Tanoue Yoshihisa, Herijgers Paul, Meuris Bart, Leunens Veerle, Lox Marleen, Flameng Willem
Department of Cardiac Surgery, Katholieke Universiteit Leuven, Belgium.
Jpn J Thorac Cardiovasc Surg. 2002 Jan;50(1):23-9. doi: 10.1007/BF02913482.
Ischemic preconditioning has been used to induce the myocardium to adapt to ischemic stress preceded by short periods of ischemia and reperfusion. We used a sheep right heart bypass model with a conductance catheter to assess the cardioprotective effect of ischemic preconditioning on 30-minute normothermic global myocardial ischemia.
Ischemic preconditioning was conducted in 6 sheep in 35-minute aortic cross-clampings interspersed with 5 minutes of reperfusion during cardiopulmonary bypass, with 6 sheep as time-matched controls. Global myocardial ischemia was subsequently achieved in 30-minute aortic cross-clamping with left ventricular unloading during normothermic cardiopulmonary bypass. Weaning from cardiopulmonary bypass was conducted 40 minutes after reperfusion. Before ischemia and 40, 70, and 100 minutes after reperfusion, left ventricular pressure-volume loops were measured using a conductance catheter during right heart bypass preparation. Left ventricular contractility, diastolic function, and mechanical efficiency were then evaluated. Right heart bypass was instituted to control the preload and to decompress the right ventricle completely, thereby eliminating parallel conductance variation.
No differences in the studied parameters were seen between ischemic-preconditioning and control groups before ischemia. Left ventricular contractility, diastolic function, and mechanical efficiency in the ischemic-preconditioning group were significantly superior to those in the control group after reperfusion.
Ischemic preconditioning attenuates postischemic myocardial dysfunction in a sheep model using 30-minute unloaded normothermic global myocardial ischemia. Ischemic preconditioning would thus be clinically significant when the ischemic damage is severe.
缺血预处理已被用于诱导心肌在经历短时间缺血和再灌注后适应缺血应激。我们使用带有电导导管的羊右心旁路模型来评估缺血预处理对30分钟常温全心肌缺血的心脏保护作用。
对6只羊进行缺血预处理,在体外循环期间进行35分钟主动脉交叉钳夹,期间穿插5分钟再灌注,另外6只羊作为时间匹配的对照组。随后在常温体外循环期间进行30分钟主动脉交叉钳夹并左心室卸载以实现全心肌缺血。再灌注40分钟后停止体外循环。在缺血前以及再灌注后40、70和100分钟,在右心旁路准备期间使用电导导管测量左心室压力-容积环。然后评估左心室收缩性、舒张功能和机械效率。建立右心旁路以控制前负荷并完全减压右心室,从而消除平行电导变化。
缺血预处理组和对照组在缺血前研究参数无差异。再灌注后,缺血预处理组的左心室收缩性、舒张功能和机械效率显著优于对照组。
在使用30分钟卸载常温全心肌缺血的羊模型中,缺血预处理可减轻缺血后心肌功能障碍。因此,当缺血损伤严重时,缺血预处理具有临床意义。