Horvath K A, Chiu E, Maun D C, Lomasney J W, Greene R, Pearce W H, Fullerton D A
Feinberg Cardiovascular Research Institute, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Ann Thorac Surg. 1999 Sep;68(3):825-9. doi: 10.1016/s0003-4975(99)00842-5.
Angiogenesis has been proposed as a potential mechanism whereby transmyocardial laser revascularization (TMLR) has provided clinical relief of angina. Experimental work has found histologic evidence supporting this, as well as an improved response when angiogenic growth factors have been added to TMLR. The purpose of this study was to demonstrate that the molecular response to TMLR was an increase in the production of endogenous vascular endothelial growth factor to promote angiogenesis.
Ameroid constrictors were placed on the proximal circumflex artery in 12 domestic pigs. After a chronic ischemic zone was established the animals were randomly divided into two groups. In the TMLR group the ischemic zone was treated with carbon dioxide laser. In the control group the ischemic zone was untreated. Six weeks later the animals were sacrificed, and sections from the ischemic zone and the nonischemic zone were submitted for immunohistochemical, histologic, and molecular analysis. Messenger RNA was obtained from northern blot analysis after being probed with vascular endothelial growth factor.
There was a twofold increase in the vascular endothelial growth factor messenger RNA in the ischemic zone of the TMLR group compared with the control group. Additionally, there was a threefold increase in the number of new blood vessels in the ischemic zone of the TMLR group compared with the control group.
Transmyocardial laser revascularization promotes angiogenesis by upregulation of vascular endothelial growth factor. The resulting angiogenesis could be the principle mechanism for the clinical efficacy of TMLR.
血管生成被认为是心肌激光血运重建术（TMLR）能够缓解心绞痛症状的潜在机制。实验研究已发现支持这一机制的组织学证据，并且在TMLR中添加血管生成生长因子时反应有所改善。本研究的目的是证明TMLR的分子反应是内源性血管内皮生长因子产生增加以促进血管生成。
在12头家猪的冠状动脉左旋支近端放置Ameroid缩窄环。在建立慢性缺血区后，将动物随机分为两组。TMLR组用二氧化碳激光治疗缺血区。对照组的缺血区不进行治疗。六周后处死动物，将缺血区和非缺血区的切片进行免疫组织化学、组织学和分子分析。用血管内皮生长因子探针杂交后，通过Northern印迹分析获得信使核糖核酸。
与对照组相比，TMLR组缺血区血管内皮生长因子信使核糖核酸增加了两倍。此外，与对照组相比，TMLR组缺血区新血管数量增加了三倍。
心肌激光血运重建术通过上调血管内皮生长因子促进血管生成。由此产生的血管生成可能是TMLR临床疗效的主要机制。
