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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00162.2001
Submitted on March 8, 2001
Accepted on May 8, 2002
1 Institute for Experimental Medical Research, Ulleval University Hospital, Oslo, Norway; Department of Cardiology, Ulleval Universityhospital, Oslo, Norway
2 Institute for Experimental Medical Research, Ulleval University Hospital, Oslo, Norway
3 Department of Medicine, Northwestern University Medical School, Chicago, Ill, USA
* To whom correspondence should be addressed. E-mail: ivar.sjaastad{at}ioks.uio.no.
Attenuated L-type Ca2+ current (ICa,L), or current-contraction gain, have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Left ventricular myocytes from Isofluran anesthetized rats 6 weeks after coronary artery ligation, inducing CHF, were current- or voltage-clamped from -70mV. In both cases contraction and contractility were attenuated in CHF-cells compared to cells from sham-operated rats (SHAM), when cells were only minimally dialyzed using high resistance microelectrodes. With patch pipettes cell dialysis caused attenuation of contractions in SHAM cells, but not CHF cells. Stepping from -50mV the following variables were not different between SHAM and CHF: peak ICa,L (4.5±0.3pApF-1 vs. 3.8±0.3pApF-1 respectively at 23°C, and 9.4±0.5pApF-1 vs. 8.4±0.5pApF-1 at 37°C); the bell-shaped voltage-contractionrelationship in Cs+ solutions (fractional shortening 15.2±1.0% vs. 14.3±0.7% respectively at 23°C, and 7.5±0.4% vs. 6.7±0.5% at 37°C); the sigmoidal voltage-contraction relationship in K+ solutions. Caffeine induced Ca2+-release and SERCA2 to phospholamban ratio were not different. Thus, in CHF contractions triggered by ICa,L were normal and the contractile deficit was only seen in un-dialyzed cardiomyocytes stimulated from -70mv
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