Apoptosis Induced By Ischemia-Reperfusion Lung Injury In Rat

Lung injury after ischemia and reperfusion(I/R), which occurs inmany clinical conditions such as cardiopulmonary bypass, pulmonaryembolism ,and lung transplantation, is a major cause of organ dysfunctionfollowing lung transplantation. Apoptosis is a distinct form of single-celldeath in response to injury, and there are strong indications that apoptosisplays an important regulatory role in various disease processes such ascancer, autoimmune disease, and others. Of particular importance in or-gan transplantation, apoptosis has recently been reported in several ani-mal models to occur after hR injury to the kidney, retina, brain, heart,liver and adrenal gland. At present, little is known about the relation be-tween hR injury and apoptosis. Using an in situ pulmonary hilum occlu-sion model of hR injury, we sought to characterize the influence of hRlung injury on apoptosis.Methods. The study contains two parts. 1. Refer to the method ofEppinger, we set up an in Situ pulmonary hilum occlusion model of hRinjury, which was convenient and physiological.2. According to reperfu-sion time, the animals were divided into eight groups and each consistedof five cases. From group Ito VI were respectively 30 minutes, 1 hour, 2hours, 4 hours, 8 hours, 12 hours after reperfusion. Group VII endure is-chemia alone and group VIII was controls. Apoptotic cells were stained bythe terminal deoxynucleotidyl transferase-mediate dUTP nick-end label-ing (TUNEL) technique. TUNEL-positive pneumocytes were counted on100 fields (X400) per specimen (mean±SD). Electron microscopy wasperformed to verify the morphologic changcs consistent with apoptosls.Results. 1. Set up a convenientand physiological model of ische-3mia-reperfusion in rat. 2. A significant apoptosis of pneumocytes occursearly after ischemia-reperfusion lung injury, that the peak in the numberof apoptotic pneumocytes occurs as early as 2 hours after reperfusion.Four hours after reperfusion, the number of apoptotic pneumocytes wasslightly less than 2 hours after reperfusion, with a further decline at 8hours and 12 hours after reperfusion. No statistically significant differ-ence between group 12 hours after reperfusion and controls. there was aslight and statistically not significant elevation of the number of apop-totic pneumocytes in lungs undergo ischemia alone compared with withcontrols.