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 re sults in significant changes in autonomic responses, including systemi c arterial pressure (AP) and heart rate (HR). These reflexively mediat ed 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 suspe nse. The present investigation examined the actions of the volatile an esthetic, halothane, on the SSR evoked by electrical stimulation of pe ripheral nerves resulting in presser or depressor alterations in AP an d associated changes in HR. Experiments were completed in rats anesthe tized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) and me chanically ventilated. After nerve isolation, either the tibial nerve or the sciatic nerve was stimulated 1, 2, and 4 times the voltage thre shold required to elicit a change in hemodynamics. Cardiovascular resp onses to nerve stimulation were recorded prior to, during, and after i ncreasing concentrations of halothane (0.25%, 0.5%, and 1.0%). Halotha ne, as expected, produced dose-dependent decreases in AP and HR as com pared 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 atte nuated 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 inhibite d 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). Electrical stimulation of the tibial nerve produced no consistent HR changes in the presence or absence of halothane, whereas stimulation o f the sciatic nerve elicited increases in HR which were significantly attenuated by halothane. In an additional group of rats, SSR responses were elicited prior to and during intravenous sodium nitroprusside (S NP) administration as a control for the decrease in baseline AP due to halothane. SNP had no effect on presser or depressor responses to ner ve stimulation. The present investigation demonstrates that indeed two distinct types of SSR may be elicited, and that administration of the volatile anesthetic, halothane, inhibits both excitatory and inhibito ry types of the SSR. These findings also support a potential antinocic eptive action of halothane.