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Articles in PresS, published online ahead of print September 12, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00537.2002
Submitted on June 28, 2002
Accepted on September 9, 2002
1 Department of Internal Medicine, University of Wurzburg, Wurzburg, Germany; Department of Biophysics, University of Wurzburg, Wurzburg, Germany
2 Department of Internal Medicine, University of Wurzburg, Wurzburg, Germany
3 Department of Biophysics, University of Wurzburg, Wurzburg, Germany
* To whom correspondence should be addressed. E-mail: M.Nahrendorf{at}Medizin.uni-wuerzburg.de.
Right ventricular (RV) weight increases dependent on time after myocardial infarction (MI) and on MI-size. Sequential changes in RV volume and hemodynamics and their relations to left ventricular (LV) remodeling after MI are unknown. We therefore examined the time course of RV remodeling in rats with LV MI. MI was produced by left coronary artery ligation in rats. Four, 8 and 16 weeks later, LV and RV hemodynamic measurements were performed and pressure-volume curves obtained. For serial measurement of RV volumes and performance, cine-MRI was performed 2 and 8 weeks after MI. The ratio of ß-MHC/
-MHC and skeletal/cardiac
-actin were detemined for the RV and LV after large MI or sham operation. RV weight increased in rats with MI, as did RV volume. RV pressure volume curves were shifted towards larger volumes 16 weeks after large MI. RV systolic pressure increased gradually over time, however, the gain of RV weight was always in excess of RV systolic pressure. The ratios of skeletal/cardiac
-actin and ß-MHC/
-MHC were increased after MI in both ventricles in a similar fashion.
Because RV wall stress was not increased after infarction, mechanical factors may not conclusively explain hypertrophy, which maintained balanced loading conditions for the right ventricle even after large LV infarction.
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