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Large artery remodeling after myocardial infarction
M A Gaballa1, T E Raya, S Goldman
1Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723, USA.
The American Journal of Physiology
|May 1, 1995
Summary
Myocardial infarction (MI) in rats causes arterial remodeling. Captopril, but not hydralazine, reversed these changes in arterial properties, permeability, and structure.
Area of Science:
- Cardiovascular physiology
- Pharmacology
- Biomedical engineering
Background:
- Myocardial infarction (MI) leads to significant arterial remodeling.
- Understanding the impact of MI on arterial hemodynamics and mechanical properties is crucial.
Purpose of the Study:
- To investigate arterial remodeling after myocardial infarction in rats.
- To evaluate the effects of captopril and hydralazine on arterial changes post-MI.
Main Methods:
- Rats underwent coronary artery ligation (MI) or sham operation.
- Animals were treated with captopril, hydralazine, or untreated water for 3 weeks.
- Arterial hemodynamics, mechanical properties, and water permeability were measured.
Main Results:
- MI rats showed increased characteristic impedance, altered material constants, and increased water permeability.
- Captopril normalized material constants and reversed water permeability, unlike hydralazine.
- MI increased arterial collagen area and decreased media thickness; captopril reduced collagen area.
Conclusions:
- Arterial remodeling, characterized by altered passive mechanical properties, water permeability, and structure, occurs after MI in rats.
- Captopril effectively reverses arterial remodeling post-MI, while hydralazine does not show the same effect.