AIM To study the effects of heat exposure and swimming on membranous structure of the small intestinalepithelium and the biochemical indexes.METHODS The distribution of the intra-membranous particles (IMPs) in enteric epithelium of SD rats andthe number of IMPs were analyzed with freeze-etching technique and TxB2, PGFIa, PRL, CORT and totalSA (TSA) were measured with the techniques of biochemistry and radio-immunity.RESULTS Heat exposure markedly affected the distributive pattern of IMPs in intestinal epithelium andmade the numbers of IMPs on the PF and EF faces of cell membrane and nuclear membrane decreased.Swimming exacerbated the above changes. And in the meantime heat exposure resulted in the massivereleasing of the body-hurting substance as TxB2 and reducing of the body-protecting substance as PGFIa.TSA increased obviously. These changes recovered partly after heat exposure, but the number of IMPs onboth PF and EF faces and certain biochemical indexes were still not restored to the levels as in the controlgroup.CONCLUSION Heat exposure and swimming can make the cellular catabolism accelerated and anabolismreduced, then bring about the numbers of IMPs of intestinal epithelium membrane and nuclear membranedecreased, and the distribution was abnormal. TxB2, PGFIa, PRL, CORT and TSA were changedabnormally during heat exposure. And above indexes showed no notable evidence of recovery after stoppingheat exposure 4 hours-24 hours; the delayed injury was obviously presented.

颌面部爆炸伤后组织血栓素A2和前列环素I2对兔脑的作用机制

Objective To detect the changes of TXA2 and PGI2 levels and discuss the significance of the level and ratio changes during maxillofacial blast injury.Methods The maxillofacial blast injury model was made by standard spherical blast sources produced by NINT.Measure dynamics of blast wave to skin surface.The metabolites of thromboxane A2( TXA2) and prostacyclin(PGI2),TXB2 and 6 keto PGF1α ,in cortex were examined before and 10min,6h,12h,24h,72h,168h after injury by radioimmunoassay.Results The pressure of central skin of blast injury was 335MPa.TXB2 and 6 keto PGF1 levels and the ratio augmented gradually after injury,and reached the peaks [(216.8± 22.5)pg/g and (102.9± 13.5)pg/g respectively] at the 24th hour,and reduced to the normal levels at the 7th day.Conclusions The blast wave can injure the cortex and vessels,thus TXA2 and PGI2 levels and the ratio increase, which aggravate injury of the cerebral cortex.