Effects of Intrathecal Morphine, Clonidine, and Midazolam on the Somato-sympathoadrenal Reflex Response in Halothane-anesthetized Cats

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Abstract
Modulatory effects of spinal opioid, .alpha.-adrenergic, and benzodiazepine receptors on the somato-sympathoadrenal reflex response, evoked by supramaximal bilateral sciatic nerve stimulation (50 times minimal motor threshold) were evaluated in halothane-anesthetized cats. Group 1 (n = 8) served as a control; group 2 (n = 7) received intrathecally (it) the opioid receptor agonist morphine (500 .mu.g); group 3 (n = 7), the .alpha.2-adrenergic agonist clonidine (200 .mu.g it); and group 4 (n = 7), the benzodiazepine receptor agonist midazolam (1 mg it). Plasma samples were collected from the adrenal vein at baseline, after it drug administration, and during sciatic nerve stimulation for the measurement of norepinephrine, epinephrine, and dopamine. In control cats (group 1), sciatic nerve stimulation evoked significant increases in adrenal vein catecholamine plasma levels, blood pressure, and heart rate. Morphine (group 2) did not have any effect on spontaneous hemodynamics and adrenal secretion. During stimulation (group 2), there were no significant increases in adrenal norepinephrine and epinephrine concentrations, whereas dopamine concentrations, blood pressure, and heart rate rose significantly. Clonidine (group 3) led to a decrease in heart rate and adrenal vein norepinephrine and epinephrine concentrations at baseline. During sciatic nerve stimulation in this group (3), significantly lower concentrations were observed in adrenal vein catecholamines compared with control, whereas the hemodynamic response was not suppressed. Midazolan suppressed baseline and stimulation-evoked adrenal vein catecholamine concentrations, but hemodynamics were not significantly affected. Although the study was conducted in a halothane-anesthetized cat model, employing single doses of agonists, the data clearly indicate a complex modulation of the somato-sympathoadrenal reflex response that is diffenerentially inhibited by spinal opioid, benzodiazepine, and .alpha.-adrenergic receptor systems.