The Evaluation of Transmyocardial Laser Revascularization with the aid of PET

(方法)成年比格犬麻醉，机械换气。进行了左开胸手术，并暴露了一颗心脏。用正电子发射断层扫描(PET)测量心肌局部血流量(RMBF)。然后结扎冠状动脉左前降支第一对角支远端，造成急性心肌梗死。然后用PET测定心肌梗死后RMBF。将犬分为两组：对照组和TMLR组。对照组关闭开胸，TMLR组用CO2激光在LAD区域建立跨壁通道。制成直径约1 mm的通道，密度为1通道/cm2，平均10个通道。用正电子发射计算机断层扫描(PET)测量RMBF。开胸手术也关闭了。分别于术后2周和2个月测量RMBF。然后，狗被榨汁，心脏被摘除。基质金属蛋白…的组织水平用酶谱和分光光度计法测定血清中多硒(Met Se，MMPs)和血小板衍化内皮细胞生长因子(PDECGF)的含量。用抗增殖细胞核抗原抗体和抗第VIII因子相关抗体双重免疫组织化学染色内皮细胞，计算微血管密度。(结果)计算梗死区13NH3吸收水平与非梗死区13NH3吸收水平的比值，以梗死区与非梗死区13NH3吸收水平的百分比作为评价指标。对照组梗死后、术后2周、2个月分别为25%、62%、49%。TMLR组梗死后、TMLR后、2周、2个月分别为36%、29%、73%、67%。两组间差异无统计学意义，TMLR不增加急性缺血心肌局部血流量。未发现任何完全开放的通道，并有肉芽组织渗入。通道周围可见大量微血管和增殖的内皮细胞。梗死区基质金属蛋白酶-2、基质金属蛋白酶-9和血小板衍生生长因子水平升高。TMLR组显著高于对照组。TMLR组的微血管密度明显高于对照组。(结论)TMLR不增加急性缺血心肌的RMBF。未发现完全开放的通道，并有肉芽组织渗入。TMLR可通过表达基质金属蛋白酶和PDECGF促进血管生成。较少

(Method) Adult beagle dogs were anesthesized and ventilated mechanically with room air. A left thoracotomy was performed and a heart was exposed. Then the regional myocardial blood flow (RMBF) by the positron emmision tomography (PET) with ^<13>NH^3 was measured. Then the left anterior descending coronary artery was ligated just distal to the first diagonal branch and acute myocardial infarction was made. Then post-MI RMBF was measured by PET.The dogs were divided into two group ; control group and TMLR group. In the control group, thoracotomy was closed, And in the TMLR group, the transmural channels were created in the LAD territory by a CO2 laser. The channels in diameter about 1mm were made with a density of 1 channel / cm2, an average of 10 channels. Then RMBF was measured by PET, too. And the thoracotomy was closed. RMBF was measured two weeks and two monthes after the operation. Then the dogs were sucrificed and the hearts were excised. The tissue level of matrix metalloproteina … More se (MMP) and platelet-derived endothelial cell growth factor (PDECGF) was measured by the zymography and spectrophotometer. In additioon, the endothelial cells were stained by double immunohistochemical technique with antiPCNA antibody and anti-Factor VIII-related antibody, and then the microvessel density was evaluated. (Results) The rate of the absorbed level of 13NH3 in the infarcted territory to non-infarcted area was caluculated, and the value was evaluated as the percentage of the pre-infarcted one. In the control group, the value of post-infarction, 2 weeks and 2 monthes after operation were 25%, 62% and 49%. In the TMLR group, the value of post-infarction, post-TMLR, 2 weeks and 2monthes were 36%, 29%, 73% and 67%. There was no significant difference between the two groups, and TMLR did not increase regional blood flow in acute ischemic myocardium. Any completely patent channels were not found, and they were infiltrated with granulation tissue. A large amount of microvessels and proliferating endothelial cells were found around the channels. The level of MMP-2, MMP-9 and PDECGF increased in the infarcted territory. They are significantly higher in the TMLR group than in the control group. The microvessel dencity was significantly higher in the TMLR group than in the control group. (Conclusion) TMLR did not increased RMBF in the acute ischemic myocardium. Thecompletely patent channels were not found, and they were infiltrated with granulation tissue. TMLR could stimulate the angiogenesis with the expression of MMP and PDECGF. Less