Am. J. Respir. Crit. Care Med., Volume 156, Number 2, August 1997, 454-458

Effects of Various Timings and Concentrations of Inhaled Nitric Oxide in Lung Ischemia-Reperfusion

SHINYA MURAKAMI, EMILE A. BACHA, GUY M. MAZMANIAN, HÉLENE DÉTRUIT, ALAIN CHAPELIER, PHILIPPE DARTEVELLE, and PHILIPPE HERVÉ, for the Paris-Sud University Lung Transplantation Group

Laboratoire de Chirurgie Expérimentale and Department of Thoracic and Vascular Surgery and Heart-Lung Transplantation, Centre Chirurgical Marie-Lannelongue, Paris-Sud University, Le Plessis Robinson, France; Department of Surgery, Kanazawa University School of Medicine, Kanazawa, Japan; and General Surgical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

Experimental studies reveal that inhaled nitric oxide (NO) can prevent, worsen, or have no effect on lung injury in the setting of ischemia-reperfusion (I-R). We tested the hypothesis that these disparate effects could be related to differences in the timing of administration and/or concentration of inhaled NO during I-R. Isolated rat lungs were subjected to 1-h periods of ischemia followed by 1-h periods of blood reperfusion. We investigated the effects of NO (30 ppm) given during ischemia, NO (30 or 80 ppm) begun immediately at reperfusion, or NO (30 ppm) given 15 min after the beginning of reperfusion, on total pulmonary vascular resistance (PVR), the coefficient of filtration (K_fc), the lung wet/dry weight ratio (W/D) of lung tissue, and lung myeloperoxidase activity (MPO). A control group did not receive NO. NO given during ischemia had no effect on K_fc or MPO, but decreased PVR. NO (30 ppm) during reperfusion (early or delayed) decreased PVR, W/D, K_fc, and MPO. NO at 80 ppm decreased PVR and MPO but not W/D or K_fc. In conclusion, NO at 30 ppm, given immediately or in a delayed fashion during reperfusion, attenuates I-R-induced lung injury. NO at 30 ppm given during ischemia or at 80 ppm during reperfusion is not protective.

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