The relationship among canine brain temperature, metabolism, and function during hypothermia

Abstract

Cerebral protection by hypothermia is commonly attributed to cerebral metabolic suppression. However, at temperatures below 28°C, the relationship of temperature to cerebral metabolic rate of oxygen consumption (CMR(O2)) has not been well characterized. Accordingly, the relationship between brain temperature and CMR(O2) was determined in eight dogs during cooling from 37 to 14°C while the EEG was continuously monitored. Cardiopulmonary bypass was initiated and control measurements were made at 37°C during anesthesia with nitrous oxide 50-60% inspired and morphine sulfate 2 mg·kg-1 intravenously (iv). Upon cooling to 27°C, the nitrous oxide was discontinued and the morphine was antagonized with naloxone 2 mg iv. Measurements were repeated at 27, 22, 18, and 14°C and in four dogs again at 37°C after nitrous oxide 50-60% had been reestablished at 27°C along with administration of morphine sulfate 2 mg·kg-1. For each temperature interval, the temperature coefficient (Q10) for CMR(O2) was calculated (Q10 = CMR(O2) at x° C / CMR(O2) at [x-10]° C). Between 37 and 27°C the Q10 was 2.23, but between 27 and 14°C the mean Q10 was doubled to 4.53. With rewarming to 37°C, CBF and CMR(O2) returned to control levels, and brain biopsies revealed a normal brain energy state. During cooling, the EEG developed burst suppression at or below 22°C. With further cooling, the periods of suppression increased; however, burst activity continued in seven of eight dogs even at 14°C. We conclude that the relationship of CMR(O2) to brain temperature is variable depending on the functional state of the brain; below 27°C progressive functional depression presumably accounts for the unexpectedly high Q10 values for CMR(O2).