The search for sterss-induced conditioning: effects of acute hypercapnia

我们研究了猪顿抑心肌缺血前或再灌注期间（预处理或后处理）急性高碳酸血症的心脏保护作用。通过PaCO 2 70 mmHg通气不足30分钟诱导高碳酸血症。12分钟缺血和90分钟再灌注产生眩晕。心肌节段缩短法评价心肌收缩力。数据用Mann-Whitney U检验进行分析。p<0.05被认为具有统计学显著性。高碳酸血症时PaCO 2和冠脉血流量显著高于对照组。昏迷无明显恢复。预处理猪再灌注后白细胞介素略有减弱。KATP通道在高碳酸血症时不被激活。急性高碳酸血症不能促进顿抑心肌的恢复。结果是冠状动脉血流量增加导致预适应刺激减弱，因此无法获得足够的预适应刺激。

We studied the cardioprotective effect of acute hypercapnia before ischemia or during reperfusion (pre- or post-conditioning) in swine stunned myocardium. Hypercapnia was induced by hypoventilation of PaCO2 70 mmHg for 30 minutes. Stunning was produced by 12-min ischemia and 90-min reperfusion. Myocardial contractility was evaluated with segment shortening. Data were analyzed with Mann-Whitney U test. p<0.05 was considered statistically significant. PaCO2 and coronary blood flow during hypercapnia were significantly higher than those in control swine. There was no significant recovery of stunning. Interleukin after reperfusion were slightly attenuated in pre-conditioned swine. KATP channels were not activated during hypercapnia. Acute hypercapnia could not enhance recovery of stunned myocardium. Attenuation of the preconditioning stimuli by the increase of coronary blood flow would be considered as the result, and therefore enough conditioning stimuli would not be obtained.