Abstract
Rats were anaesthetised with pentobarbitone, cooled to 2°, held in cardiac arrest for 30 minutes, and rewarmed with artificial respiration. On rewarming 86% of the rats restarted breathing if they had been artificially respired during cooling, whereas only 9% restarted if they had not been respired during cooling. Blood O[2] saturation, CO2 content, pH, Na[+], K[+], phosphate, and lactate measurements indicated that the latter rats were hypoxic relative to the former. The hearts of the rats artificially respired during cooling stopped before - or at the same time as - a sharp fall in their carotid arterial pressures; in those not respired during cooling, cardiac arrest occurred about 29 seconds after the fall in blood pressure. It was inferred that hypoxia in the presence of hypothermia led to a massive vasodilatation, related to the inability of the rats, which had not been respired during cooling, to recover on rewarming with artificial respiration. When rats which had not been respired during cooling were rewarmed and artificially respired, the further measure of intermittent pressure (3-4 mm. Hg.) on the abdomen, 240 times/min. for 2 min. , caused spontaneous respiration to restart in 45% of these animals about 40 minutes later. In most of the animals in which spontaneous respiration did not return, the heart did not resume beating on rewarming. In vitro perfusion of Eagle's balanced salt solutions caused the isolated hearts from cooled unrespired rats to resume beating. Centripetal injections into the carotid artery had a similar in vivo perfusion effect, and such injections followed by abdominal pumping allowed 70-90% of the cooled unrespired rats to recover on rewarming.