nhaled Nitric Oxide Attenuates Apoptosis in schemia-Reperfusion Injury of the Rabbit Lung

rabbit lung Inhaled nitric oxide attenuates apoptosis in ischemia-reperfusion injury of the Background. Lung ischemia-reperfusion injury occurs after lung transplantation and various clinical procedures. Recently, apoptosis was reported to be induced after ischemia-reperfusion. We investigated the effects of inhaled nitric oxide (NO) on lung ischemia-reperfusion and apoptosis after ischemia-reperfusion. Methods. As a control group, the left pulmonary hilum of Japanese white rabbits (n ‫؍‬ 10) was occluded for 120 minutes and reperfused for 120 minutes. In the inhaled NO group (n ‫؍‬ 10), 20 parts per million nitric oxide was inhaled during reperfusion. The sham-operated group was ligated at the right hilum and perfused by the left lung only for 120 minutes. The mean pulmonary arterial pressures and PaO 2 were measured during reperfusion. The wet-to-dry weight ratio of the left lower lobe of the lung was calculated. The number of apoptotic cells was estimated using the terminal deoxynucleotidyl trans-ferase-mediated dUTP-biotin nick-end labeling (TUNEL) technique. The TUNEL staining for a time course study was done using 15 control animals that were killed by exsanguination at 15, 30, and 60 minutes after reperfusion.