Anesthesia rapidly suppresses insulin pulse mass but enhances the orderliness of insulin secretory process

Induction of anesthesia is accompanied by modest hyperglycemia and a decreased plasma insulin concentration. Most insulin is secreted in discrete pulses occurring at ∼6- to 8-min intervals. We sought to test the hypothesis that anesthesia inhibits insulin release by disrupting pulsatile insulin secretion in a canine model by use of direct portal vein sampling. We report that induction of anesthesia causes an abrupt decrease in the insulin secretion rate (1.1 ± 0.2 vs. 0.7 ± 0.1 pmol·kg^-1·min^-1, P < 0.05) by suppressing insulin pulse mass (630 ± 121 vs. 270 ± 31 pmol, P < 0.01). Anesthesia also elicited an ∼30% higher increase in insulin pulse frequency (P < 0.01) and more orderly insulin concentration profiles (P < 0.01). These effects were evoked by either sodium thiamylal or nitrous oxide and isoflurane. In conclusion, anesthesia represses insulin secretion through the mechanism of a twofold blunting of pulse mass despite an increase in orderly pulse frequency. These data thus unveil independent amplitude and frequency controls of β-cells' secretory activity in vivo.