Inhibition of nitric oxide biosynthesis and carotid arteriovenous anastomotic shunting in the pig.

1. The role of nitric oxide (NO) biosynthesis in the regulation of blood flow through arteriovenous anastomoses was evaluated in the carotid circulation of the anaesthetized pig. For this purpose, the effect of intracarotid (i.c.) administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME: 0.1, 0.3 and 1.0 mg kg-1; n = 6) or saline (n = 6) was studied on the distribution of common carotid blood flow, using the radioactive microsphere method. 2. Apart from the highest dose, L-NAME caused no major changes in the systemic haemodynamic variables. Both cardiac output and systemic vascular conductance were reduced by L-NAME (1 mg kg-1), being reversed partly by L-arginine (100 mg kg-1, i.c.). In both groups, L-arginine slightly reduced mean arterial blood pressure. 3. Total common carotid artery blood flow as well as its distribution over the capillary and arteriovenous anastomotic fraction remained stable after saline injection. In contrast, L-NAME caused a dose-dependent decline in common carotid artery blood flow and conductance and this decline was confined entirely to its arteriovenous anastomotic part. 4. Subsequent intracarotid injection of L-arginine (100 mg kg-1) reversed the reduction in total carotid conductance almost completely and that in the arteriovenous anastomotic region partially. Additionally, L-arginine increased capillary conductance significantly in the L-NAME--as well as the saline-treated animals. 5. These results indicate that the L-arginine-NO pathway contributes little to the regulation of tissue perfusion in the porcine carotid circulation. In contrast, NO seems to play an important role in shunting arterial blood through arteriovenous anastomoses in the anaesthetized pig.