国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
4期
256-259
,共4页
急性肺损伤%缺血再灌注%细胞凋亡%白介素1β%一氧化氮
急性肺損傷%缺血再灌註%細胞凋亡%白介素1β%一氧化氮
급성폐손상%결혈재관주%세포조망%백개소1β%일양화담
Acute lung injury%Ischemia reperfusion%Apoptosis%Interleukin-1β%Nitric oxide
目的 探讨大鼠肾缺血再灌注后肺组织细胞凋亡及血清细胞因子的的变化,分析其在肾缺血再灌注后肺损伤发病机制中的作用.方法 用无损伤动脉夹钳夹大鼠双侧肾蒂45 min制成肾缺血再灌注损伤模型.观察缺血再灌注后2 h、6 h、12 h、24 h、72 h血清白介素1β(IL-1β)和一氧化氮(NO)的浓度,病理切片观察肺组织病理学及细胞凋亡的改变.结果 缺血再灌注后肺组织细胞凋亡、血清IL-1β和NO的浓度逐渐增加,以再灌注12 h最明显,24 h后逐渐下降.缺血再灌注各时间点肺组织损伤变化与各项检测指标的变化规律相一致.结论 肾缺血再灌注后释放的细胞因子IL-1β和NO可能是肺组织细胞凋亡和肺损伤的原因之一.
目的 探討大鼠腎缺血再灌註後肺組織細胞凋亡及血清細胞因子的的變化,分析其在腎缺血再灌註後肺損傷髮病機製中的作用.方法 用無損傷動脈夾鉗夾大鼠雙側腎蒂45 min製成腎缺血再灌註損傷模型.觀察缺血再灌註後2 h、6 h、12 h、24 h、72 h血清白介素1β(IL-1β)和一氧化氮(NO)的濃度,病理切片觀察肺組織病理學及細胞凋亡的改變.結果 缺血再灌註後肺組織細胞凋亡、血清IL-1β和NO的濃度逐漸增加,以再灌註12 h最明顯,24 h後逐漸下降.缺血再灌註各時間點肺組織損傷變化與各項檢測指標的變化規律相一緻.結論 腎缺血再灌註後釋放的細胞因子IL-1β和NO可能是肺組織細胞凋亡和肺損傷的原因之一.
목적 탐토대서신결혈재관주후폐조직세포조망급혈청세포인자적적변화,분석기재신결혈재관주후폐손상발병궤제중적작용.방법 용무손상동맥협겸협대서쌍측신체45 min제성신결혈재관주손상모형.관찰결혈재관주후2 h、6 h、12 h、24 h、72 h혈청백개소1β(IL-1β)화일양화담(NO)적농도,병리절편관찰폐조직병이학급세포조망적개변.결과 결혈재관주후폐조직세포조망、혈청IL-1β화NO적농도축점증가,이재관주12 h최명현,24 h후축점하강.결혈재관주각시간점폐조직손상변화여각항검측지표적변화규률상일치.결론 신결혈재관주후석방적세포인자IL-1β화NO가능시폐조직세포조망화폐손상적원인지일.
Objective To investigate changes of apoptosis in lung and serum cytokines, and to explore the role of them in lung injury after renal ischemia reperfusion. Methods The animal model of renal ischemia reperfusion injury was made by clamping bilateral renal pedicle for 45 minutes. At 2 h, 6 h,12 h,24 h,72 h after ischemia reperfusion,the serum interleukin-1β(IL-1β) and nitric oxide (NO) were detected,the changes of histopathology and apoptosis in lung were observed. Results After ischemia reperfusion,lung apoptosis,serum IL-1β and NO gradually increased. They reached to a peak value at 12 h after ischemia reperfusion. They gradually decreased at 24 h after ischemia reperfusion. The changes of lung injury were consistent to the changes of detected parameters at each time point after ischemia reperfusion. Conclusions IL-1β and NO released after renal ischemia reperfusion may be one of the reasons of apoptosis and injury in lung.
