The Effect of Halothane Anaesthesia upon Cerebral Oxygen Consumption in the Rat

Abstract

The influence of halothane (0.6 and 2%) upon cerebral (cortical) blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) was studied in artificially ventilated rats, using a modified technique of Kety & Schmidt (1948). The values obtained in halothane anaesthesia were compared to those recorded in nitrous oxide anaesthesia, or to those measured in unanesthetized animals given an analgesic drug (fentanyl citrate). Although it could be confirmed that halothane induces vasodilatation in the brain, there were relatively small differences in CBF between the groups. The results demonstrate that, in the rat, halothane depresses CMRo2 in a dose-dependent way. With 0.6% halothane, CMRo2 was reduced by 20-30% and, with 2% halothane, CMRo2 was reduced by about 50%. Thus, in the rat the effect of 2% halothane upon metabolic rate is comparable to that observed in barbiturate anaesthesia.

Perfusion imaging

“…g-' -min-' previously reported in the literature ( 10). This result is evidence that the assumptions of complete saturation of blood water and negligible relaxation of the spins until after exchange with tissue water which are used to quantitate perfusion are valid.…”

31P NMR saturation transfer measurements of the steady state rates of creatine kinase and ATP synthetase in the rat brain

“…The latter has no measureable effect on cerebral oxygen consumption in rats [28], while halothane produces significant, dose-dependent reductions in cerebral oxygen consumption [29]. Halothane at 0.6% was found to reduce cerebral oxygen consumption in rats by 25% [29]. This is the maximum reduction we would expect in our experiments.…”

“…Our experiments were carried out under light halothane anaesthesia, those in [26,27] under 70% Nz0/30% OZ. The latter has no measureable effect on cerebral oxygen consumption in rats [28], while halothane produces significant, dose-dependent reductions in cerebral oxygen consumption [29]. Halothane at 0.6% was found to reduce cerebral oxygen consumption in rats by 25% [29].…”

Glutamate metabolism in cerebral mitochondria after ischemia and post‐ischemic recovery during aging: relationships with brain energy metabolism

“…Although halothane in low concentration (0.6 vol%) reduced the cerebral metabolic rate of oxygen by 25% (Harp et al . ), glycolytic flux and cerebral energy state remained steady under anesthesia with 1.0 vol% halothane, except for a decrease in glucose concentrations (Nilsson and Siesjö , ). However, (i) to prevent the influence of halothane on ischemic tissue reported by Smith et al .…”