Intestinal ischemia and reperfusion impairs vasomotor functions of pulmonary vascular bed

Objective To investigate the effects of intestinal ischemia and reperfusion (I/R) on the pulmonary vascular endothelium and smooth muscle. Summary Background Data Respiratory failure is an important cause of death and complications after intestinal I/R. Although the mechanism of respiratory failure in this setti ng is complex and poorly understood, recent studies of lung injury suggest that endothelial dysfunction may play a significant role. Methods A rat model of acute lung injury was studied after 60 minutes of superior m esenteric arterial occlusion followed by either 120 or 240 minutes of reper fusion. The pulmonary vasomotor function was examined in isolated lungs per fused at a constant flow rate. Results Sixty minutes of intestinal ischemia followed by 120 or 240 minutes of repe rfusion led to a significant reduction in the ability of the pulmonary vasc ulature to respond to angiotensin ii, acetylcholine, and calcium ionophore but not to nitroglycerin. The vasoconstriction response to N-G-nitro-L-argi nine methyl eater, which is a measure of basal nitric oxide release, was di minished in the 240-minute reperfusion group. Intestinal I/R was also assoc iated with pulmonary leukosequestration and increased pulmonary microvascul ar leakage. Conclusions Basal and agonist-stimulated release of nitric oxide from the pulmonary vas cular endothelium and the ability of pulmonary smooth muscle to contract in response to angiotensin II were impaired by intestinal I/R. Such functiona l impairment in both pulmonary vascular endothelium and smooth muscle may c ontribute to the alveolocapillary dysfunction and pulmonary hypertension fo und in acute lung injury after intestinal I/R.