CAJ | 학술논문

背景:脑死亡供体已成为当前器官移植的主要来源.研究有效的方法与手段,保护供体器官,提高器官质量至关重要.目的:观察热休克蛋白70在脑死亡状态致肺损伤中的作用.方法:60只家兔随机均分为3组,即正常对照组:不行手术;假手术组:行股动脉插管、气管插管及颅骨钻孔置管术,不行颅内加压脑死亡术;脑死亡组:行股动脉插管、气管插管、颅骨钻孔置管及颅内加压脑死亡术,呼吸机维持脑死亡状态.各组均在术后2,4,6,8 h 记录动脉血压及心率的变化.苏木精-伊红染色光镜观察肺脏结构改变, RT-PCR 和免疫组化检测各组肺脏热休克蛋白70的 mRNA 及蛋白表达.结果与结论:脑死亡组较假手术组血压与心率尚未发现显著变化(P >0.05).假手术组各时间点肺脏组织损伤不明显.2-6 h 内,随着时间延长,脑死亡组家兔肺脏损伤逐渐加重(P <0.05),但8 h 出现一定程度好转.热休克蛋白70 mRNA与蛋白表达呈时间依赖性增高(P <0.05),始于2 h,于8 h 最高.结果证实,热休克蛋白70可能介入脑死亡状态诱导的肺脏损伤,发挥自身防御性保护作用.
배경:뇌사망공체이성위당전기관이식적주요래원.연구유효적방법여수단,보호공체기관,제고기관질량지관중요.목적:관찰열휴극단백70재뇌사망상태치폐손상중적작용.방법:60지가토수궤균분위3조,즉정상대조조:불행수술;가수술조:행고동맥삽관、기관삽관급로골찬공치관술,불행로내가압뇌사망술;뇌사망조:행고동맥삽관、기관삽관、로골찬공치관급로내가압뇌사망술,호흡궤유지뇌사망상태.각조균재술후2,4,6,8 h 기록동맥혈압급심솔적변화.소목정-이홍염색광경관찰폐장결구개변, RT-PCR 화면역조화검측각조폐장열휴극단백70적 mRNA 급단백표체.결과여결론:뇌사망조교가수술조혈압여심솔상미발현현저변화(P >0.05).가수술조각시간점폐장조직손상불명현.2-6 h 내,수착시간연장,뇌사망조가토폐장손상축점가중(P <0.05),단8 h 출현일정정도호전.열휴극단백70 mRNA여단백표체정시간의뢰성증고(P <0.05),시우2 h,우8 h 최고.결과증실,열휴극단백70가능개입뇌사망상태유도적폐장손상,발휘자신방어성보호작용.
BACKGROUND: Donation after brain death has been the main source for organ transplantation. It is important to develop an effective method to protect the organ and improve its quality. OBJECTIVE: To investigate the effect of heat shock protein 70 on rabbit brain death induced lung injury. METHODS: The 60 rabbits were randomly divided into three groups: rabbits in the normal control group without surgery;the rabbits in the sham-operation group received femoral artery catheterization, endotracheal intubation and burr hole catheter, did not received the intracranial pressure; and the rabbits in the brain death group were treated with femoral artery catheterization, endotracheal intubation, burr hole catheter and intracranial pressure, and the ventilator was used to maintain a brain-dead state. Each group was further divided into four time points at 2, 4, 6 and 8 hours. The blood pressure and the heart rate were measured at each point. The changes of lung morphology were observed by hematoxylin-eosin staining. The mRNA and the protein expression of heat shock protein 70 were measured by reverse transcription-PCR and immunohistochemistry. RESULTS AND CONCLUSION: There was no significant difference in the blood pressure and the heart rate between the brain death group and sham-operation group (P > 0.05). The lung injuries in the sham-operation group at different time points were not obvious. From 2 to 6 hours, the lung injuries in the brain-death groups were getting worse in a time-dependent manner (P < 0.05), but somewhat amelioration at 8 hours group was observed when compared with the previous time group. The mRNA and the protein expression of heat shock protein 70 were gradual y increased at 2 hours in a time-dependent manner (P < 0.05) and reached peak at 8 hours. These findings confirm that heat shock protein 70 can ameliorate brain death induced lung injury and play their defensive protection effect.