the arterial O2 content produced a considerable augmentation of flow. 100% O2 consistently resulted in an 11% diminution of flow. Inhalation of 5 and 7% CO2 produced no significant alteration in flow even though the arterial CO2 content increased an avg. of 6 vol. %. Decrease in blood pH caused marked increases in coronary flow.