Effects of hypercapnia on metabolism, temperature, and ventilation during heat and fever.

We wished to determine whether 1) acute hypercapnia in cats changes metabolic heat production to affect temperature regulation and 2) heat exposure and fever affect the normal response. The effects of breathing 4% CO2 on O2 consumption (VO2), rectal temperature (Tre), and ventilation (V) were measured in five conscious resting cats. Cats were exposed to a normal (24-27 degrees C) chamber temperature (Ta) and a warm (33-34 degrees C) chamber Ta. Fever was produced by intravenous injection of Escherichia coli endotoxin (0.02 microgram/kg) at a normal Ta. In normothermic cats, hypercapnia decreased VO2 by approximately 40%, despite an increased V (approximately 100%), but Tre decreased only transiently and slightly compared with studies in which air was breathed throughout. During heat studies, average V was elevated but VO2 was markedly lower than at the normal Ta; Tre gradually increased. Hypercapnia combined with heat did not cause additional increases in VO2, nor did it cause a decrease in VO2, as at a normal Ta; however, the rate of rise of Tre during heat was slowed by hypercapnia. During febrigenesis, hypercapnia prevented the transient increase in VO2 observed when air was breathed and delayed the rate of rise in Tre. As Tre was falling in fever, hypercapnia depressed VO2 but did not affect Tre compared with fever studies in which air was breathed. Unlike heat exposure, hypercapnia had a further additive stimulatory effect on the increase in V at the onset of fever, and it increased V during the falling phase of fever when V had returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)