摘要
目的 探讨经皮激光心肌血运重建术 (PMR)治疗心肌缺血的机制。方法 取体重 14～18kg的雄性杂种健康犬 10条 ,随机分为PMR组和对照组 ,每组 5条。对两组犬均以不完全结扎冠状动脉 (冠脉 )左前降支的方法复制慢性心肌缺血模型。PMR组在冠脉结扎术后 2周采用Ho :YAG激光系统在缺血心壁施行PMR ,每条犬平均打孔 (15± 3)个。PMR组在冠脉结扎前和PMR后 1、4、12周 ,对照组在冠脉结扎前、冠脉结扎后 3、6和 14周 ,以心肌核素显像检查心肌灌注状况 ,以超声心动图测量左室射血分数 (LVEF)。PMR组在 1、4周检测结束后各处死 1条犬 ,12周检测结束后处死 3条犬 ;对照组在 14周检测结束后处死全部 5条犬。取犬心肌组织作形态学观察及血管计数。PMR术后 2 4h病理标本取自PMR预实验犬。结果 (1)心肌灌注积分 :PMR组冠脉结扎前为 3 2± 0 6 ,PMR后 12周为 0 3± 0 2 ;对照组冠脉结扎前为 3 1± 0 5 ,结扎后 14周为 1 2± 0 3。两组下降幅度的差异有显著意义 (P <0 0 5 )。 (2 )LVEF :PMR组冠脉结扎前为 4 2 6± 6 5 ,PMR后 12周为 5 5 8± 7 6 (P <0 0 5 ) ;对照组冠脉结扎前为 4 3 2± 8 7,结扎后 14周为 4 5 2± 6 3。两组增加幅度的差异有显著意义 (P <0 0 5 )。 (3)PMR犬心肌PMR区域每视野微血管?
Objective To evaluate the cardiac angiogenesis after percutaneous myocardial laser revascularization (PMR). Methods The left anterior descending coronary arteries of 10 healthy mongrel dogs weighing 14-18 kg were ligated partially so as to construct a model of chronic cardiac ischemia. Then the dogs were randomly divided into 2 groups of 5 dogs: PMR and control groups. Cardiogenesis Holmium:YAG laser system was used to make endomyocardial channels (15±3 channels/dog) in the ischemic ventricular walls in PMR group 2 weeks after the ligation. Sham procedure was conducted on the control group. Myocardial perfusion was examined by single photon emission computed tomography (SPECT) and left ventricle ejection fraction (LVEF) was examined by cardiac ultrasound before the ligation and 1, 4, and 12 weeks after PRM in the PMR group and before and 3, 6, and 14 weeks after the ligation in the control group. In the PRM group one dog was killed after the SPECT and LVEF examination 1 and 4 weeks after the PRM respectively and the remaining 3 dogs were killed after the SPECT and LVEF examination 12 weeks after the PRM. The dogs in the control group were killed after the SPECT and LVEF examination 14 weeks after the ligation. Myocardial pathology and cardiac angiogenesis analysis were conducted in both groups. Results Three months after PMR or coronary artery ligation, the SPECT scores of the PMR and control groups decreased from 3.2±0.6 and 3.1±0.5 to 0.3±0.2 and 1.2±0.3 respectively (both P<0.05), the LVEF of the 2 groups increased from 42.6±6.5 and 43.2±8.7 to 55.8±7.6 and 42.6±6.5 respectively (both P<0.05). Microscopy showed that the amount of micrangii was 45.6±7.4 vessel/field in the PMR region of the PRM group, significantly much more than that in the non-ischemic region of the PRM group(18.2±4.7), the ischemic region of the control group (21.4±5.6), and the non-ischemic region of the control group (17.3±6.9,all P<0.05). Conclusion PMR promotes angiogenesis in the ischemic myocardial wall, thus improving
出处
《中华医学杂志》
CAS
CSCD
北大核心
2003年第23期2083-2086,共4页
National Medical Journal of China
