Establishment of a long-surviving murine model of myocardial infarction: Qualitative and quantitative conventional microscopic findings during pathological evolution

被引:15
作者
Kumashiro, H [1 ]
Kusachi, S [1 ]
Moritani, H [1 ]
Ohnishi, H [1 ]
Nakahama, M [1 ]
Uesugi, T [1 ]
Ayada, Y [1 ]
Nunoyama, H [1 ]
Tsuji, T [1 ]
机构
[1] Okayama Univ, Sch Med, Dept Internal Med 1, Okayama 7008558, Japan
关键词
ischemia; pathology; coronary artery disease; rodent;
D O I
10.1007/s003950050129
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Ongoing basic molecular analyses are being performed in mice, and a simple long-surviving murine model of myocardial infarction (MI) would be very useful in this regard. Although a few studies have induced hll in mice by coronary artery ligation, the induction involves a complex technique and has a relatively high mortality rate. In addition, the identification of the basic pathological sequence is essential to the interpretation of experimental results. We developed a simple technique for the induction of MI in mice and examined qualitative and quantitative conventional microscopic findings during the pathological evolution over a 28-day observation period, Male BALB/c mice weighing approximately 25 - 30 g were anesthetized and then ventilated with a positive pressure ventilator. The heart was exposed by thoracotomy. Left coronary artery occlusion was performed by thermocoagulation using a thermocoagulation knife at the level of the tip of the left atrium, After establishing this surgical method, we used it to induce hll in 71 mice. The operative and postoperative mortality rates of this model were 5.6 % (4/71) and 12.6% (9/71), respectively. In 3 (5.2 %) of the 58 surviving mice, the area of infarct was not sufficient. The infarct area in the remaining 55 mise was 40 +/- 9 % of the entire perimeter of the left ventricle. Conventional microscopic examinations with hematoxylin-eosin and Masson-trichrome staining disclosed that all of the characteristic histopathological features of MI occurred 1 - 2 days earlier than those in rats. Our surgical technique provides a sufficient infarct area. with an acceptable mortality rate. The present study clarified the histopathological sequence in this long surviving murine MI model.
引用
收藏
页码:78 / 84
页数:7
相关论文
共 16 条
  • [1] Myocyte apoptosis during acute myocardial infarction in the mouse localizes to hypoxic regions but occurs independently of p53
    Bialik, S
    Geenen, DL
    Sasson, IE
    Cheng, R
    Horner, JW
    Evans, SM
    Lord, EM
    Koch, CJ
    Kitsis, RN
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (06) : 1363 - 1372
  • [2] BRING RJ, 1956, AM JMED SCI, V232, P533
  • [3] A COMPARATIVE-STUDY WITH VARIOUS ANESTHETICS IN MICE (PENTOBARBITAL, KETAMINE-XYLAZINE, CARFENTANYL-ETOMIDATE)
    ERHARDT, W
    HEBESTEDT, A
    ASCHENBRENNER, G
    PICHOTKA, B
    BLUMEL, G
    [J]. RESEARCH IN EXPERIMENTAL MEDICINE, 1984, 184 (03) : 159 - 169
  • [4] FISHBEIN MC, 1978, AM J PATHOL, V90, P57
  • [5] TARGETING GENE-EXPRESSION TO SPECIFIC CARDIOVASCULAR CELL-TYPES IN TRANSGENIC MICE
    HUNTER, JJ
    ZHU, H
    LEE, KJ
    KUBALAK, S
    CHIEN, KR
    [J]. HYPERTENSION, 1993, 22 (04) : 608 - 617
  • [6] Overexpression of heat shock protein 72 in transgenic mice decreases infarct size in vivo
    Hutter, JJ
    Mestril, R
    Tam, EKW
    Sievers, RE
    Dillmann, WH
    Wolfe, CL
    [J]. CIRCULATION, 1996, 94 (06) : 1408 - 1411
  • [7] Transgenic animals as models in the study of the neurobiological role of polyamines
    Kauppinen, RA
    Alhonen, LI
    [J]. PROGRESS IN NEUROBIOLOGY, 1995, 47 (06) : 545 - &
  • [8] The role of transgenic knockout models in defining the pathogenesis of viral heart disease
    Liu, P
    Penninger, J
    Aitken, K
    Sole, M
    Mak, T
    [J]. EUROPEAN HEART JOURNAL, 1995, 16 : 25 - 27
  • [9] Myocardial ischemia and reperfusion: A murine model
    Michael, LH
    Entman, ML
    Hartley, CJ
    Youker, KA
    Zhu, J
    Hall, SR
    Hawkins, HK
    Berens, K
    Ballantyne, CM
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 269 (06): : H2147 - H2154
  • [10] Mulder P, 1997, CIRCULATION, V95, P1314