Influence Of Hepatic Inflow Occlusion On Apoptosis Of Lung Cells In Rat

Objective:To explore the influence of hepatic inflow occlusion on lungs apoptosisof lung cells. To investigate the potential role of apoptosis in the development ofinjury.Materials and Methods:48 S-D rats, regardless of sex, weight 180-220g. wererandomized into six groups: Control group (C group, n=8):without occlusion ofhepatic ;ischemia group(I group,n=8); with 60 min of occlusion of hepatic and noreperfusion; From ischemia reperfusion 2h group (I/R2h group n=8)group toischemia reperfusion 12h group (I/R 12h groupn=8) with 2, 4, 8, 12 hoursaccording the different reperfusion time after 60 min ischemia. Species were takendirectly after thoracic incision. The lower lobes of the left lungs and the right lungswere obtained for histologic evaluation and wreigt deteckiong. Broncho alveolarlavage fluid(BALF) and serum were collected . lung index(LI), lung permeabilityindex(LPI), Lung water content,and the ratio of neutrophils were determined.Apoptotic cells were stained by the terminal deoxynucleotidyi transferase-mediatedUTP nick-end labeling(TUNEL) technique. Average TUNEL-positivepneumocytes were counted on 10 fields(×400) per specimen. All datas wererepresented as Mean±Standard Deviation and analyzed with one-way analysis ofvariance and q test .P<0.05 was considered as significance. All the statisticalanalysis was carried on via SPSS 10.0 in personal computer.Results:Pulmonary H-E stain showed edma(both interstitial and alveolar) andnutrophil infiltration in alveolar tissue. alveolar spaces were narrowed andneutrophils exuded.With prolongation of time the destructive change of thealveolar wall was worsened. The changes began in the early stage of reperfusionperiod(but not in control group) and became prominent at8h of hepatic inflowocclusion. BALF protein content, LPI increased after initiating reperfusion,especially in group I/R8h(P<0.01 vs C group﹚. PMN was significantly higher inI/R8h groups than that in C group(P<0.01vs C group﹚. W/D, LI, TLW increasdafter 2h of post-reperfusion and reached a peak value at 8h post-reperfusion andbegan to decrease at 12h of post-reperfusion.apoptosis of pneumocytes occursearly after reperfusion, and the peak in the number of apoptotic pneumocytesoccurs as early as 4h after reperfusion. 8 hours after reperfusion, the number ofapoptotic pneumocytes was slightly less than 4 hours after reperfusion, with afurther deline at 12 hours after reperfusion.there was a not significant elevation ofthe number of apoptotic pneumocytes in lungs undergo ischemia alone comparedwith controls.Conlusions:Hepatic inflow occlusion can make influence on lungs.Apoptosis mayplay an important role in the pathogenesis of lung injury caused by Hepatic inflowocclusion. Apoptosis, as a pathogenetic mechanism, accelerates the inflammatoryresponses .