Yamamoto N, Kohmoto T, Gu A, DeRosa C, Smith C R, Burkhoff D
Department of Surgery, Columbia University, New York, New York 10032, USA.
J Am Coll Cardiol. 1998 May;31(6):1426-33. doi: 10.1016/s0735-1097(98)00086-2.
This study sought to test whether transmyocardial laser revascularization (TMLR) stimulates angiogenesis in an animal model of chronic ischemia.
TMLR relieves angina and may also improve blood flow in patients who are not candidates for traditional therapies. The mechanisms of these benefits are not fully defined.
Ischemia was created in 14 dogs by proximal left anterior descending coronary ameroid constrictors. TMLR was performed in the anterior wall (approximately 1 channel/cm2) of seven dogs; the remaining dogs served as the ischemic control group. Myocardial blood flow was measured (colored microspheres) at rest and during chemical stress (adenosine) in the acute setting and after 2 months.
TMLR did not influence blood flow in the acute setting. After 2 months, resting blood flow increased comparably in the anterior wall in both groups to approximately 80% of normal. However, the TMLR-treated dogs demonstrated an approximately 40% increase in blood flow capacity during stress in the ischemic territory compared with untreated dogs (left anterior descending coronary artery/left circumflex coronary artery flow 0.53+/-0.16 in the control group vs. 0.73+/-0.08 in TMLR animals, p < 0.05). Vascular proliferation, assessed by bromodeoxyuridine incorporation and proliferating cell nuclear antigen positivity in endothelial and smooth muscle cells was about four times greater in the TMLR group than in the control group (p < 0.001). The density of vessels with at least one smooth muscle cell layer was approximately 1.4 times greater in the myocardium surrounding the TMLR channel remnants than in control ischemic tissue (p < 0.001).
In this canine model of chronic ischemia, TMLR significantly enhances angiogenesis as evidenced by the increased number of vessels lined with smooth muscle cells, markedly increased vascular proliferation and increased blood flow capacity during stress.
本研究旨在测试经心肌激光血运重建术（TMLR）是否能在慢性缺血动物模型中刺激血管生成。
TMLR可缓解心绞痛，对于那些不适合传统治疗的患者，它还可能改善血流。这些益处的机制尚未完全明确。
通过在14只犬的左冠状动脉前降支近端植入阿梅氏环缩器来制造缺血。对7只犬的前壁进行TMLR（约1个通道/平方厘米）；其余犬作为缺血对照组。在急性情况下以及2个月后，分别于静息状态和化学应激（腺苷）期间测量心肌血流量（彩色微球法）。
在急性情况下，TMLR对血流无影响。2个月后，两组前壁的静息血流均可比地增加至正常的约80%。然而，与未治疗的犬相比，接受TMLR治疗的犬在应激期间缺血区域的血流能力增加了约40%（对照组左冠状动脉前降支/左旋支冠状动脉血流为0.53±0.16，TMLR组为0.73±0.08，p<0.05）。通过溴脱氧尿苷掺入以及内皮和平滑肌细胞中增殖细胞核抗原阳性评估的血管增殖，TMLR组比对照组大约高4倍（p<0.001）。在TMLR通道残余物周围的心肌中，至少有一层平滑肌细胞的血管密度比对照缺血组织大约高1.4倍（p<0.001）。
在这个慢性缺血的犬模型中，TMLR显著增强了血管生成，这表现为平滑肌细胞内衬血管数量增加、血管增殖明显增加以及应激期间血流能力增加。
