我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

经皮激光心肌血运重建术治疗缺血性心脏病的实验研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2002年第1期
页码:
38-41,42
栏目:
论著
出版日期:
2002-01-01

文章信息/Info

Title:
The experimental research of percutaneous transmyocardial laser revas cularization treating ischemic heart disease
作者:
周云飞11 卢才义1 陈 宏2 江一清1 王红月3 马潞娜4 姚克纯5 王 军1
空军总医院: 1. 心内科, 4. 核医学科, 5. 超声诊断科; 2. 空军北京医院心内科; 3. 阜外医院病理科, 北京 100036
Author(s):
ZHOW Yun-fei LU Cai-yi CHEN Hong JIANG Yi-qing WANG Hong-yueMA Lu-na YAO Ke-chunWANG Jun
General Hospital of Air Force,Beijing 100036, China
关键词:
心电描记术 超声心动描记术 动物模型 心肌缺血 经皮激光心肌血运重建术
Keywords:
electrocardiography echocardiography animal model ischemic myocardiumpercutaneous transmyocardial laser revascularization
分类号:
R454. 2; R542. 22
DOI:
-
文献标识码:
A
摘要:
目的 探讨经皮激光心肌血运重建术(PMR) 治疗缺血性心脏病的疗效及其作用机制。方法 犬22只, 用结扎冠状动脉左前降支法建立犬心肌缺血模型后, 随机分为PMR 组和对照组, 对照组不予处理, 分别于术后24h, 1周, 1,3月观察。应用单光子发射计算机体层摄影(SPECT)、超声心动图(UCG) 及心肌病理组化染色观察打孔部位心肌的灌注、功能及激光孔道的变化。结果 PMR 组心肌灌注缺损较术前减轻2~ 3 分, 对照组心肌灌注损伤仍为2~3分, PMR 组静息状态下心肌射血分数从术前(40.2±3.5)% 增加为术后(51.6±3. 0)% ,对照组静息状态下心肌射血分数从术前(42.7±2.6)% 增加为术后(45.3±2.8)%; 心肌打孔孔道急性期保持开放, 但早在术后1 周即已闭塞, 远期孔道及周边有新生小血管形成; 组织化学染色显示打孔区域微血管密度为46±7 条?视野(×100) , 对照组为16±4 条?视野(×100) (P<0.05)。结论 PMR 使缺血心肌的供血和功能得到改善, 通过通畅的激光孔道向缺血心肌供血可能不是PMR 的治疗机制, 而激光孔道及其周围新生微血管的形成已发生导致心肌内固有的微循环及其辅助循环的结构重构, 可能是PMR 术后心肌缺血改善及局部心肌舒缩功能提高的原因。
Abstract:
AIM To investigate into the curative effect and action machanism of percutaneous trans myocardial laser revascularization (PMR) on ischemic myocardium by animal experiment.METHODS 22 dogs were divided into two groups: PMR group and control group after their left anterior descending branches had been ligated. Each group was observed on three time phase points as 24 h, 1st week, 1st, 3rd month. The PMR groups was handled with PMR while the control group had not reatment. The changes of myocardial perfusion, function and laser channels were studied by applying SPECT , UCG and pathologic researsh. RESULTS The myocardial perfusion defection in laser treated areas alleviated 2~ 3′than before and the resting myocardium EF value changed from (40. 2±3. 5)% to (51. 6±3. 0)%. The density of microvessels in laser treated areas was 46±7 roots/field of vision (×100) while the control group′s was 16±4 roots/field of vision (×100) (P < 0. 05). CONCLUSION PMR improve the blood-supply and function of ischemic myocardium. It may not be the just mechansim of PMR that the ischemic myocardium was reperfused through patency channel transporting blood from left ventricle to myocardium wall. On the contrary, the forming and grnerating of microvessels in or surrounding lased channel caused remodeling of inherent microcirculation and its aid circulation may be the true mechanism of PMR to improve perfusion and function of ischemic myocardium.

参考文献/References

[1] Kordenat RK, Kezdi P, Stanley F I. A new catheter technique for producing experimental coronary thrombosis and selective coronary visualization[J]. Am Heart J , 1972, 83: 360- 367.

[2] 陈士良, 臧益民, 朱妙章, 等. 冠状动脉狭窄对血流量的影响[J].生理学报, 1989. 41: 91.

[3] Osterle SN , Schuler G,Lauer B, et al. Percutaneous myocardial laser revascularization: initial human experience [J]. Clin Cardiology , 1997 (Supple I) : 1205.

[4] 安春雷, 屈 正, 曹喜湘. 激光心肌血运重建术对心功能的影响[J]. 心脏杂志, 2001, 13 (2) : 153.

[5] Osterle SN. Beyond stents: third generation coronary devices[J]. Ann Thorac Surg , 1998, 66: 1045- 1049.

[6] Cooley DA , Frazier OH, Kadipasaoglu KA , et al.Transmyocardial laser revascularization: anatomic evidence of long term channel patency[J]. Tex Heart Inst J , 1994, 21: 220.

[7] Mirhoseini M , Shelgikar S, Cayton SN. New concepts inrevscularization of themyocardium [J]. Ann Thorac Surg , 1988,45: 415- 420.

[8] Horvath KA , Cohn LH, Cooly DA , et al. TMLR: results of amulticenter for trial with transmyocardial laser revascularization used as a therapy for end-stage coronary artery disease [J]. J Thorac Cardiovasc Surg , 1997, 113 (9) : 645- 655.[9] Krabstch T, Schaper F, Tulsner J. Histological findings after11 (5) : 326- 331.

[10] Schweitzer W , Schnerder J , Maass D, et al. TMLR histopathology of laser channels in 10 postopratively deceased patients 1 to 18 days after treatment with a CO2 lasr [J].Pathology , 1997, 18 (157) : 374- 384.

[11] Burkhoff D, Fisher PE, Apfelbaum M , et al. Histologic appearance of transmyocardial laser channels after 421/2 weeks[J]. Ann Thorac Surg , 1996, 61 (5) : 1532- 1534.

[ 12 ]Kohmoto T, Fisher PE, Gu A , et al. Does blood flow through holmium: YA Gtrans myocardial laser channels? [J]. Ann Thorac Surg , 1996, 61: 861- 868.[13] Piffare R, Tasuja ML , Lynch RD, et al. Myocardial revascularization by transmyocardial acupuncture [J]. J Thorac Cardiovasc Surg , 1969, 58: 424- 431.

[14] Roethy W , Yamamoto N , Burkhoff D. An examination of potential mechanisms underlying transmyocardial laser revascularization induced increases in myocardial blood flow[J]. Semin Thorac Cardiovasc Surg , 1999, 11 (1) : 24- 28.

[15] Yamamoto N , Kohmoto T, Gu A , et al. Angiogenesis isenhanced in ischemic canine myocardium by transmyocardiallaser revascularization [J]. J Am Coll Cardiol, 1998, 31: 1426- 1433.[16] Kohmoto T, Derosa CM , Yamamoto N , et al. Evidence of vascular growth associated with laser treatment of normal canine myocardium [J]. Ann Thorac Surg , 1998, 65 (5) : 1360- 1367.

[17] Pelletier MP, Giaid A , Sivaraman S, et al. Angiogenesis and growth factor expression in a model of transmyocardial laser revascularization [J]. Ann Thorac Surg , 1998, 66 (1) : 12 -18.

[18] Hughes GC, Lowe JE, Kypson AD, et al. Neovascularization after TMR in a model of chronic ischemia [J]. Ann Thorac Surg , 1998, 66 (16) : 2029- 2036.

[19]Asahara T,Murohara T, Sullivan A , et al. Isolation of putative progenitor endothelial cells for angiogenesis [J]. Science,1997, 275: 964- 967.

备注/Memo

备注/Memo:
收稿日期: 2001-04-03.
更新日期/Last Update: 2002-01-01