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出 处:《中国医药导刊》2009年第9期1539-1541,共3页Chinese Journal of Medicinal Guide
摘 要:目的:观察缺血后处理(IPO)对肺缺血再灌注期间肺组织NOS活性和NO含量的影响,探讨IPO对肺缺血再灌注损伤的保护作用机制。方法:24只健康SD大鼠,雌雄不拘,随机分成3组(n=8):假手术组(S组)、缺血再灌注组(I/R组),缺血后处理组(IPO组)。采用开胸夹闭和开放左肺门建立大鼠缺血再灌注损伤模型,S组不缺血持续灌注150min;I/R组缺血40min,再灌注105min;IPO组缺血40min后,短暂再灌注30s,缺血30s,反复3次,然后再恢复灌注102min。分别检测各组肺组织NOS活性、NO含量及iNOS表达,测定动脉血氧分压(PaO_2)、肺组织湿/干熏比(W/D),观察肺组织病理变化。结果:与S组比较,I/R组和IPO组NOS活性、No_2含量显著增加(均P<0.01),iNOS表达明显升高;PaO_2降低,肺组织W/D显著升高,病理损伤明显,与I/R组比较,IPO组NOS活性和NO含量升高(P<0.05),但iNOS表达无差异(F>0.05);PaO_2显著升高,肺组织W/D明显降低,病理损伤明量减轻。结论:激活eNOS,增加内源性NO含量可能是早期缺血后处理减轻肺缺血再灌注损伤的可能机制。Objective: To observe effect of ischemic postconditioning(IPO) on pulmonary NOS activity and NO content during lung ischemia- reperfusion (I/R) injury ,and to explore its protective mechanism. Methods: Twenty-four healthy SD rats weighing 210±20g were randomly divided into 3 groups (n=8 each): sham operation group (S group); I/R group: hilum of left lung was clamped for 40 min followed by 105 rain reperfusion ; IPO group: left lung hilum was clamped for 40 min and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion before restoring full perfusion for 102 min; Arterial partial pressure of oxygen (PaO2) was assessed; When the experiment finishes, the left lung was removed for determination of the activity of NOS and NO content, wet/dry lung weight ratio, and for pathological investigation. Results: As compared with S group, the activity of NOS ,the levels of NO and expression of iNOS in UR and IPO groups were higher(P〈0.01).The PaO2 in UR and IPO groups was significantly lower than that in S group, while the lung wet/dry weight ratio in two the experimental groups was significantly increased (P〈0.05 or P〈0.01).To be compared with I/R group, the activity of NOS and the levels of NO in IPO group were higher(P〈0.05),while there was no difference in the expression ofiNOS between I/R and IPO group(P〉0.05), the PaO2 in IPO group was higher than that UR group ,while the lung wet/dry weight ratio in IPO group was significantly lower. Pathological changes of lungs in IPO group apparently weaken. Conclusion: The activation of eNOS and NO release played an important role in protective effect of Ischemic Postconditionittg on lung ischemia-reperfusion injury.
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