1996
DOI: 10.1161/01.cir.94.8.1894
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Creatine Kinase System in Failing and Nonfailing Human Myocardium

Abstract: In failing and nonfailing donor human myocardium, there is a combined decrease of CK activity and creatine that may impair the ability to deliver ATP to energy-consuming systems.

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Cited by 273 publications
(203 citation statements)
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“…ATPase activity also has been shown to be decreased in the failing human heart, but at least part of the decrease is explained by the decrease in mitochondrial content (Unverferth et al 1988). The energy buffering and transfer capacity into the cells is compromised in end-stage HF, partly due to a decrease in CK activity (Khuchua et al 1992;Saks et al 1991) and a diminution of creatine concentration (Kalsi et al 1999;Nascimben et al 1996). These observations agree with P NMR studies suggesting that a low PCr/ATP ratio is a consequence of the creatine pool depletion.…”
Section: Anatomical Sites In the Heartmentioning
confidence: 53%
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“…ATPase activity also has been shown to be decreased in the failing human heart, but at least part of the decrease is explained by the decrease in mitochondrial content (Unverferth et al 1988). The energy buffering and transfer capacity into the cells is compromised in end-stage HF, partly due to a decrease in CK activity (Khuchua et al 1992;Saks et al 1991) and a diminution of creatine concentration (Kalsi et al 1999;Nascimben et al 1996). These observations agree with P NMR studies suggesting that a low PCr/ATP ratio is a consequence of the creatine pool depletion.…”
Section: Anatomical Sites In the Heartmentioning
confidence: 53%
“…End-stage HF was associated with multiple mitochondrial functional injuries, e.g., a decrease of ETC activities per muscle mass, most notably CI (Scheubel et al 2002), CIII (Buchwald et al 1990;Jarreta et al 2000;Marin-Garcia et al 1995), and CIV (Arbustini et al 1998;Quigley et al 2000), and a decrease in OXPHOS capacity in the presence of substrates directing electrons into CI in permeabilized fibers (Saks et al 1991;Sharov et al 2000). Part of the loss of mitochondrial ETC activity or OXPHOS per g of muscle is explainable by a decrease in mitochondrial content occurring also in endstage HF (Kalsi et al 1999;Nascimben et al 1996;Quigley et al 2000). The similarity in CS activity between end-stage HF and control groups (Maurer and Zierz 1994) may be explained by the age differences between groups, because the CS activity increases with age (Marin-Garcia et al 1998).…”
Section: Anatomical Sites In the Heartmentioning
confidence: 99%
“…Failing myocardium in many animal models and in human myocardium has been demonstrated to have changes in action potential durations, contraction/relaxation parameters, time courses of the calcium transient, and in the force-interval relationships Liao et al 1996;Nascimben et al 1996). However, changes in these characteristics of heart failure appear to be model dependent .…”
Section: Discussionmentioning
confidence: 99%
“…However, facilitated diffusion provided by CK and AK phosphotransfer systems that could bridge diffusional barriers essentially dissipates nucleotide gradients imposed by membrane AT-Pases and diffusional restrictions. Under cardiomyocyte stress, phosphotransfer flux through CK is significantly damped [92][93][94] such that with only a moderate drop in bulk cytosolic ATP, CK could no longer effectively dissipate nucleotide gradients precipitating a significant fall in submembrane CrP, and generation of an amplified nucleotide response at the K ATP channel site (Fig. 2) [16].…”
Section: The K Atp Channel Complex As a Component Of The Cellular Enementioning
confidence: 99%
“…In heart failure, cardiomyocytes undergo extensive remodeling including diminished mitochondrial respiration, suppressed creatine kinase flux, decreased energy storage, and cytoskeletal disruption, although bulk cytosolic ATP levels are preserved [20,92,93]. These changes impact metabolic signal generation, signal trafficking through phosphotransfer and diffusional effects by altered cellular architecture, among other factors, that affect the ability of cellular distress to be properly communicated to K ATP channels.…”
Section: K Atp Channel Regulation In Cardiac Diseasementioning
confidence: 99%