摘要
①目的 了解猪同种原位心脏移植术后早期一氧化氮 (NO)、一氧化氮合酶 (NOS)含量的变化 ,及其与早期缺血再灌注损伤的关系。②方法 建立猪同种原位心脏移植模型。供心在移植前低温保存 (Thomas液 ,4℃ ) 4h ,移植成功心脏复搏后 2h取材。应用组织化学方法测定心肌组织中NO、NOS的含量 ,应用核酸原位末端标记法 (TUNEL)测定心肌细胞凋亡指数 ,作为评价心肌缺血再灌注损伤的指标。以正常心肌及单纯缺血心肌组织作为对照。③结果 移植后心肌组织NO、NOS的含量较缺血组与正常组低 ,差异有显著意义 (F =2 7.2 2 9、16 .2 0 3,q =5 .716~ 6 .4 12 ,P <0 .0 1)。移植组心肌细胞凋亡指数与正常组及缺血组比较明显升高 ,差异有显著性(F =16 3.884 ,q =7.4 82、6 .975 ,P <0 .0 1)。心肌组织NO、NOS含量与心肌细胞凋亡指数呈负相关关系 (r =- 0 .886、- 0 .795 ,P <0 .0 1)。④结论 猪心脏移植后早期心肌缺血再灌注损伤所致的细胞死亡主要表现为心肌细胞凋亡 ;再灌注期间内源性NO。
Objective To investigate the changes of NO and NOS contents in the heart tissues during ischemic reperfusion after porcine orthotopic heart transplantation(POHT), and to determine the relationship between NO and NOS and ischemic reperfusion injuries. Methods The POHT models were established. The donor hearts were preserved for four hours in cold storage(Thomas liquid, 4 ℃) before the transplantation. Two hours after the surgery, the grafts were taken for detection. The contents of NO and NOS were measured histochemically. Apoptosis of myocardium was detected for apoptosis index(AI) as the index of ischemic reperfusion injury with in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL). The results were compared with those of the normal and ischemic heart tissues. Results The contents of NO and NOS in the grafts were significantly lower than those in the ischemia and the control hearts(F=27.229,16.203;q=5.716- 6.412;P<0.01). The AI of the grafts increased significantly (F=163.884;q=7.482,6.975;P<0.01). The content of NO and NOS had negative correlation with myocardial apoptosis(r=-0.886,-0.795; P<0.01). Conclusion The main form of cell death of early ischemic reperfusion after the procedure is myocardial cell apoptosis. Decreased production of endogenous NO and NOS contributes to the early ischemic reperfusion injury after the transplantation.
出处
《齐鲁医学杂志》
2004年第6期471-473,共3页
Medical Journal of Qilu
基金
青岛市科技局重点资助项目 ( 2 0 0 1KNS 2E 5 1)
关键词
一氧化氮
一氧化氮合酶
心脏移植
再灌注损伤
凋亡
nitric oxide
nitric-oxide synthase
heart transplantation
reperfusion injury
apoptosis