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Ann Thorac Surg 1995;60:1169-1175
© 1995 The Society of Thoracic Surgeons
Section of Thoracic Surgery and Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan
Background. Inhaled nitric oxide (•NO) has been found to be a potent pulmonary vasodilator. We assessed whether •NO, through this function or others, could alleviate lung reperfusion injury.
Methods. Rats underwent thoracotomy, with clamps used to create left lung ischemia. After 90 minutes of ischemia, clamps were released, permitting reperfusion for either 30 minutes or 4 hours. Additional animals received inhaled •NO via the ventilator to determine its effects on reperfusion injury.
Results. Lung injury, measured by increased vascular permeability using iodine-125–labeled bovine serum albumin leakage, was significantly increased in ischemic-reperfused animals compared with time-matched shams not undergoing ischemia. Inhaled •NO delivered at the start of reperfusion worsened injury at 30 minutes but was protective at 4 hours. The increased injury could be avoided either by delaying •NO for 10 minutes or by treating the animals with superoxide dismutase before reperfusion. •NO reversed postischemic pulmonary hypoperfusion at 4 hours, as measured by labeled microspheres. Lung neutrophil content was significantly reduced at 4 hours in •NO-treated animals.
Conclusions. •NO is toxic early in reperfusion, due to its interaction with superoxide, but is protective at 4 hours of reperfusion, due to reversal of postischemic lung hypoperfusion and reduction of lung neutrophil sequestration.
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