The role of nitric oxide in subcutaneous and transmural gut tissue oxygenation

The influence of inhibiting the nitric oxide (NO) synthetase on tissue perfusion as indicated by tissue oxygen tensions was determined. Tissue oxygen probes were placed subcutaneously and on serosal and mucosal surfaces of colon of anesthetized adult rats. After a control period, the inhibitor of NO formation, N^G-nitro-L-arginine methyl ester (L-NMMA), was given intravenously and followed 20 min later by infusion of substrate for NO synthetase, L-arginine. Mean arterial blood pressure (MAP), subcutaneous tissue oxygen tension (P_SQO₂), serosal tissue oxygen tension (P_SO₂), and mucosal tissue oxygen tension (P_MO₂) were simultaneously measured. Baseline values for the measured parameters were MAP = 95 ± 9 mmHg, P_SQO₂ = 61 ± 7 mmHg, P_SO₂ = 65 ± 7 mmHg, and P_MO₂ = 9 ± 2 mmHg. The infusion of L-NMMA induced a significant increase in MAP to 123 ± 7 mmHg (p < .001) and P_SQO₂ to 72 ± 7 mmHg (p < .001). P_SO₂ did not change significantly from baseline after L-NMMA infusion. A significant decrease in P_MO₂ to 4 ± 2 mmHg was noted after L-NMMA infusion (p < .001). The administration of L-arginine promptly returned all measured parameters to baseline levels within 10 min of infusion. A transmural Po₂ gradient exists across the colon with P_MO₂ far lower than P_SO₂. P_SQO₂ approximates P_SO₂ at baseline and P_SO₂ is not altered by inhibition of the NO synthetase. The 45% reduction in mucosal PO₂ after L-NMMA, which was reversed by L-arginine infusion, suggests that nitric oxide participates in splanchnic vasomotor control with a preferential effect in the mucosal vasculature. The observed decrease in mucosal PO₂ observed after inhibition of NO production is similar to the worsened hypoxia previously measured during hemorrhagic shock. Further work clarifying the local control mechanisms of gut tissue Po₂ can direct therapies to increase gut tissue oxygenation.