Gao Li-Wei, Xie Rui-Qin, Cui Wei, Liu Fan, Liu Jing, Hu Hai-Juan, Lu Jing-Chao, Pei Wei-Na, Yang Xiao-Hong
Department of Cardiology, the Second Hospital of Hebei Medical University , Shijiazhuang 050000, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jan;28(1):28-32.
In this study, we try to find the better protocol of limb ischemia postconditioning by observing different protective effects of limb ischemic postconditioning (different strength and time windows in rabbits).
42 healthy New Zealand rabbits were randomly divided into 7 groups (n = 6): Sham; Control (CON); Skeletal muscle postconditioning (SP); 6 min-delayed skeletal muscle postconditioning (6M-DSP); 1 min-delayed skeletal muscle postconditioning (1M-DSP); Strengthen skeletal muscle postconditioning (SSP); Weakened skeletal muscle postconditioning (WSP). Acute ischemia/reperfusion (I/R) model was induced by 45 minutes occlusion on left circumflex coronary artery (LCX) and 2 hours reperfusion in all anesthetized open-chest rabbits except the Sham. Limb ischemia was induced by external iliac arteries occlusion and reperfusion through artery clamps. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining. Blood serum creatine kinase (CK) activity and lactate dehydrogenase (LDH) activity were measured at baseline,the end of ischemia, after 1 hour and 2 hours of reperfusion respectively.
Compared with the CON, the weight ratio and area ratio of myocardial infarction size were significantly decreased by 49.97% and 43.78% in SP, by 42.32% and 42.68% in 1M-DSP, by 48.36% and 48.86% in SSP (P < 0.05). But there was no significant difference between SP and 1M-DSP and SSP (P > 0.05). Otherwise, compared with the CON, myocardial infarct size was not significantly reduced in 6M-DSP or WSP (P > 0.05). The change of CK was similar to the trend of myocardial infarct size.
The limb ischemia strength of 5 mini/1 minR x 1 cycle could significantly reduce the myocardial ischemia/ reperfusion injury in rabbits, if it was achieved before myocardial reperfusion.
在本研究中，我们试图通过观察肢体缺血后处理（不同强度和时间窗，以家兔为实验对象）的不同保护作用，找出更好的肢体缺血后处理方案。
42只健康的新西兰家兔被随机分为7组（n = 6）：假手术组；对照组（CON）；骨骼肌后处理组（SP）；延迟6分钟骨骼肌后处理组（6M - DSP）；延迟1分钟骨骼肌后处理组（1M - DSP）；强化骨骼肌后处理组（SSP）；弱化骨骼肌后处理组（WSP）。除假手术组外，所有麻醉开胸家兔均通过左回旋支冠状动脉（LCX）闭塞45分钟和再灌注2小时诱导急性缺血/再灌注（I/R）模型。通过动脉夹夹闭和再灌注髂外动脉诱导肢体缺血。通过三苯基四氮唑（TTC）染色评估心肌梗死范围。分别在基线、缺血结束时、再灌注1小时和2小时测量血清肌酸激酶（CK）活性和乳酸脱氢酶（LDH）活性。
与对照组相比，SP组心肌梗死面积的重量比和面积比显著降低49.97%和43.78%，1M - DSP组降低42.32%和42.68%，SSP组降低48.36%和48.86%（P < 0.05）。但SP组与1M - DSP组和SSP组之间无显著差异（P > 0.05）。此外，与对照组相比，6M - DSP组或WSP组心肌梗死面积未显著减小（P > 0.05）。CK的变化与心肌梗死面积的趋势相似。
如果在心肌再灌注前实现，5分钟缺血/1分钟再灌注×1个周期的肢体缺血强度可显著减轻家兔心肌缺血/再灌注损伤。
