Chronic Animal Experimant Using Transmycardial Laser Revascularization (TMLR)

激光心肌血运重建术(TMLR)使心肌通过形成微孔来增加血液供应。尽管TMLR改善了心绞痛的临床症状，但其确切的机制以及长期效果尚不清楚。本研究旨在探讨TMLR对组织血流量和神经感受器破坏的慢性影响。在所有动物中，TMLR在左前降支和第一斜角动脉(D1)周围建立了30个微通道。然后，第1组(n=7)结扎D1，第2组(n=7)结扎完整。术后12个月，第2组动物也结扎d1。测量两组的节段性室壁运动(RWM)和全血流量(TBF)。此外，将缓激肽注射到TMLR区周围的心肌中，以评估对交感神经受体的反应，这一点经免疫组织化学证实。结果1组TMLR区RWM严重减少或停滞，并伴有较差的TBF，组织学显示明显的纤维化。第2组的RWM也有所减少，但优于第1组基本恢复的TBF。2组对缓激肽的反应维持，而1组反应较差。两组心外膜周围均可见酪氨酸羟化酶。结论TMLR可增加TBF，但不能改善RWM。由于TMLR不破坏神经感受器，推测TMLR后心绞痛的缓解主要是由于TBF的改善而不是神经感受器的破坏。

Transmyocardial laser revascularization (TMLR) enables myocardium to increase blood supply by creation of micropores. Although the clinical symptom of angina pectoris was improved by TMLR, the precise mechanism as well as long term results are unclear. The purpose of this study is to investigate chronic effects of TMLR on tissue blood flow (TBF) and destruction of neuroreceptors.<Methods> Fourteen swine were used in this study. In all animals, 30 microchannels by TMLR were created around the left anterior descending artery and the first diagonal artery (D1). Then, D1 was ligated in group 1 (n=7), and was intact in group 2 (n=7). Twelve months after operation, D1 of group 2 animals was also ligated. Regional wall motion (RWM) and TBF was measured in both groups. Furthermore, Bradykinin was injected into the myocardium around TMLR area to evaluate response to sympathetic neuroreceptors, which were confirmed by immunohistochemistry. <Results> In group 1, RWM of TMLR area was severely reduced or akinetic in association with poor TBF, and histology revealed marked fibrosis. In group 2, RWM was also reduced, but was better than in group 1 with substantially restored TBF. The response to Bradykinin was maintained in group 2, while it was poor in group 1. Tyrosine hydroxylase was observed around epicardium in both groups. <Conclusion> TMLR increased TBF, but failed to improve RWM. Since neuroreceptors were not destroyed by TMLR, it was speculated that angina pectoris was predominantly relieved after TMLR due to improvement of TBF rather than destruction of neuroreceptors.