Dissociation of glucagon's central and peripheral hemodynamic effects: mechanisms of reduction and redistribution of canine hindlimb blood flow.

Effects of parenterally administered pharmacologic doses of glucagon on canine hindlimb blood flow were studied. Cardiac output (CO), mean arterial pressure (MAP), total peripheral resistance (TPR), common femoral artery flow (CFAQ), common femoral artery resistance (CFAR), percentage shunt in the hindlimb (AVA%) determined by 99mTc microsphere technique, the volume of hindlimb shunt flow (AVAQ), and the volume of hindlimb nutrient capillary flow (NCQ) were determined at baseline and at 10, 20, and 30 min during continuous intravenous infusion of 1 &kg/min glucagon (n = 8). Blood glucagon and glucose levels were measured at all time periods. Glucagon infusion significantly increased CO throughout the infusion, while reducing MAP and TPR. Unexpectedly, CFAQ decreased significantly despite the increase in CO. CFAR increased despite the reduction of TPR during glucagon infusion. The reduction of CFAQ was associated with diminished nonshunt hindlimb NCQ and increased AVA%. Changes in CFAQ, AVA%, AVAQ, and NCQ did not correlate in a linear fashion with the changes in either blood glucose or glucagon levels by linear regression analysis. Glucagon appeared to cause a major redistribution of peripheral blood flow. Hindlimb arteriolar dilatation was not an effect of this hormone in this experimental model. Glucagon appeared to have a salutary central hemodynamic effect, but was detrimental to canine extremity perfusion.