CAJ | 학술논문

目的探讨缺血预处理(IP)对心肌细胞的保护作用及其机制.方法 2004年4月至2004年12月期间在我科行瓣膜置换手术的患者36例,根据是否采取缺血预处理分为预处理组(20例)和对照组(16例),比较两组炎症因子白细胞介素(IL)-8、IL-10、肿瘤坏死因子-α(TNF-α)和心肌细胞转录因子NF.KB p65蛋白的变化情况,分析IP对机体炎症反应的影响.结果两组患者细胞因子IL-8、IL-10、TNF-α均在主动脉开放6 h时达到高峰,术后5 d均恢复到术前水平.预处理组开放后6 h、术后1 d、术后2 d IL-8和TNF-a水平明显低于对照组(P<0.05),IL-10水平显著高于对照组(P<0.05).复灌后两组心肌细胞中NF-KB p65蛋白表达明显增多,预处理组表达量明显低于对照组(P<0.05),与术后1 d TNF-α呈正相关.结论缺血预处理可能通过降低机体的炎症反应途径达到心肌细胞保护的效果.
목적 탐토결혈예처리(IP)대심기세포적보호작용급기궤제.방법 2004년4월지2004년12월기간재아과행판막치환수술적환자36례,근거시부채취결혈예처리분위예처리조(20례)화대조조(16례),비교량조염증인자백세포개소(IL)-8、IL-10、종류배사인자-α(TNF-α)화심기세포전록인자NF.KB p65단백적변화정황,분석IP대궤체염증반응적영향.결과 량조환자세포인자IL-8、IL-10、TNF-α균재주동맥개방6 h시체도고봉,술후5 d균회복도술전수평.예처리조개방후6 h、술후1 d、술후2 d IL-8화TNF-a수평명현저우대조조(P<0.05),IL-10수평현저고우대조조(P<0.05).복관후량조심기세포중NF-KB p65단백표체명현증다,예처리조표체량명현저우대조조(P<0.05),여술후1 d TNF-α정정상관.결론 결혈예처리가능통과강저궤체적염증반응도경체도심기세포보호적효과.
Objective To explore the mechanism of human myocardial ceils protection after ischemia/reperfusion (I/R) injury by preconditioning with ischemia. Methods Data of thirty-six patients underwent valve replacement were collected. They were divided into the ischemic preconditioning group (IP group, 20 cases) and non-ischemic preconditioning group ( contrast group, 16 cases) according to whether they were given single cycle reperfusion before cardioplegia or not. Serum level of interleukin-8,10 and tumor necrosis factor-alpha (TNF-α) were measured with ELISA. Expression of myocardial nuclear facter-κB p65 was analyzed. Results The inflammatory factor IL-8, IL-10 and TNF-aincreased to the highest level in serum on hours 6 after declamping and recovered to normal level on day-5 after declamping. On hour-6, D-1 and D-2 after declamping, serum level of IL-8 and TNF-α were significantly lower in IP group than those in the contrast group ( P < 0.05 ), but serum level of IL-10 was higher in IP group (P <0.05). Expression of myocardial NF-κB p65 increased in both groups after reperfusion,and its level was higher in the contrast group than that in IP group (P < 0.05). Conclusion Ischcmic preconditioning have the effect of protection of human myocardial cells after ischemia/reperfusion injury through decreasing systemic inflammatory response following ischemia reperfusion injury.