Abstract

The mechanism behind hyperemia in skeletal muscle during insulin-induced hypoglycemia was investigated in 42 anesthetized male Wistar rats using the microdialysis ethanol technique of monitoring nutritive blood flow. Microdialysis probes were inserted bilaterally into the gastrocnemius muscle and perfused with a modified Krebs-Henseleit buffer containing 20 mmol/l ethanol and one or more of the following compounds: propranolol (10(-6) mol/l), phentolamine (10(-6) mol/l), and calyculin A (1.0 mumol/l). Muscle blood flow increased, as indicated by a decrease in the ethanol outflow:inflow ratio (P < 0.001, n = 6), during hypoglycemia induced by a bolus intravenous infusion of insulin (680 mU/kg body wt). This increase was not present during normoglycemia or during hypoglycemia and local beta-adrenergic blockade via propranolol. However, the hyperemic response was potentiated during hypoglycemia and local alpha-adrenergic blockade via phentolamine. A normal hyperemic response to hypoglycemia was detected during simultaneous alpha- and beta-adrenergic blockade. This response was eliminated on further supplementation of the microdialysis perfusion medium with calyculin A. Therefore, although stimulation of the alpha- and beta-adrenergic receptors does occur during insulin-induced hypoglycemia, it is not essential for the induction of hyperemia in this state. It may be concluded that hyperinsulinemia results in vasodilatation during hypoglycemia, although hyperinsulinemia does not have an effect on skeletal muscle blood flow under normoglycemic conditions.