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Ann Thorac Surg 1995;60:1169-1176
© 1995 The Society of Thoracic Surgeons
Section of Thoracic Surgery and Department of Pathology, University of Michigan Medical Center, Ann Arbor, Michigan, USA
* Address reprint requests to Dr Deeb, University of Michigan Hospitals, 1500 E. Medical Center Dr, 2124F Taubman Center TC/0344, Ann Arbor, MI 48109.
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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