Distinct mouse coronary anatomy and myocardial infarction consequent to ligation

被引:73
作者
Kumar, D
Hacker, TA
Buck, J
Whitesell, LF
Kaji, EH
Douglas, PS
Kamp, TJ
机构
[1] Univ Vermont, Dept Med, Burlington, VT USA
[2] Univ Wisconsin, Dept Med, Sect Cardiovasc Med, Madison, WI USA
关键词
anterior wall; left ventricle; myocardial infarction; coronary artery anatomy;
D O I
10.1097/00019501-200502000-00008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This study describes the coronary anatomy of C57BL/6 mice and the functional impact of that anatomy on myocardial infarctions induced by ligation of the left coronary artery. In contrast to humans, a distinct septal coronary artery was observed in all mice arising either from a separate ostium from the right sinus of Valsalva or as a branch of the right coronary artery. Ligation of the left coronary artery at the site of its emergence from under the left atrium resulted in reproducible large myocardial infarctions involving the anterolateral, posterior, and apical regions of the heart as evidenced by histology and echocardiography. Interestingly, the septum was spared from infarction as predicted by the presence of the distinct septal branch found in mice. Thus, the distinct mouse coronary artery anatomy results in different regionality of infarction compared with man and large laboratory animals, and this may affect on the associated pathological remodeling of the heart. Background The objective of this study was to describe the coronary anatomy of C57BL/6 mice and determine the functional impact of that anatomy on myocardial infarctions induced by ligation of the left coronary artery. Methods C57BL/6 mice were used to visualize mouse coronary anatomy and to generate myocardial infarction. Mouse coronary artery visualization was performed on isolated hearts using injection of Silastic sealant into the aortic arch. After left thoracotomy myocardial infarction was produced by ligating the left coronary artery at the site of the vessels' emergence past the tip of the left atrium. Echocardiography was performed to analyze heart function, and histology was performed to delineate myocardial infarction. Results The different septal coronary artery was observed in all mice arising either from a separate ostium from the right sinus of Valsalva or as a branch of the right coronary artery. The mouse left coronary artery passed obliquely across the left ventricular free wall similar to the ramus intermedius coronary artery variant in man. Ligation of the left coronary artery as it emerged from under the left atrium resulted in reproducible large infarctions involving the anterolateral, posterior, and apical regions of the heart as demonstrated by histology and echocardiography. Notably, the septum was spared from infarction as predicted by the presence of the distinct septal coronary artery found in mice. Conclusions Mouse coronary anatomy is distinct compared to man or large laboratory animals, and myocardial infarctions resulting from ligation of the mouse left coronary artery spare the septum, which may affect the pathological remodeling of the heart. (C) 2005 Lippincott Williams Wilkins.
引用
收藏
页码:41 / 44
页数:4
相关论文
共 14 条
[1]   Myocyte apoptosis during acute myocardial infarction in the mouse localizes to hypoxic regions but occurs independently of p53 [J].
Bialik, S ;
Geenen, DL ;
Sasson, IE ;
Cheng, R ;
Horner, JW ;
Evans, SM ;
Lord, EM ;
Koch, CJ ;
Kitsis, RN .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (06) :1363-1372
[2]   ECHOCARDIOGRAPHIC ASSESSMENT OF LEFT-VENTRICULAR HYPERTROPHY - COMPARISON TO NECROPSY FINDINGS [J].
DEVEREUX, RB ;
ALONSO, DR ;
LUTAS, EM ;
GOTTLIEB, GJ ;
CAMPO, E ;
SACHS, I ;
REICHEK, N .
AMERICAN JOURNAL OF CARDIOLOGY, 1986, 57 (06) :450-458
[3]   STUDIES ON EXPERIMENTAL MYOCARDIAL-INFARCTION - DOGS OR BABOONS [J].
FLAMENG, W ;
VANHAECKE, J ;
VANDEPLASSCHE, G .
CARDIOVASCULAR RESEARCH, 1986, 20 (04) :241-247
[4]   Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction [J].
Harada, K ;
Sugaya, T ;
Murakami, K ;
Yazaki, Y ;
Komuro, I .
CIRCULATION, 1999, 100 (20) :2093-2099
[5]   Animal models of human cardiovascular disease, heart failure and hypertrophy [J].
Hasenfuss, G .
CARDIOVASCULAR RESEARCH, 1998, 39 (01) :60-76
[6]   Overexpression of heat shock protein 72 in transgenic mice decreases infarct size in vivo [J].
Hutter, JJ ;
Mestril, R ;
Tam, EKW ;
Sievers, RE ;
Dillmann, WH ;
Wolfe, CL .
CIRCULATION, 1996, 94 (06) :1408-1411
[7]   Regeneration of ischemic cardiac muscle and vascular endothelium by adult stem cells [J].
Jackson, KA ;
Majka, SM ;
Wang, HG ;
Pocius, J ;
Hartley, CJ ;
Majesky, MW ;
Entman, ML ;
Michael, LH ;
Hirschi, KK ;
Goodell, MA .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (11) :1395-1402
[8]   Establishment of a long-surviving murine model of myocardial infarction: Qualitative and quantitative conventional microscopic findings during pathological evolution [J].
Kumashiro, H ;
Kusachi, S ;
Moritani, H ;
Ohnishi, H ;
Nakahama, M ;
Uesugi, T ;
Ayada, Y ;
Nunoyama, H ;
Tsuji, T .
BASIC RESEARCH IN CARDIOLOGY, 1999, 94 (02) :78-84
[9]   IN-VIVO ASSESSMENT OF LV MASS IN MICE USING HIGH-FREQUENCY CARDIAC ULTRASOUND - NECROPSY VALIDATION [J].
MANNING, WJ ;
WEI, JY ;
KATZ, SE ;
LITWIN, SE ;
DOUGLAS, PS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (04) :H1672-H1675
[10]   Bone marrow cells regenerate infarcted myocardium [J].
Orlic, D ;
Kajstura, J ;
Chimenti, S ;
Jakoniuk, I ;
Anderson, SM ;
Li, BS ;
Pickel, J ;
McKay, R ;
Nadal-Ginard, B ;
Bodine, DM ;
Leri, A ;
Anversa, P .
NATURE, 2001, 410 (6829) :701-705