BACKGROUND: In infants, nonshivering thermogenesis from brown adipose tissue 
provides an important source of heat for thermoregulation. Infants are known to 
have a high susceptibility to hypothermia during anesthesia. To investigate 
whether this could be due to an inhibition of nonshivering thermogenesis by 
anesthetics, the effect of preincubation with volatile anesthetics on the 
norepinephrine-induced heat production of brown adipocytes was investigated.
METHODS: Brown adipocytes from hamsters were isolated with a collagenase 
digestion method and preincubated with volatile anesthetics. The cells were 
stimulated with norepinephrine, and heat production, measured as oxygen 
consumption, was monitored polarographically.
RESULTS: Norepinephrine addition led to a 20-fold increase in the rate of oxygen 
consumption (thermogenesis). However, preincubation of cells with 3% halothane 
reduced the response to norepinephrine by more than 70%. The potency of 
norepinephrine (the median effective concentration) was not affected by 
halothane. Full effect of halothane was reached quickly, and after halothane 
withdrawal, the thermogenic response recovered, although rather slowly. 
Halothane, isoflurane, and enflurane were approximately equipotent inhibitors of 
thermogenesis, with concentrations of approximately 0.7% resulting in 50% 
inhibition. The inhibitory effect of 1% halothane was unaffected by the presence 
of 74% nitrous oxide, but nitrous oxide alone also reduced thermogenesis.
CONCLUSIONS: Volatile anesthetics severely attenuated the thermogenic response 
to norepinephrine of isolated brown-fat cells. It is inferred that 
brown-adipose-tissue heat production is reduced during (and probably also some 
time after) anesthesia. Because infants are dependent on brown-fat-derived 
nonshivering thermogenesis for thermal balance, the inhibition by volatile 
anesthetic agents of brown-adipocyte heat production may at least partly explain 
the susceptibility of infants to hypothermia during and after anesthesia.