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1 Dept. of Physiology & Biophysics, Univ. of Illinois at Chicago, Chicago, Illinois, United States; Department of Cardiology, Jeroen Bosch Hospital, Netherlands
2 Dept. of Physiology & Biophysics, Univ. of Illinois at Chicago, Chicago, Illinois, United States
3 Dept. of Physiology & Biophysics, Univ. of Illinois at Chicago, Chicago, Illinois, United States
* To whom correspondence should be addressed. E-mail: pdetombe{at}uic.edu.
The cellular mechanisms underlying the development of congestive heart failure (HF) are not well understood. Accordingly, we studied myocardial function in isolated right ventricular trabeculae from rats in which HF was induced by left ventricular myocardial infarction (MI). Both early stage (12 weeks post MI; E-pMI) and late, end-stage HF (28 weeks post-Mi; L-pMI) were studied. HF was associated with decreased sarcoplasmic reticulum Ca2+ ATPase protein levels (28% E-pMI; 52% L-pMI). HF affected neither sodium/calcium exchange, ryanodine receptor, nor phospholamban protein levels. Twitch force at saturating extracellular [Ca2+] was depressed in HF (30% E-pMI; 38% L-pMI), concomitant with a marked increase in sensitivity of twitch force toward extracellular [Ca2+] (26% E-pMI; 68% L-pMI). Ca2+ saturated myofilament force development in skinned trabeculae was unchanged in E-pMI, but significantly depressed in L-pMI (45%). Tension dependent ATP hydrolysis rate was depressed in L-pMI (49%), but not in E-pMI. Our results suggest a hierarchy of cellular events during the development of HF, starting with altered calcium homeostasis during the early phase followed by myofilament dysfunction at end-stage HF.
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