Stengl Milan, Sykora Roman, Krouzecky Ales, Chvojka Jiri, Novak Ivan, Varnerova Veronika, Kuncova Jitka, Nalos Lukas, Sviglerova Jitka, Matejovic Martin
Department of Physiology, Charles University in Prague, Faculty of Medicine and Teaching Hospital in Plzen, Plzen, Czech Republic.
Crit Care Med. 2008 Dec;36(12):3198-204. doi: 10.1097/CCM.0b013e31818f9eda.
Sepsis has been defined as the systemic host response to infection with an overwhelming systemic production of both proinflammatory and anti-inflammatory mediators. Continuous hemofiltration has been suggested as possible therapeutic option that may remove the inflammatory mediators. However, hemodialysis and hemofiltration were reported to influence cardiac electrophysiologic parameters and to increase the arrhythmogenic risk. We hypothesize that sepsis affects electrophysiologic properties of the pig heart and that the effects of sepsis are modified by hemofiltration.
Laboratory animal experiments.
Animal research laboratory at university medical school.
Forty domestic pigs of either gender.
In anesthetized, mechanically ventilated, and instrumented pigs sepsis was induced by fecal peritonitis and continued for 22 hours. Conventional or high-volume hemofiltration was applied for the last 10 hours of this period.
Electrocardiogram was recorded before and 22 hours after induction of peritonitis. RR, QT, and QTc intervals were significantly shortened by sepsis. The plasma levels of interleukin-6 and tumor necrosis factor-alpha were increased in sepsis. High-volume hemofiltration blunted the sepsis-induced increase in tumor necrosis factor-alpha. Action potentials were recorded in isolated ventricular tissues obtained at the end of in vivo experiments. Action potential durations were significantly shortened in septic preparations at all stimulation cycle lengths tested. Both conventional and high-volume hemofiltrations lead to further shortening of action potential durations measured afterward in vitro. This action potential duration shortening was reversed by septic hemofiltrates obtained previously by conventional or high-volume hemofiltration. Tumor necrosis factor-alpha (500 ng/L) had no effect on action potential durations in vitro.
In a clinically relevant porcine model of hyperdynamic septic shock, both sepsis and continuous hemofiltration shortened duration of cardiac repolarization. The continuous hemofiltration was not associated with an increased prevalence of ventricular arrhythmias. Tumor necrosis factor-alpha or interleukin-6 did not contribute to the observed changes in action potential durations.
脓毒症被定义为机体对感染的全身性宿主反应，伴有促炎和抗炎介质的大量全身性产生。持续血液滤过被认为是一种可能去除炎症介质的治疗选择。然而，据报道血液透析和血液滤过会影响心脏电生理参数并增加致心律失常风险。我们假设脓毒症会影响猪心脏的电生理特性，且血液滤过会改变脓毒症的影响。
实验室动物实验。
大学医学院的动物研究实验室。
40只雌雄不限的家猪。
在麻醉、机械通气并安装仪器的猪身上，通过粪便性腹膜炎诱导脓毒症，并持续22小时。在此期间的最后10小时进行常规或高容量血液滤过。
在腹膜炎诱导前和诱导后22小时记录心电图。脓毒症使RR、QT和QTc间期显著缩短。脓毒症时白细胞介素-6和肿瘤坏死因子-α的血浆水平升高。高容量血液滤过减弱了脓毒症诱导的肿瘤坏死因子-α的升高。在体内实验结束时从分离的心室组织中记录动作电位。在所有测试的刺激周期长度下，脓毒症标本的动作电位时程显著缩短。常规和高容量血液滤过均导致随后在体外测量的动作电位时程进一步缩短。这种动作电位时程的缩短可被先前通过常规或高容量血液滤过获得的脓毒症血液滤过液逆转。肿瘤坏死因子-α（500 ng/L）在体外对动作电位时程无影响。
在一个具有临床相关性的高动力性脓毒症休克猪模型中，脓毒症和持续血液滤过均缩短了心脏复极时间。持续血液滤过与室性心律失常的发生率增加无关。肿瘤坏死因子-α或白细胞介素-6对观察到的动作电位时程变化无作用。
