CO_2激光心肌打孔缓解心绞痛的祛神经作用机制的实验研究

Denervation Mechanism of Transmyocardial Laser Treatment for Angina Pectoris

目的观察激光打孔术后早期是否有祛心肌交感神经的作用,为激光心肌血运重建术的临床应用提供理论依据。方法健康杂种犬20只,随机分为4组(每组5只):(1)对照组、(2)缺血组、(3)激光打孔组、(4)酚处理组(阳性对照组)。心脏交感神经结构和功能采用如下方法进行检测:于处理前及2周后行缓激肽涂擦刺激心脏交感神经并观察平均动脉压的变化,高压液相色谱电化学检测器法测定局部心肌组织内儿茶酚胺含量。结果各组处理前均有缓激肽刺激所致的平均动脉压的下降。实验后第2周,3、4组对缓激肽的心脏表面刺激无血流动力学的改变,与1、2组相比差别有显著性意义(P<0.05);3、4组局部心肌组织内儿茶酚胺NE和DA的含量较低,与1、2组相比差别有显著性意义(P<0.05)。结论(1)激光心肌血运重建术可破坏心脏交感神经及串行其内的感觉神经,(2)激光心肌血运重建术术后早期临床症状的改善可通过心绞痛传导通路的阻断来解释。(3)单纯激光心肌血运重建术(TMLR)应限于晚期冠心病严重心绞痛不能行冠状动脉搭桥术(CABG)或经皮冠状动脉腔内成形术(PTCA)而需缓解症状者。

Objective We hypothesized that transmyocardial laser treatment by domestic CO_2 laser device damages cardiac sympathetic nerve fibers that convey the pain of angina pectoris, and evaluated clinical application of transmyocardial laser revascularization(TMLR) to treat myocardial ischemia. Methods Twenty mongrel dogs divided randomly into 4 groups: (1)sham-operated negative control animals undergoing thoracotomy and pericardiotomy alone,(2)mutiple ligation of the coronary arteries to creat acute myocardial ischemia,(3)40 minutes after creation of acute myocardial ischemia, drilling with high power CO_ 2 laser,(4)chemical destruction of cardiac nerves by application of 85% phenol to the epicardium. Regional myocardial catecholamine release determined by high pressure liquid chromatography (HPLC) and electrochemical detection(EC). Epicardial application of bradykinin before treatment and 2 weeks after the operation, the resulting central nervous system-mediated decrease in systemic mean arterial pressure was measured. Results Before treatment, changes in systemic arterial pressure were seen with bradykinin stimulation in all dogs.Two weeks after treatment, no hemodynamic response was seen after stimulation of laser or phenol-treated areas, but a normal response was seen in control and ischemia groups with significant difference(P<0.05). The catecholamine content in regional myocardium detected by HPLC-EC also demonstrated significant difference between groups 1 and 2 vs 3 and 4 (P<0.05). NE and DA level in laser- or phenol- treated myocardium was much lower than that of control and ischemia groups. Conclusions (1) Transmyocardial laser treatmemt destroys cardiac nerve fibers, including sensory nerve which is contained in sympathetic nerves. (2) Symptom improvement after TMLR could be interpreted by destruction of cardiac nerve fibers conducting angina pectoris seen clinically.(3) The application of TMLR should be limited to reduce intractable angina pectoris in patients suffered advanced coronary artery disease who can not accept treatment of CABG or PTCA.