CAJ | 학술논문

目的：建立兔烫伤合并海水浸泡的实验模型，探讨烫伤合并海水浸泡复合损伤对肠道损害的影响。方法新西兰兔63只，制作20%TBSA动物烫伤模型后，随机分为单纯烫伤对照组（A组）（n=21）、烫伤后浸泡淡水组（B组）（n=21）和烫伤后浸泡海水组（C组）（n=21），每小组分别在伤后2、4和8 h处死7只动物，抽取心室血及取标本。检测血浆中超氧化物歧化酶（SOD）和脂质过氧化物（LPO）水平，检测肠道组织中PGs含量，形态学观察小肠的炎症反应情况及结构损伤状况，采用SP法检测小肠粘膜细胞中Bax和Bcl-2蛋白的表达情况。结果小肠形态学观察，总体上C组小肠组织炎症反应情况、结构损伤状况较A组和B组严重；C组兔小肠组织中PGs含量、血浆中SOD活力在海水浸泡2、4、8 h后较同期A组和B组明显减少，组间差异有显著性（P<0.01），各时相点间差异有显著性（P<0.01），随着浸泡（或致伤）时间延长含量或活力逐渐减少；C组兔血浆中LPO含量在海水浸泡2、4、8 h后较同期A组和B组明显增加，组间差异有显著性（P<0.01），不同时相点间差异有显著性（P<0.01），随着浸泡（或致伤）时间延长含量逐渐升高；C组兔小肠粘膜组织中凋亡蛋白Bax和Bcl-2的表达在海水浸泡4、8 h后较同期A组和B组明显增强，组间差异有显著性（P<0.01），不同时相点间差异有显著性（P<0.01），随着浸泡（或致伤）时间延长Bax和Bcl-2表达逐渐增强。结论烧伤合并海水浸泡会加重肠粘膜结构破坏和屏障功能损伤，表现在小肠炎症反应和结构损伤状况的加重，小肠组织中PGs含量和血浆中SOD活力降低，血浆中LPO含量升高，小肠粘膜上皮细胞中凋亡蛋白Bax和Bcl-2的表达增强。
목적：건립토탕상합병해수침포적실험모형，탐토탕상합병해수침포복합손상대장도손해적영향。방법신서란토63지，제작20%TBSA동물탕상모형후，수궤분위단순탕상대조조（A조）（n=21）、탕상후침포담수조（B조）（n=21）화탕상후침포해수조（C조）（n=21），매소조분별재상후2、4화8 h처사7지동물，추취심실혈급취표본。검측혈장중초양화물기화매（SOD）화지질과양화물（LPO）수평，검측장도조직중PGs함량，형태학관찰소장적염증반응정황급결구손상상황，채용SP법검측소장점막세포중Bax화Bcl-2단백적표체정황。결과소장형태학관찰，총체상C조소장조직염증반응정황、결구손상상황교A조화B조엄중；C조토소장조직중PGs함량、혈장중SOD활력재해수침포2、4、8 h후교동기A조화B조명현감소，조간차이유현저성（P<0.01），각시상점간차이유현저성（P<0.01），수착침포（혹치상）시간연장함량혹활력축점감소；C조토혈장중LPO함량재해수침포2、4、8 h후교동기A조화B조명현증가，조간차이유현저성（P<0.01），불동시상점간차이유현저성（P<0.01），수착침포（혹치상）시간연장함량축점승고；C조토소장점막조직중조망단백Bax화Bcl-2적표체재해수침포4、8 h후교동기A조화B조명현증강，조간차이유현저성（P<0.01），불동시상점간차이유현저성（P<0.01），수착침포（혹치상）시간연장Bax화Bcl-2표체축점증강。결론소상합병해수침포회가중장점막결구파배화병장공능손상，표현재소장염증반응화결구손상상황적가중，소장조직중PGs함량화혈장중SOD활력강저，혈장중LPO함량승고，소장점막상피세포중조망단백Bax화Bcl-2적표체증강。
Objective To investigate the effect of seawater exposure on intestinal injury in rabbits with scald burns and explore the mechanisms. Methods Sixty-three rabbits with scald burns covering 20%total body surface area were randomized equally into scald control group (group A), scald with freshwater exposure group (group B), and scald with seawater exposure group (group C). At 2, 4 and 8 h after scald burns, 7 rabbits from each group were sacrificed for detecting plasma superoxide dismutase (SOD) and lipid peroxide (LPO) levels and intestinal contents of prostaglandins (PGs) and for examining the intestinal pathologies; immunohistochemistry was used to detect the expression of Bax and Bcl-2 proteins in the small intestinal epithelium. Results The rabbits in group C showed severer intestinal mucosal and barrier function damages than those in groups A and B. The plasma SOD activity and intestinal PGs contents were significantly lowered in group C than in groups A and B at 2, 4, and 8 h postburn (P<0.01) and reduced as the postburn time extended (P<0.01). In group C, plasma LPO content was the highest among the groups (P<0.01) and increased significantly with the seawater exposure time (P<0.01). The expression of Bax and Bcl-2 in the intestinal mucosal tissues was also the highest in group C (P<0.01) at 4 h and 8 h postburn and increased significantly with time (P<0.01). Conclusion Seawater exposure exacerbates scald burn-induced intestinal mucosal and barrier function damages in rabbits mainly by aggravating intestinal inflammation and structural damage, as evidenced by decreased intestinal PGs contents and plasma SOD activity, increased plasma PLO content, and enhanced Bax and Bcl-2 protein expressions in the intestinal mucosa.