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1 Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
2 Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, FL, USA
* To whom correspondence should be addressed. E-mail: phofmann{at}physio1.utmem.edu.
We have proposed that pharmacological preconditioning, leading to PKC-
activation, in hearts improves
postischemic functional recovery through a decrease in actomyosin ATPase activity and subsequent ATP conservation.
The purpose of the present study was to determine if moderate, PKC-independent decreases in actomyosin ATPase are sufficient to improve myocardial postischemic function. Rats were given propylthiouracil (PTU) for 8 days to induce a 25% increase in 
-myosin heavy chain with a 28% reduction in actomyosin ATPase activity. PTU-treated rat hearts subjected to 30 minutes of global ischemia had a significantly higher recovery of postischemic left ventricular developed pressure (LVDP) when compared to Control hearts (57.9 ± 6.2% of preischemic values versus 32.6 ± 5.1%, respectively). Concomitant with this, PTU-treated hearts had a delayed onset of rigor contracture during ischemia and a higher global ATP content following ischemia. In the second part of our study, we demonstrated human troponin T (TnT) transgenic mouse hearts also had a lower maximal actomyosin ATPase and a higher global ATP content following ischemia. Mouse hearts, with and without a point mutation at F110I of human TnT, had a 55.4 ± 5.5% and 62.5 ± 14.5% recovery of postischemic LVDP compared to a 20.0 ± 2.9% recovery in non-transgenic mouse hearts following 35 minutes of global ischemia. These results are consistent with the hypothesis that moderate decreases in actomyosin ATPase activity result in net ATP conservation which is sufficient to improve postischemic contractile function.
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