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We investigated whether the nitric oxide (NO) system is involved in the augmentation of pulmonary vascular tone and vascular resistance after pulmonary ischemia/reperfusion. Rats underwent pulmonary artery ligation or sham operation and were divided into three groups, namely the control group, 1-week pulmonary ischemia/reperfusion (IR) group, and 2-week IR group. In the IR groups, reperfusion was continued for 1 week (1-week IR group) or 2 weeks (2-week IR group). In the control group, reperfusion was maintained for 4 weeks. A micro-occlusion technique was used to induce ischemia in the IR groups. Pulmonary vascular reactivity was assessed by assessing systemic arterial pressure, systemic arterial blood gases, lung weight gain, mean pulmonary arterial pressure, and calculated pulmonary vascular resistance. Real-time polymerase chain reaction was used to examine changes in mRNA expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) in lung tissue. Western blotting was used to examine protein changes in eNOS and iNOS in lung tissue. The expression of iNOS and the expression of eNOS protein were significantly decreased in the 2-week IR group compared with the control group. Pulmonary ischemia/reperfusion increased the mean pulmonary arterial pressure and the calculated pulmonary vascular resistance compared with the control group. Pulmonary ischemia/reperfusion also increased the expression of iNOS and decreased the expression of eNOS protein. Pulmonary ischemia/reperfusion also decreased the pulmonary vasodilator response after pulmonary artery ligation. Pulmonary ischemia/reperfusion diminished pulmonary vasodilation and augmented pulmonary vasoconstriction. The NO system mediates pulmonary ischemia/reperfusion-induced vasoconstriction and vasodilation after pulmonary artery ligation. Pulmonary ischemia/reperfusion decreases pulmonary NO synthase expression and attenuates the pulmonary vasodilator response after pulmonary artery ligation.
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