慢性缺血模型中经心肌激光血运重建术后的新生血管形成

Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia.

作者信息

Hughes G C, Lowe J E, Kypson A P, St Louis J D, Pippen A M, Peters K G, Coleman R E, DeGrado T R, Donovan C L, Annex B H, Landolfo K P

机构信息

Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.

出版信息

Ann Thorac Surg. 1998 Dec;66(6):2029-36. doi: 10.1016/s0003-4975(98)01095-9.

DOI:10.1016/s0003-4975(98)01095-9

PMID:9930489

Abstract

BACKGROUND

The mechanism of clinical improvement after transmyocardial laser revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study sought to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia.

METHODS

Six miniature pigs underwent subtotal left circumflex coronary artery occlusion to reduce resting blood flow to 10% of baseline. After 2 weeks in the low-flow state, dobutamine stress echocardiography and positron emission tomography were performed to document ischemic, viable myocardium. The animals then underwent TMR and were sacrificed 6 months later for histologic and immunohistochemical analysis.

RESULTS

Histologic analysis of the lased left circumflex region demonstrated many hypocellular areas filled with connective tissue representing remnant TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predominantly at the periphery of the channels. Immunohistochemical analysis confirmed the presence of endothelial cells within neovessels. Vascular density analysis revealed a mean of 29.2+/-3.6 neovessels per high-power field in lased ischemic myocardium versus 4.0+/-0.3 (p<0.001) in nonlased ischemic myocardium.

CONCLUSIONS

This study provides evidence that neovascularization is present long term in regions of ischemic, viable myocardium after TMR. Angiogenesis may represent the mechanism of clinical improvement after TMR.

摘要

背景

心肌激光血运重建术（TMR）后临床症状改善的机制尚不清楚。一种假说认为，TMR通过新生血管形成增加心肌灌注。本研究旨在确定在慢性心肌缺血猪模型中TMR后是否发生血管生成。

方法

6只小型猪接受左回旋支冠状动脉次全闭塞，使静息血流降至基线的10%。在低血流状态下2周后，进行多巴酚丁胺负荷超声心动图和正电子发射断层扫描，以记录缺血、存活心肌。然后动物接受TMR，6个月后处死进行组织学和免疫组织化学分析。

结果

对激光照射的左回旋支区域进行组织学分析，发现许多细胞减少区域充满结缔组织，代表残留的TMR通道。组织化学染色显示新生血管高度紊乱，与主要位于通道周边的血管生成一致。免疫组织化学分析证实新生血管内存在内皮细胞。血管密度分析显示，激光照射的缺血心肌每高倍视野平均有29.2±3.6条新生血管，而非激光照射的缺血心肌为4.0±0.3条（p<0.001）。