Spanier T, Smith C R, Burkhoff D
Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
J Clin Laser Med Surg. 1997 Dec;15(6):269-73. doi: 10.1089/clm.1997.15.269.
While clinical reports indicate that significant relief of angina is achieved with transmyocardial laser revascularization (TMLR), the mechanisms of benefit are still a matter of considerable controversy. Studies in our laboratory, as well as in the laboratories of other investigators, have challenged the classic hypothesis that benefits are derived from blood flow through chronically patent channels. While several alternatives have been proposed, our work has focused on investigating the possibility that TMLR stimulates vascular growth in the region around the TMLR channels. We have performed studies looking at histologic markers of vascular growth (including vessel counting and cellular proliferation assays) in order to test this hypothesis, the results of which are reviewed. In brief, we find that TMLR markedly enhances myocardial vascular growth above what is seen normally in ischemic myocardium. We hypothesize that the underlying mechanism relates to liberation of growth factors by inflammatory cells, which are recruited in response to the laser induced myocardial injury. Clarification of whether this mechanism contributes to observed clinical benefits is of fundamental importance, since such understanding may suggest means of enhancing the process.
虽然临床报告表明经皮激光心肌血运重建术（TMLR）能显著缓解心绞痛，但其获益机制仍存在很大争议。我们实验室以及其他研究者实验室的研究，对经典假说提出了质疑，该假说认为获益源于通过长期通畅通道的血流。虽然已经提出了几种替代方案，但我们的工作重点是研究TMLR是否会刺激TMLR通道周围区域的血管生长。我们进行了一些研究，观察血管生长的组织学标志物（包括血管计数和细胞增殖分析）以检验这一假说，现将研究结果进行综述。简而言之，我们发现TMLR能显著增强心肌血管生长，超过缺血心肌的正常水平。我们推测其潜在机制与炎症细胞释放生长因子有关，这些炎症细胞是因激光诱导的心肌损伤而被募集的。明确这一机制是否有助于观察到的临床获益至关重要，因为这样的理解可能会提示增强这一过程的方法。
