Effect of sympathetic blockade by spinal anesthesia on pancreatic islet function in man

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Abstract
The effect of resting sympathetic nervous system activity on pancreatic islet function was assessed in 20 patients receiving spinal anesthesia prior to elective surgical procedures. High thoracic sensory dermatone spinal anesthesia with tetracaine hydrochloride (T2-T6 level) suppressed plasma norepinephrine (NE), epinephrine (E) and mean arterial pressure (MAP) below preanesthesia levels and inhibited the acute insulin response (AIR) to glucose (5 g i.v.) by 56 .+-. 6%, .hivin.x .+-. SE, n = 5 (P < 0.01). There was no suppression of NE, E or MAP in 6 patients receiving low spinal anesthesia (T9-T12 level), and the AIR to glucose was unchanged. Overall, there was a relationship between the change of plasma NE during spinal anesthesia and the AIR to glucose, expressed as a percentage of the baseline AIR (r = 0.82, n = 14, P < 0.001). In 6 patients receiving high spinal anesthesia (T5 level), the AIR to arginine (5 g i.v.) was also inhibited by 28 .+-. 8% (P < 0.02). The acute glucagon response to arginine increased by 26 .+-. 4% (P < 0.005) during high spinal anesthesia. Thus, inhibition of the resting adrenergic tone by high spinal anesthesia was associated with a fall of plasma insulin responses to both glucose and arginine and an increased glucagon response to arginine. Baseline adrenergic input may be important for the maintenance of normal islet function in man.