Normal contractions triggered by I(Ca,L) in ventricular myocytes from rats with postinfarction CHF.
I. Sjaastad, J. B�kenes, F. Swift, J. Wasserstrom, and O. Sejersted.
Am. J. Physiol. Heart Circ. Physiol. 283 (3): H1225-36 (September 2002)

Attenuated L-type Ca$^2+$ current (I(Ca,L)), or current-contraction gain have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Six weeks after coronary artery ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized rats were current or voltage clamped from -70 mV. In both cases, contraction and contractility were attenuated in CHF cells compared with cells from sham-operated rats 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 -50 mV, the following variables were not different between sham and CHF, respectively: peak I(Ca,L) (4.5 +/- 0.3 vs. 3.8 +/- 0.3 pApF(-1) at 23 degrees C and 9.4 +/- 0.5 vs. 8.4 +/- 0.5 pApF(-1) at 37 degrees C), the bell-shaped voltage-contraction relationship in Cs$^+$ solutions (fractional shortening, 15.2 +/- 1.0\% vs. 14.3 +/- 0.7\%, respectively, at 23 degrees C and 7.5 +/- 0.4\% vs. 6.7 +/- 0.5\% at 37 degrees C) and the sigmoidal voltage-contraction relationship in K$^+$ solutions. Caffeine-induced Ca$^2+$ release and sarcoplasmic reticulum Ca$^2+$-ATPase-to-phospholamban ratio were not different. Thus CHF contractions triggered by I(Ca,L) were normal, and the contractile deficit was only seen in undialyzed cardiomyocytes stimulated from -70 mV.

URL: http://dx.doi.org/10.1152/ajpheart.00162.2001
DOI: 10.1152/ajpheart.00162.2001
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@article{Sjaa_2002_H1225,
  abstract = {Attenuated L-type {C}a$^{2+}$ current (I(Ca,L)), or current-contraction
	gain have been proposed to explain impaired cardiac contractility
	in congestive heart failure (CHF). Six weeks after coronary artery
	ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized
	rats were current or voltage clamped from -70 mV. In both cases,
	contraction and contractility were attenuated in CHF cells compared
	with cells from sham-operated rats 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 -50 mV, the following variables were
	not different between sham and CHF, respectively: peak I(Ca,L) (4.5
	+/- 0.3 vs. 3.8 +/- 0.3 pApF(-1) at 23 degrees C and 9.4 +/- 0.5
	vs. 8.4 +/- 0.5 pApF(-1) at 37 degrees C), the bell-shaped voltage-contraction
	relationship in {C}s$^+$ solutions (fractional shortening, 15.2 +/-
	1.0\% vs. 14.3 +/- 0.7\%, respectively, at 23 degrees C and 7.5 +/-
	0.4\% vs. 6.7 +/- 0.5\% at 37 degrees C) and the sigmoidal voltage-contraction
	relationship in {K}$^{+}$ solutions. Caffeine-induced {C}a$^{2+}$
	release and sarcoplasmic reticulum {C}a$^{2+}$-ATPase-to-phospholamban
	ratio were not different. Thus CHF contractions triggered by I(Ca,L)
	were normal, and the contractile deficit was only seen in undialyzed
	cardiomyocytes stimulated from -70 mV.},
  added-at = {2009-06-03T11:20:58.000+0200},
  author = {Sjaastad, Ivar and B�kenes, Janny and Swift, Fredrik and Wasserstrom, J. Andrew and Sejersted, Ole M},
  biburl = {https://www.bibsonomy.org/bibtex/244ca8970d69a9ab5639c9b286c7df273/hake},
  description = {The whole bibliography file I use.},
  doi = {10.1152/ajpheart.00162.2001},
  file = {Sjaa_2002_H1225.pdf:Sjaa_2002_H1225.pdf:PDF},
  interhash = {5024208e04a530642170e2aef4e0b4c1},
  intrahash = {44ca8970d69a9ab5639c9b286c7df273},
  journal = {Am. J. Physiol. Heart Circ. Physiol.},
  key = 39,
  keywords = {5-HT4, AMP, ATPase, Abstract, Action Adrenergic Adrenergic, Agents, Anesthesia, Anesthetics, Animals, Antibodies, Antibody Binding, Blotting, C57BL, Caffeine, Calcium Calcium, Calcium-Binding Carbazoles, Cardiac, Cardiomegaly, Cardiotonic Carrier Cell Cells, Channels, Comparative Competitive, Computer-Assisted, Concentration, Confocal, Congestive, Constriction, Contraction, Coronary Cultured, Cyclic Diagnosis, Differential, Direct, Doppler, Dose-Response Drug, Echocardiography, English Failure, Female, Fentanyl, Fibers, Fibroblasts, Fluorescent Formamides, Heart Hematoporphyrins, Hemodynamic Humans, Hydrogen-Ion Image Immunoelectron, Immunohistochemistry, In Inbred Indoles, Infarction, Interpretation, Ischemia, Isoproterenol, Ketamine, L-Type, Left, Line, Male, Medetomidine, Membrane Mesoporphyrins, Messenger, Mice, Microscopy, Microtubules, Molecular Monoclonal, Muscle Myocardial Myocardium, Phenomena, Potentials, Proteins, Relationship, Structure, Study, Technique, Ventricles, Vessels, Vitro, alpha-Agonists, alpha-Antagonists, beta-Agonists, beta-Antagonists, {C}a$^{2+}$-Transporting},
  month = Sep,
  number = 3,
  pages = {H1225-36},
  timestamp = {2009-06-03T11:21:30.000+0200},
  title = {Normal contractions triggered by I(Ca,L) in ventricular myocytes
	from rats with postinfarction CHF.},
  url = {http://dx.doi.org/10.1152/ajpheart.00162.2001},
  volume = 283,
  year = 2002
}

%0 Journal Article
%1 Sjaa_2002_H1225
%A Sjaastad, Ivar
%A B�kenes, Janny
%A Swift, Fredrik
%A Wasserstrom, J. Andrew
%A Sejersted, Ole M
%D 2002
%J Am. J. Physiol. Heart Circ. Physiol.
%K 5-HT4, AMP, ATPase, Abstract, Action Adrenergic Adrenergic, Agents, Anesthesia, Anesthetics, Animals, Antibodies, Antibody Binding, Blotting, C57BL, Caffeine, Calcium Calcium, Calcium-Binding Carbazoles, Cardiac, Cardiomegaly, Cardiotonic Carrier Cell Cells, Channels, Comparative Competitive, Computer-Assisted, Concentration, Confocal, Congestive, Constriction, Contraction, Coronary Cultured, Cyclic Diagnosis, Differential, Direct, Doppler, Dose-Response Drug, Echocardiography, English Failure, Female, Fentanyl, Fibers, Fibroblasts, Fluorescent Formamides, Heart Hematoporphyrins, Hemodynamic Humans, Hydrogen-Ion Image Immunoelectron, Immunohistochemistry, In Inbred Indoles, Infarction, Interpretation, Ischemia, Isoproterenol, Ketamine, L-Type, Left, Line, Male, Medetomidine, Membrane Mesoporphyrins, Messenger, Mice, Microscopy, Microtubules, Molecular Monoclonal, Muscle Myocardial Myocardium, Phenomena, Potentials, Proteins, Relationship, Structure, Study, Technique, Ventricles, Vessels, Vitro, alpha-Agonists, alpha-Antagonists, beta-Agonists, beta-Antagonists, {C}a$^{2+}$-Transporting
%N 3
%P H1225-36
%R 10.1152/ajpheart.00162.2001
%T Normal contractions triggered by I(Ca,L) in ventricular myocytes
	from rats with postinfarction CHF.
%U http://dx.doi.org/10.1152/ajpheart.00162.2001
%V 283
%X Attenuated L-type Ca$^2+$ current (I(Ca,L)), or current-contraction
	gain have been proposed to explain impaired cardiac contractility
	in congestive heart failure (CHF). Six weeks after coronary artery
	ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized
	rats were current or voltage clamped from -70 mV. In both cases,
	contraction and contractility were attenuated in CHF cells compared
	with cells from sham-operated rats 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 -50 mV, the following variables were
	not different between sham and CHF, respectively: peak I(Ca,L) (4.5
	+/- 0.3 vs. 3.8 +/- 0.3 pApF(-1) at 23 degrees C and 9.4 +/- 0.5
	vs. 8.4 +/- 0.5 pApF(-1) at 37 degrees C), the bell-shaped voltage-contraction
	relationship in Cs$^+$ solutions (fractional shortening, 15.2 +/-
	1.0\% vs. 14.3 +/- 0.7\%, respectively, at 23 degrees C and 7.5 +/-
	0.4\% vs. 6.7 +/- 0.5\% at 37 degrees C) and the sigmoidal voltage-contraction
	relationship in K$^+$ solutions. Caffeine-induced Ca$^2+$
	release and sarcoplasmic reticulum Ca$^2+$-ATPase-to-phospholamban
	ratio were not different. Thus CHF contractions triggered by I(Ca,L)
	were normal, and the contractile deficit was only seen in undialyzed
	cardiomyocytes stimulated from -70 mV.

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Normal contractions triggered by I(Ca,L) in ventricular myocytes from rats with postinfarction CHF.
I. Sjaastad, J. B�kenes, F. Swift, J. Wasserstrom, and O. Sejersted.
Am. J. Physiol. Heart Circ. Physiol. 283 (3): H1225-36 (September 2002)

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Normal contractions triggered by I(Ca,L) in ventricular myocytes from rats with postinfarction CHF.I. Sjaastad, J. B�kenes, F. Swift, J. Wasserstrom, and O. Sejersted. Am. J. Physiol. Heart Circ. Physiol. 283 (3): H1225-36 (September 2002)

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Cite this publication

Normal contractions triggered by I(Ca,L) in ventricular myocytes from rats with postinfarction CHF.
I. Sjaastad, J. B�kenes, F. Swift, J. Wasserstrom, and O. Sejersted.
Am. J. Physiol. Heart Circ. Physiol. 283 (3): H1225-36 (September 2002)