L-arginine protects the mesenteric vascular circulation against cardiopulmonary bypass-induced vascular dysfunction

The aim of our study was to determine whether addition of the nitric oxide donor l-arginine at reperfusion may prevent the cardiopulmonary bypass (CPB)-induced vascular alterations in the intestine.

Twelve dogs underwent 90-minute hypothermic CPB. After 60 minutes, the cardiac arrest-treated group (n = 6) received 40 mg/kg intravenous bolus l-arginine, followed by 3 mg/kg/min infusion for 20 minutes. Hemodynamic parameters, blood gases, lactate, and glucose were monitored. Reactive hyperemia (RH) in response to superior mesenteric artery ischemia and vasorelaxation to systemically administered vasoactive drugs (acetylcholine [ACH] and sodium nitroprusside) were assessed before and after CPB and defined as percent change of vascular resistance.

In the control group, CPB reduced reactive hyperemia (RH) (-26 +/- 15% vs -53 +/- 5%), and the response to ACH (-30 +/- 3% vs -42 +/- 7%). In the treated group, the post-CPB endothelial dysfunction was reversed (-37 +/- 1%, P <.05 vs control group) and RH partially recovered (-34 +/- 4%, P <.05). Administration of l-arginine resulted in a higher mesenteric oxygen delivery, increased nitrite/nitrate production, and lower lactate release from the mesenteric vascular circulation after reperfusion.

CPB disrupts some of the regulatory functions of the endothelial cell in the mesenterium and these are mostly related to nitric oxide unavailability. Systemic supplementation of l-arginine at reperfusion prevents the CPB-induced mesenteric endothelial dysfunction in association with an increased blood distribution and a reduced metabolic impairment.