CAJ | 학술논문

目的　探讨激光心肌血管重建术（TMLR）对急性缺血心肌血流量和氧代谢的作用与机制。方法　18只犬随机等分为正常对照组、心肌缺血组、激光治疗组。采用连续型N d∶YAG激光行TMLR。测左前降支冠状动脉（LAD）结扎前、结扎后30 min和60 min的心肌血流量（MBF），动脉血氧含量（Ca.O2）和冠状窦血氧含量（Ccs.O2），心肌氧耗量（MVO2）和心肌氧利用率（MEO2）。结果　(1)缺血组和激光组LAD结扎后30 min，MBF分别为39.06 ml±5.33 ml ／(100 g心肌*min)和51.35 ml±3.42 ml／(100 g心肌*min)(P＜0.05)；结扎后60 min，MBF分别为35.77 ml±8.23 ml／(100 g心肌*min) 和52.18 ml±4.82 ml／(100 g心肌*min)(P＜0.05) 。(2)缺血组和激光组LAD结扎后60 min，Ccs.O2分别为7.35 ml/dl±1.47 ml/dl 和5.82 ml/dl±1.84 ml/dl(P＜0.05)；结扎后30 min， MVO2分别为2.95 ml±1.35 ml／(100 g心肌*min)和4.42 ml±1.04 ml／(100 g心肌 *min)(P＜0.05)，结扎后60 min，MVO2分别为2.35 ml±1.10 ml／(100 g心肌*min)和4.38 ml±0.93 ml／(100 g心肌*min)(P＜0.05)；结扎后60 min，MEO2分别为(44.83±9.83)%和(59.3 3±10.07)%(P＜0.05)。结论　TMLR可有效增加缺血心肌血流量和改善心肌细胞氧代谢。
목적　탐토격광심기혈관중건술（TMLR）대급성결혈심기혈류량화양대사적작 용여궤제。 방법　18지견수궤등분위정상대조조、심기결혈조、격광치료조。채용련속형N d∶YAG격광행TMLR。측좌전강지관상동맥（LAD）결찰전、결찰후30 min화60 min적심기혈 류량（MBF），동맥혈양함량（Ca.O2）화관상두혈양함량（Ccs.O2），심기양 모량（MVO2）화심기양이용솔（MEO2）。 결과　(1)결혈조화격광조LAD결찰후30 min，MBF분별위39.06 ml±5.33 ml ／(100 g심기*min)화51.35 ml±3.42 ml／(100 g심기*min)(P＜0.05)；결찰후60 min，MBF분별위35.77 ml±8.23 ml／(100 g심기*min) 화52.18 ml±4.82 ml／(100 g심기*min)(P＜0.05) 。(2)결혈조화격광조LAD결찰후60 min，Ccs.O2분별위7.35 ml/dl±1.47 ml/dl 화5.82 ml/dl±1.84 ml/dl(P＜0.05)；결찰후30 min， MVO2분별위2.95 ml±1.35 ml／(100 g심기*min)화4.42 ml±1.04 ml／(100 g심기 *min)(P＜0.05)，결찰후60 min，MVO2분별위2.35 ml±1.10 ml／(100 g심기*min)화4.38 ml±0.93 ml／(100 g심기*min)(P＜0.05)；결찰후60 min，MEO2분별위(44.83±9.83)%화(59.3 3±10.07)%(P＜0.05)。 결론　TMLR가유효증가결혈심기혈류량화개선심기세포양대사。
Objective　To investigate the effect and mechanism of transmyocardial laser revascularizationMethods　18 adult dogs were randomly and evenly divided into the cont rol, ischemic and TMLR groups. Continuous wave Nd∶YAG laser was used to TML R. The parameters included myocardial blood flow (MBF), concentration of oxygen in the blood of artery and coronary sinus (Ca.O2 ＆ Ccs.O2）, myocar dial oxygen uptake （MVO2）and myocardial oxygen extraction（MEO2）before an d 30 min and 60 min after ligation of ligating the left anterior descending coro nary artery (LAD). Results　(1) In the ischemic and the TMLR groups, MBF 30 min after th e LAD ligation were 39.06 ml±5.33 ml／(100 g myocardium*min) and 51.35 ml± 3.42 ml／(100 g myocardium*min) (P＜0.05), respectively , MBF 60 min after the LAD ligation were 35.77 ml±8.23 ml／(100 g myocardium * min) and 52.18 ml±4.82 ml／(100 g myocardium* min) (P＜0.05), respectively. (2) In the ischemic and the TMLR groups, Ccs.O 2 60 min after the LAD ligation were 7.35 ml/dl±1.47 ml/dl and 5.82 ml±1.84 ml /dl (P＜0.05), MVO2 30 min after the LAD ligation were 2.95 ml ±1.35 ml／(100 g myocardium* min) and 4.42 ml±1.04 ml／(100 g myocardium* min) (P＜0.05), respectively, MVO2 60 min after the LA D ligation were 2.35 ml±1.10 ml／(100 g myocardium*min) and 4.38±0.93 ml ／(100 g myocardium*min) (P＜0.05), respectively, and M EO2 60 min after the LAD ligation were (44.83±9.83)% and (59.33±10.07)% (P＜0.05), respectively. Conclusions　TMLR may effectively improve myocardial blo od flow and myocardial oxygen metabolism in acute myocardial ischemia.