© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Mouse model of myocardial remodelling after ischemia: role of intercellular adhesion molecule-1
aDivision of Cardiology, Department of Internal Medicine, University of Innsbruck, Innsbruck, Austria
bInstitute for Medical Chemistry and Biochemistry, University of Innsbruck, Innsbruck, Austria
cInstitute for Biomedical Ageing Research, Austrian Academy of Sciences, Rennweg 10, A-6020 Innsbruck, Austria
* Corresponding author. Tel.: +43-512-583-9190; fax: +43-512-583-9198 qingbo.xu{at}oeaw.ac.at
Objective: We studied the effects of temporary myocardial ischemia and reperfusion on myocyte injury and ventricular remodelling in wildtype and intercellular adhesion molecule-1- (ICAM-1) deficient mice. Methods: ICAM-1–/– and ICAM-1+/+ mice were subjected to 30 min of myocardial ischemia and subsequent reperfusion for 2 h, 1 week and 3 weeks, respectively. The evaluation of tissue damage and scar size was performed with histological sections stained with hematoxilin and eosin. Serum levels of troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were evaluated as an index of cardiac cellular damage. Immunohistological analysis was employed to determine cell compositions in ischemic regions. Results: After myocardial ischemia (30 min) and 2 h reperfusion, elevation in serum troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were found in both groups, but significantly reduced in ICAM-1–/– mice compared with wildtype mice (P<0.05). Absence of a functional ICAM-1 gene in ICAM-1–/– mice resulted in a marked reduction of ischemia–reperfusion injury at the early stage. The damage score and size of the infarct area were lower in ICAM-1 –/– mice by 30 min of ischemia and 2 h of reperfusion (1.4±0.54 vs. 2.4±0.47, P<0.05). The percentage of MAC-1-positive cells in the ischemic region and the border zone was also significantly diminished in groups of ICAM-1–/– mice. Surprisingly, the scar size in ventricles in animals 1 or 3 weeks after ischemia was similar between ICAM-1–/– and ICAM-1+/+ mice, although the number of infiltrated MAC-1 positive cells in the scar in wildtype mice was higher. Conclusion: Our results demonstrate that the absence of ICAM-1 expression results in less myocardial damage induced by ischemia–reperfusion at the early stage, but does not influence the size of myocardial infarction and scar formation.
KEYWORDS Infarction; Ischemia; Reperfusion; Remodelling
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