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Does myocardial infarction induced by left coronary artery ligation cause differential changes in sarcoplasmic reticulum calcium transport in the left and right ventricles of rats?
Does myocardial infarction induced by left coronary artery ligation cause differential changes in sarcoplasmic reticulum calcium transport in the left and right ventricles of rats?
In a rat model of post-myocardial infarction heart failure, sarcoplasmic reticulum calcium pump mechanisms undergo differential remodeling, with decreased activity in the left ventricle and transiently increased activity in the right ventricle.
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Differential post-MI SR Ca2+ uptake in rat LV versus RV; hypothesis-generating for ventricular-specific remodeling in human HF.
To examine the status of sarcoplasmic reticulum (SR) with respect to Ca2+ transport in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated for 4, 8, and 16 wk. The left heart function was assessed with an intraventricular pressure transducer, and SR membrane fractions from the right ventricle and the viable left ventricle were isolated for measuring the ATP-dependent Ca2+ uptake activities. In comparison to sham-operated controls, SR Ca2+ uptake activity was decreased in viable left ventricle of the experimental animals at 4, 8, and 16 wk. On the other hand, SR Ca2+ uptake activity in the right ventricle was increased at 4 and 8 wk, but no change was apparent at 16 wk of coronary occlusion. The decrease in SR Ca2+ uptake in left ventricle and increase in right ventricle were associated with corresponding changes in maximal velocity values without any alterations in the affinity for Ca2+. These opposite changes in the right and left ventricles were dependent on the scar size as well as time after inducing the myocardial infarction. The SR Ca(2+)-stimulated adenosinetriphosphatase activity was decreased in left ventricle and increased in the right ventricle from 4 wk experimental animals. The results suggest differential remodeling of the SR membranes with respect to Ca(2+)-pump mechanisms in left and right ventricles during the development of congestive heart failure.
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Afzal et al. (1992) studied this question.
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