Objective: Jejunal nitric oxide (NO) formation is impaired during mucosal hypoperfusion. This study was undertaken to investigate whether this phenomenon could result from a restricted mucosal availability of NO-synthase substrates, ie, oxygen and/or L-arginine.
Design: Controlled study using laboratory animals.
Setting: University animal research laboratory.
Subjects: Eighteen chloralose-anesthetized, ventilated, juvenile Landrace domestic pigs.
Interventions: Mesenteric hypoperfusion was induced by intrapericardial infusion of Ringer's solution to achieve decreased cardiac output by creation of cardiac tamponade.
Measurements and main results: Animals were prepared for jejunal intraluminal perfusion with 150 mM NaCl or 3 mM L-arginine solution in an isolated intestinal segment and then subjected to cardiac tamponade. Jejunal mucosal NO formation was measured with a tonometric technique. Mesenteric blood flow was measured as portal blood flow, and mucosal perfusion was measured by laser Doppler flowmetry. Regional oxygen consumption and delivery were calculated from arterial and portal blood samples. Cardiac tamponade reduced jejunal NO formation (-52%), mesenteric oxygen delivery (-75%), oxygen consumption (-39%), and mucosal perfusion (-43%). Oxygenation of the jejunal intraluminal perfusate completely restored the intestinal NO levels within 30 mins, whereas presence of L-arginine was without effect.
Conclusions: The study indicates that oxygen rather than L-arginine is the rate-limiting factor for mucosal NO production during acute reduced splanchnic perfusion.