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探讨缺血再灌注对在体兔窦房结细胞凋亡的影响。取家兔 90只随机分为对照组 ,缺血 10 ,30 ,6 0 ,12 0min组及缺血 10 ,30 ,6 0 ,12 0min再灌注 4h组 ,每组 10只。通过结扎及放松右冠状动脉起始部制作窦房结缺血再灌注损伤模型 ,当达各预定时间点后 ,迅速切取窦房结组织固定 ,用TUNEL法检测窦房结细胞凋亡。结果 :①对照组、缺血10 ,30min组均未观察到明显的窦房结细胞凋亡现象。②缺血 6 0 ,12 0min组及缺血再灌注 4组中共有 6 8.3% (41/6 0 )的兔子窦房结细胞出现不同程度的凋亡现象 ,表明该部分兔子的窦房结动脉起源于右冠状动脉。③缺血 6 0 ,12 0min两组窦房结细胞凋亡率分别为 8.6 %与 16 .1% ,而缺血 10 ,30 ,6 0 ,12 0min再灌注 4h 4组中窦房结细胞凋亡率分别为 2 3.5 %、34.5 %、4 4 .7%与 31.2 %。结论 :缺血再灌注可诱导在体兔窦房结细胞凋亡 ,且随缺血时间延长 ,细胞凋亡率逐渐增加 ;再灌注组细胞凋亡率较相同时间缺血组明显增加 ,表明缺血再灌注损伤介导了窦房结细胞凋亡。
To investigate the effect of ischemia / reperfusion on the apoptosis of sinoatrial node cells in rabbits. Totally 90 rabbits were randomly divided into control group, ischemia group of 10, 30, 60, 120 min and ischemia reperfusion group of 10, 30, 60, 120 min for 4h. The model of sinoatrial ischemia-reperfusion injury was made by ligating and relaxing the beginning of the right coronary artery. After reaching the predetermined time points, the sino-atrial node tissue was quickly removed and the apoptosis of sino-atrial node cells was detected by TUNEL. Results: ① In the control group, no apparent apoptosis of sinoatrial node cells was observed in 10 min and 30 min ischemia groups. ② A total of 6 8.3% (41/60) of rabbit sinoatrial node cells in 60 min ischemia and 60 min ischemia reperfusion groups showed different degrees of apoptosis, indicating that the sinoatrial node artery Originated in the right coronary artery. ③ The apoptosis rate of sinoatrial node cells in ischemic group was 8.6% and 16.1% at 60 and 120 minutes, respectively, while the apoptosis of sinoatrial node cells in 4h and 4 groups after ischemia 10, 30, 60 and 120 min Mortality rates were 23.5%, 34.5%, 44.7% and 31.2% respectively. CONCLUSION: Ischemia-reperfusion can induce apoptosis of sino-atrial node cells in rabbits, and the apoptosis rate of sino-atrial node cells gradually increases with the prolongation of ischemia. The apoptosis rate in reperfusion group is significantly increased compared with the same time ischemia group, Blood reperfusion injury mediates apoptosis of sinoatrial node cells.