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目的:观察兔脑死亡后不同时间点肺组织的细胞凋亡情况和相关基因的表达变化,探究脑死亡状态致肺损伤发生的分子机制。方法:40只健康家兔随机数表法分为2组,假手术组(n=20):行气管插管、股动脉插管及钻孔开颅手术,置入Foley 3F气囊导管后不加压;脑死亡组(n=20):成功建立兔脑死亡模型。各组在术后2,6及8h记录动脉血压和心率变化,RT-PCR检测各组Bcl-2相关X蛋白(Bax)的mRNA表达,免疫组织化学法检测肺组织caspase 3的表达,并用TUNEL法检测肺组织的细胞凋亡情况。结果:脑死亡后2,6,8h家兔动脉血压、心率差异无统计学意义(P>0.05)。脑死亡组各时间点caspase 3阳性表达细胞数较假手术组均有升高(P<0.05)。TUNEL染色显示,脑死亡组细胞凋亡指数在6h和8h达到80%,提示肺损伤逐渐加重,这与促凋亡基因Bax mRNA表达的趋势一致。结论:脑死亡状态可导致肺脏损伤,随着脑死亡时间的延长逐渐加重,且该变化与相关凋亡基因的过表达有关。脑死亡状态维持6h以上,肺脏细胞凋亡情况最为严重。
OBJECTIVE: To observe the apoptosis of lung tissue and the expression of related genes at different time points after brain death in rabbits, and to explore the molecular mechanism of lung injury induced by brain death. Methods: Forty healthy rabbits were randomly divided into two groups: sham operation group (n = 20): endotracheal intubation, femoral artery cannulation and craniotomy. Without Foley 3F balloon catheter Pressure; brain death group (n = 20): A model of brain death was established successfully. The arterial blood pressure and heart rate were recorded at 2, 6 and 8 hours after operation. The mRNA expression of Bcl-2 and Bax in each group was detected by RT-PCR. The expression of caspase 3 in lung tissue was detected by immunohistochemical method. Act detection of lung tissue apoptosis. Results: There was no significant difference in arterial blood pressure and heart rate between 2 and 6 h after brain death (P> 0.05). The number of caspase 3 positive cells in brain death group was higher than that in sham operation group at each time point (P <0.05). TUNEL staining showed that apoptosis index of brain death group reached 80% at 6h and 8h, suggesting that lung injury gradually aggravated, which is consistent with the trend of Bax mRNA expression. CONCLUSION: The brain death state can lead to lung injury, which gradually aggravates with the prolongation of brain death, and the change is related to the overexpression of related apoptosis genes. The state of brain death maintained more than 6h, lung cell apoptosis is the most serious.