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Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload
G L Brower1, J R Henegar, J S Janicki
1Department of Physiology and Pharmacology, Auburn University, Alabama 36849-5517, USA.
The American Journal of Physiology
|November 1, 1996
Summary
Chronic volume overload from an arteriovenous (A-V) fistula causes significant left ventricular (LV) dilation and hypertrophy in rats. While systolic function initially declines, remodeling over 8 weeks helps preserve it.
Area of Science:
- Cardiovascular Physiology
- Cardiac Remodeling
Background:
- Chronic volume overload is a common cause of left ventricular (LV) dysfunction.
- The precise temporal adaptations of LV mass, volume, and function following chronic volume overload are not fully understood.
Purpose of the Study:
- To characterize the time course of left ventricular (LV) remodeling and functional changes induced by chronic volume overload via an infrarenal arteriovenous (A-V) fistula in rats.
Main Methods:
- Rats with an A-V fistula were compared to age-matched controls at 1, 2, 3, 5, and 8 weeks post-surgery.
- Left ventricular (LV) end-diastolic pressure, size, and function were assessed using isovolumetric pressure-volume relationships in blood-perfused isolated hearts.
Main Results:
- Progressive LV hypertrophy (192%) and dilation (172%) were observed, peaking at 8 weeks.
- Ventricular stiffness decreased significantly (257% at 8 weeks).
- LV end-diastolic pressure peaked at 3 weeks, followed by a decline and further dilation at 5 weeks, correlating with reduced stiffness. Myocardial contractility was reduced, but remodeling preserved systolic function by 8 weeks.
Conclusions:
- Chronic volume overload induces substantial LV dilation and hypertrophy.
- Ventricular stiffness decreases over time, and despite reduced contractility, compensatory remodeling aids in preserving systolic function by 8 weeks.