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Ventricular function and contractile proteins in the infarcted overloaded rat heart
D L Geenen1, A Malhotra, D Liang
1Department of Medicine, Montefiore Medical Center, Bronx, New York.
Cardiovascular Research
|April 1, 1991
Summary
Surviving heart muscle after infarction cannot increase size when exposed to sustained high afterload. However, overall cardiac function in situ remains stable despite this challenge.
Area of Science:
- Cardiovascular Physiology
- Cardiac Remodeling
- Myocardial Infarction
Background:
- Myocardial infarction (MI) leads to significant cardiac remodeling.
- The adaptive capacity of surviving myocardium to increased afterload post-MI is not fully understood.
Purpose of the Study:
- To investigate if surviving myocardium in infarcted rat hearts can adapt to sustained increases in afterload.
- To assess cardiac mass, ventricular function, and actomyosin ATPase activity under induced stress.
Main Methods:
- Female Wistar rats underwent coronary artery ligation to induce myocardial infarction.
- A subset experienced superimposed renal artery constriction 4 weeks post-infarction.
- Cardiac mass, ventricular function, and actomyosin ATPase activity were compared to sham-operated controls.
Main Results:
- Infarcted hearts showed increased weight but reduced systolic pressure and +/- dP/dt compared to controls.
- No further functional decline was observed with superimposed renal artery constriction.
- Actomyosin ATPase activity was depressed, with a greater shift to V3 myosin isoenzyme in the combined infarct and constriction group.
Conclusions:
- Surviving myocardium post-infarction fails to increase cardiac mass under chronic increased afterload.
- Actomyosin ATPase activity is depressed under these conditions.
- In situ cardiac function is maintained despite the inability to hypertrophy and depressed enzymatic activity.