Hemodynamic splanchnic and renal changes associated with administration of arginine-hydrochloride in dogs.

Abstract

The relationship of arginine-mediated release of endogenous glucagon and insulin to renal and splanchnic arterial blood flow, blood pressure, and heart rate was studied in dogs. Intravenous injection of argininehydrochloride (arg-HCl) in logarithmically increasing doses increased the concentration of glucagon (pGl) in the femoral artery from 143 ± 39 pg/ml (pre-injection) to 282 ± 49 pg/ml (following maximum dosage of arg-HCl) and insulin concentration from 23 ± 5 to 41 ± 11 µU/ml. Sodium chloride (NaCl) and urea, isovolemic and isosmolar to arg-HCl, failed to change pGl and insulin. Arg-HCl depressed arterial blood pressure from 93 ± 13 (preinjection) to 60 ± 14 mm Hg (maximum dose), NaCl increased it from 89 ± 13 to 99 ± 13 mm Hg. The blood flow increase due to arg-HCl was comparable with that due to NaCl in renal as well as in celiac and left gastric artery. The former was more pronounced in superior and inferior pancreaticoduodenal artery by 61 and 102%, and in gastroduodenal and superior mesenteric artery by 11 and 35%. Infusion of arg-HCl increased pGl from 294 ± 90 to 731 ± 200 pg/ml, and insulin from 23 ± 5 to 63 ± 18 µU/ml; the resulting blood flow increase, however, only differed in both pancreatic arteries by 10–20% from the rise during NaCl infusion where no change of pGl was observed and a decline occurred in insulin from 64 ± 21 to 27 ± 8 µU/ml. It is concluded that physiological levels of pGl have no systemic effect on arterial blood flow. A local flow increasing effect of glucagon and/or insulin on the arteries next to the pancreas is discussed.