CAJ | 학술논문

目的建立细菌性老龄大鼠多器官损伤模型.方法将大鼠随机分为老龄对照组、老龄模型组和青年对照组、青年模型组.采用气管插管法注入肺炎克雷伯杆菌引起肺部炎症,根据脏器有关生化指标变化、病理学改变及动物死亡率等情况评价该模型.结果青年模型组和老龄模型组制模24 h后大鼠死亡率分别为33.3%(5/15)和60.0%(15/25).与同龄对照组比较,青年模型组和老龄模型组外周血白细胞计数和中性粒细胞比例明显增高(P均<0.01);肺、心、肝功能障碍发生率为60%～100%;肺动脉血氧分压(PaO2)明显下降,动脉血二氧化碳分压(PaCO2)显著上升(P<0.05或P<0.01);血清肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)和丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)明显增高(P<0.05或P<0.01);脏器组织学发生了明显的病理学改变.与青年模型组比较,老龄模型组肺PaO2明显下降、PaCO2显著上升;血清CK、CK-MB、LDH和ALT、AST明显增高(P<0.05或P<0.01);肺、心、小肠病理损伤评分显著增高(P均<0.05),肝、肾亦有增高趋势.结论成功地制备了细菌性老龄大鼠多器官损伤模型,符合老年"肺启动"机制多器官功能障碍综合征(MODS)特征,该模型制备简便,成功率高.脏器损伤重、死亡率高为老龄大鼠多器官损伤的特点.
목적 건립세균성노령대서다기관손상모형.방법 장대서수궤분위노령대조조、노령모형조화청년대조조、청년모형조.채용기관삽관법주입폐염극뢰백간균인기폐부염증,근거장기유관생화지표변화、병이학개변급동물사망솔등정황평개해모형.결과 청년모형조화노령모형조제모24 h후대서사망솔분별위33.3%(5/15)화60.0%(15/25).여동령대조조비교,청년모형조화노령모형조외주혈백세포계수화중성립세포비례명현증고(P균<0.01);폐、심、간공능장애발생솔위60%～100%;폐동맥혈양분압(PaO2)명현하강,동맥혈이양화탄분압(PaCO2)현저상승(P<0.05혹P<0.01);혈청기산격매(CK)、기산격매동공매(CK-MB)、유산탈경매(LDH)화병안산전안매(ALT)、천동안산전안매(AST)명현증고(P<0.05혹P<0.01);장기조직학발생료명현적병이학개변.여청년모형조비교,노령모형조폐PaO2명현하강、PaCO2현저상승;혈청CK、CK-MB、LDH화ALT、AST명현증고(P<0.05혹P<0.01);폐、심、소장병리손상평분현저증고(P균<0.05),간、신역유증고추세.결론 성공지제비료세균성노령대서다기관손상모형,부합노년"폐계동"궤제다기관공능장애종합정(MODS)특정,해모형제비간편,성공솔고.장기손상중、사망솔고위노령대서다기관손상적특점.
Objective To reproduce a model of bacterial multiple organ injury (MOI) in aged rats. Methods Male Sprague-Dawley (SD) rats were used. The young rats were divided into young control group (YCG, n=10) and young model group (YMG, n=15), and the elderly, aged control group (ACG, n = 10) and aged model group (AMG, n = 25). The model of rats with Klebsiella pneumoniae pneumonia was produced by tracheal instillation of the bacteria, and injury to various organs was observed and evaluated with changes in biochemical parameters, pathological pictures and mortality. Results Between YMG and AMG, the mortality rates were 33. 33% (5/15) and 60. 00% (15/25), respectively, at 24 hours after instillation of the bacteria. Compared with YCG and ACG, the neutrophil percentage and white blood cell (WBC) counts in peripheral blood increased significantly in YMG and AMG groups (all P＜0. 01), the rates of dysfunction of the lungs, the heart and the liver, were 60%- 100%. The respiratory dysfunction was evidenced by an increase in the arterial partial pressure of carbon dioxide (PaCO2, P＜0. 01), and a decrease in the arterial partial pressure of oxygen (PaO2, P＜0. 05 or P＜0. 01). Myocardial dysfunction was shown by a the sharp increase in creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB) and lactate dehydrogenase (LDH), and that of the liver by changes in alanine aminotransferase (ALT) and aspartate aminotransferase (AST, P＜0. 05 or P＜0. 01). The pathological changes under light and electronic microscopy were obvious, and the main feature was infiltration of the inflammatory cells. Compared with YMG, PaO2 in AMG dropped significantly, PaCO2 increased, CK, CK-MB, LDH, ALT and AST also increased significantly (P＜0. 05 or P＜0. 01). The scores of pathological injury in the lungs, the heart and the small intestine in the AMG were obviously higher than that in YMG group (all P＜0. 05), and the same was trend in the liver and the kidney. Conclusion The model of bacterial MOI in aged rats is reproduced successfully, and it mimics the pathogenesis of multiple organ dysfunction syndrome (MODS) which initiates from infection in the lungs. The model is simple and convenient to replicate with a high success rate. The MOI in the aged rats is characterized by the severity of the organ injury and a high mortality rate.