[Role of nitric oxide in warm ischemia of the transplanted kidney].

Objective: Nitric oxide (NO) is a gas considered to have two roles: cytoprotective, derived from its vasodilating and anti-platelet aggregation effects, and cytotoxic, due to its free oxygen radical. It is produced by NO synthase; nitrites and nitrates are its end products. We investigated the role of NO in ischemia-perfusion injury.
Methods: For the study, we utilized dogs weighing 15 to 25 kg. Autotransplantation of the left kidney and right nephrectomy were performed. Group I comprised 9 dogs submitted to renal autotransplantation; group II comprised 6 dogs submitted to renal autotransplantation after 24 h cold ischemia; group III comprised 6 dogs submitted to renal autotransplantation after 24 h cold ischemia and subsequent warm ischemia of 30 min; group IV comprised 9 dogs submitted to renal autotransplantation after 24 h cold ischemia and 60 min warm ischemia.
Results: A significant fall in nitrite levels was observed in dogs that had some type of surgical injury. Nitrate levels increased significantly in dogs that had warm ischemia. At 30 min reperfusion, a significant increase in the production of constitutive enzyme was observed in all groups. A significant increase in inducible enzyme at 30 min reperfusion was observed in the first three groups and no inducible enzyme was produced in the group that had more injury from ischemia (group IV).
Conclusion: Nitrites are markers of the injury produced by surgery. Nitrates clearly express the injury to the organs caused by warm ischemia-reperfusion. The cNOS enzyme increases after surgery in response to surgical insult or stress. The iNOS enzyme increases in the kidneys that have suffered ischemia and are viable. Non-viable kidneys express no enzymatic activity (cNOS, iNOS).