ROLE OF NITRIC-OXIDE IN THE REGULATION OF REGIONAL BLOOD-FLOW AND METABOLISM IN ANESTHETIZED PIGS

To investigate the contribution of nitric oxide in the regulation of r egional blood flow and metabolism in vivo, we administered incremental doses of N-omega-L-arginine-methyl ester (L-NAME 1, 3, 10, 30 and 100 mg kg(-1), intravenously) in isoflurane anaesthetized pigs. The pulmo nary vascular bed exhibited a greater sensitivity to the L-NAM E-induc ed presser effects compared with the systemic arterial bed as the slop e of the dose-response curve was steeper (42.9 +/- 4.3 vs. 24.3 +/- 3. 6, P < 0.05) and the dose of I-NAME required to induce a 25% pressure increase was lower (PD25 Of 6.2 +/- 2.5 vs. 22.8 +/- 5.2 mg kg(-1), P < 0.05). I-NAME infusion produced a dose-dependent reduction in cardia c output that was evenly distributed among the mesenteric, femoral, he patic and carotid arterial circulation as demonstrated by unchanged re gional blood flows-to-cardiac output ratios, except in the kidney wher e the L-NAM E-induced vasoconstriction was most pronounced (renal bloo d flow/cardiac output decreased from 6.2 +/- 0.6 to 3.7 +/- 0.7% after 100 mg kg(-1) of I-NAME, P < 0.05). After the administration of I-NAM E 30 mg kg(-1), intestinal O-2 uptake (Vo(2)) increased (+39 +/- 3%, P < 0.05) whereas renal Vo(2) tended to decrease (-19 +/- 4%, P = 0.07) and whole body Vo(2) remained unchanged. Plasma noradrenaline and adr enaline concentrations did not change significantly with L-NAME infusi on. These data demonstrate that in anaesthetized pigs, endogenous nitr ic oxide is most important for the regulation of pulmonary and renal b lood flows and in spite of unchanged global metabolic demand, nitric o xide inhibition leads to an increase in intestinal Vo(2) associated wi th enhanced gut motility without rise in circulating lactate levels.