Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction.

Abstract:

:Left ventricular (LV) dilatation following myocardial infarction (MI) is a major determinant of the patient's prognosis, and myocardial energy metabolism may play a key role in LV remodeling. We aimed to investigate the relative timing of LV dilatation to LV function, myocardial energy regulation by uncoupling protein (UCP)-2, and cellular damage in the noninfarct zone. Myocardial infarction was produced in Sprague-Dawley rats by ligation of the coronary artery. The LV end-diastolic dimension (mm) increased (8.9+/-0.3 vs 6.8+/-0.8 in sham-operated rats, P<0.01) in association with elevation of the LV end-diastolic pressure (mmHg) (18+/-5 vs 6+/-2 in sham-operated rats) at 1 week following the ligation. At 4 weeks, the UCP-2 expression (180% of that in sham-operated rats) and LV end-diastolic dimension increased further (11.1+/-0.5, P<0.01) but there was no change in the LV end-diastolic pressure. The mechanisms for LV dilatation were quite different between the early and late stages after MI. In the late stage, augmentation of UCP-2 expression in the noninfarct zone may be related to the LV dilatation. Further examinations regarding the possibility of the protective role of UCP-2 are needed.

journal_name

Heart Vessels

journal_title

Heart and vessels

authors

Guo P,Mizushige K,Noma T,Murakami K,Namba T,Ishizawa M,Tsuji T,Kimura S,Kohno M

doi

10.1007/s00380-004-0805-5

subject

Has Abstract

pub_date

2005-03-01 00:00:00

pages

61-5

issue

2

eissn

0910-8327

issn

1615-2573

journal_volume

20

pub_type

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