The effects of halothane on pressor and depressor responses elicited via the somatosympathetic reflex: a potential antinociceptive action.

The specific stimulation of various somatic sensory afferent nerves results in significant changes in autonomic responses, including systemic arterial pressure (AP) and heart rate (HR). These reflexively mediated responses have been termed the "somatosympathetic reflex" (SSR). The SSR is mediated at spinal and supraspinal sites within the central nervous system (CNS), and may, in part, represent a nociceptive response. The present investigation examined the actions of the volatile anesthetic, halothane, on the SSR evoked by electrical stimulation of peripheral nerves resulting in pressor or depressor alterations in AP and associated changes in HR. Experiments were completed in rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) and mechanically ventilated. After nerve isolation, either the tibial nerve or the sciatic nerve was stimulated 1, 2, and 4 times the voltage threshold required to elicit a change in hemodynamics. Cardiovascular responses to nerve stimulation were recorded prior to, during, and after increasing concentrations of halothane (0.25%, 0.5%, and 1.0%). Halothane, as expected, produced dose-dependent decreases in AP and HR as compared to baseline controls. Electrical stimulation of the tibial nerve during control resulted in graded decreases in mean arterial pressure (MAP) with increasing current densities. Halothane significantly attenuated the depressor response to tibial nerve stimulation (decrease in MAP at maximal stimulation: 3 +/- 2 mm Hg with 1.0% halothane vs 21 +/- 2 mm Hg during control). Stimulation of the sciatic nerve resulted in current-dependent increases in AP which were significantly inhibited in the presence of halothane (increase in MAP at maximal stimulation: 7 +/- 3 mm Hg with 1.0% halothane vs 34 +/- 5 mm Hg during control).(ABSTRACT TRUNCATED AT 250 WORDS)