Liu Ke-Xuan, Li Yun-Sheng, Huang Wen-Qi, Chen Shu-Qing, Wang Zhong-Xin, Liu Jia-Xin, Xia Zhengyuan
Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, Zhongshan 2th Road, 510080 Guangzhou, China.
Intensive Care Med. 2009 May;35(5):933-42. doi: 10.1007/s00134-009-1428-1. Epub 2009 Feb 4.
To test the hypothesis that immediate but not delayed ischemic postconditioning (IPo) during reperfusion attenuates intestinal injury, and that ischemic preconditioning (IPC) and IPo may confer synergy in intestinal protection.
Prospective laboratory animal study with concurrent control.
Adult Sprague-Dawley rats.
Intestinal ischemia/reperfusion (II/R) injury in rats was produced by clamping superior mesenteric artery for 60 min followed by 60 min reperfusion; IPC was elicited by 10 min ischemia and 10 min reperfusion before index ischemia; IPo was performed by three cycles of 30 s reperfusion and 30 s ischemia initiated either immediately at the onset of reperfusion (IPo) or after reperfusion for 3 min (delayed-IPo). Combination of IPC and IPo was performed by combining both protocols.
Intestinal ischemia/reperfusion resulted in significant intestinal injury evidenced as significant increase in Chiu's scores and wet-to-dry intestine weight ratio accompanied with increases in plasma levels of tumor necrosis factor-alpha and interleukin-6, as well as increases in the intestinal tissue lipid peroxidation product malonediadehyde and myeloperoxidase activity as compared to control animals (all P < 0.05). All these changes were significantly attenuated either by IPC or IPo or their combination (P < 0.05), and not by delayed-IPo (P > 0.05). IPC and IPo showed synergistic protection compared with either protocol alone.
Ischemic postconditioning reduces intestinal injury, in part, by inhibiting oxidative injury, neutrophils filtration and proinflammatory response. The early period of reperfusion is critical to intestinal protection by IPo, and intestinal protection with IPo can be enhanced by IPC.
验证以下假设，即在再灌注期间即刻而非延迟进行缺血后处理（IPo）可减轻肠道损伤，且缺血预处理（IPC）与IPo可能在肠道保护中具有协同作用。
前瞻性实验室动物研究，设同期对照。
成年Sprague-Dawley大鼠。
通过夹闭肠系膜上动脉60分钟，随后再灌注60分钟制作大鼠肠缺血/再灌注（II/R）损伤模型；在指数缺血前，通过10分钟缺血和10分钟再灌注诱导IPC；IPo在再灌注开始时即刻（IPo）或再灌注3分钟后（延迟IPo）进行三个周期的30秒再灌注和30秒缺血。通过联合两种方案进行IPC与IPo的联合应用。
与对照动物相比，肠缺血/再灌注导致显著的肠道损伤，表现为Chiu评分和肠湿重与干重之比显著增加，同时血浆肿瘤坏死因子-α和白细胞介素-6水平升高，以及肠组织脂质过氧化产物丙二醛和髓过氧化物酶活性增加（均P < 0.05）。IPC、IPo或其联合应用均能显著减轻所有这些变化（P < 0.05），而延迟IPo则不能（P > 0.05）。与单独使用任一方案相比，IPC和IPo显示出协同保护作用。
缺血后处理部分通过抑制氧化损伤、中性粒细胞浸润和促炎反应减轻肠道损伤。再灌注早期对IPo的肠道保护至关重要，IPC可增强IPo的肠道保护作用。
