Halothane induces depressor responses to noxious stimuli in the rat.

The effect of halothane on hemodynamic responses to noxious stimuli was investigated in anesthetized male Sprague-Dawley rats. It was found that increasing the end-tidal halothane concentration from sub-MAC to supra-MAC levels was frequently associated with a reversal of the mean arterial pressure response to a noxious stimulus from a pressor response to depressor response. The depressor responses could be produced by noxious stimuli at several sites but were of greatest frequency (100%) and magnitude (up to -80 mmHg) after clamp application at the base of the tail. The depressor responses were often, but not always, accompanied by decreases in heart rate. The correlation coefficient between the changes in heart rate and the changes in mean arterial pressure caused by noxious stimuli was +0.61 (n = 9). The authors further characterized the depressor responses in an additional 18 rats. The depressor responses were not influenced by vagotomy or muscarinic cholinergic blockade and were associated with concurrent decreases in both cardiac output and systemic vascular resistance. The hemodynamic changes associated with the depressor responses were consistent with a centrally mediated withdrawal of sympathetic tone. Knowledge of this effect of halothane on the arterial blood pressure and heart rate responses to noxious stimuli may be important for correctly interpreting animal responses to noxious stimuli in the presence of general anesthetic agents, particularly because animals are frequently used to characterize both the potency and the hemodynamic effects of anesthetic agents. The presence of depressor responses also indicates that mean arterial pressure responses to noxious stimuli cannot be used as a linear index of anesthetic depth in rats anesthetized with halothane.