AIM: We examined the cellular basis for depressed cardiac contractility
in rats with congestive heart failure (CHF) secondary to myocardial
infarction. METHODS: Six weeks after ligation of the left coronary
artery, CHF was confirmed by haemodynamic measures and echocardiographic
demonstration of reduced myocardial contractility in vivo. Papillary
muscles from CHF animals developed less force than those from sham
operated (SHAM) animals. Cell shortening was measured in isolated
ventricular myocytes voltage-clamped with high resistance electrodes.
Ca$^2+$ transients were measured in fluo-4 loaded myocytes. RESULTS:
Contractions triggered by depolarizing test steps from a post conditioning
potential of -70 mV were significantly smaller and had significantly
reduced velocity of shortening in CHF compared with SHAM myocytes.
However, contractions initiated from -40 mV, were similar in amplitude
and velocity of shortening in CHF and SHAM cells. L-type Ca$^2+$
current was not significantly different between CHF and SHAM cells,
whether activated from -70 or -40 mV. Therefore, in SHAM cells, excitation-contraction
coupling exhibited higher gain when contractions were initiated from
negative (-70 mV), as compared with depolarized potentials (-40 mV).
However, in CHF myocytes, excitation-contraction coupling gain was
selectively depressed with steps from -70 mV. This depression of
gain in CHF was not accompanied by a significant reduction in sarcoplasmic
reticulum Ca$^2+$ content. Isoproterenol increased Ca$^2+$
transients less in CHF than SHAM myocytes. CONCLUSION: In this post-infarction
model of CHF, the contractile deficit was voltage dependent and the
gain of excitation-contraction coupling was selectively depressed
for contractions initiated negative to -40 mV.
%0 Journal Article
%1 Sjaa_2005_45
%A Sjaastad, I.
%A Birkeland, J. A.
%A Ferrier, G.
%A Howlett, S.
%A Skomedal, T.
%A Bj�rnerheim, R.
%A Wasserstrom, J. A.
%A Sejersted, O. M.
%D 2005
%J Acta Physiol. Scand.
%K , 15847643
%N 1
%P 45-58
%R 10.1111/j.1365-201X.2005.01431.x
%T Defective excitation-contraction coupling in hearts of rats with
congestive heart failure.
%U http://dx.doi.org/10.1111/j.1365-201X.2005.01431.x
%V 184
%X AIM: We examined the cellular basis for depressed cardiac contractility
in rats with congestive heart failure (CHF) secondary to myocardial
infarction. METHODS: Six weeks after ligation of the left coronary
artery, CHF was confirmed by haemodynamic measures and echocardiographic
demonstration of reduced myocardial contractility in vivo. Papillary
muscles from CHF animals developed less force than those from sham
operated (SHAM) animals. Cell shortening was measured in isolated
ventricular myocytes voltage-clamped with high resistance electrodes.
Ca$^2+$ transients were measured in fluo-4 loaded myocytes. RESULTS:
Contractions triggered by depolarizing test steps from a post conditioning
potential of -70 mV were significantly smaller and had significantly
reduced velocity of shortening in CHF compared with SHAM myocytes.
However, contractions initiated from -40 mV, were similar in amplitude
and velocity of shortening in CHF and SHAM cells. L-type Ca$^2+$
current was not significantly different between CHF and SHAM cells,
whether activated from -70 or -40 mV. Therefore, in SHAM cells, excitation-contraction
coupling exhibited higher gain when contractions were initiated from
negative (-70 mV), as compared with depolarized potentials (-40 mV).
However, in CHF myocytes, excitation-contraction coupling gain was
selectively depressed with steps from -70 mV. This depression of
gain in CHF was not accompanied by a significant reduction in sarcoplasmic
reticulum Ca$^2+$ content. Isoproterenol increased Ca$^2+$
transients less in CHF than SHAM myocytes. CONCLUSION: In this post-infarction
model of CHF, the contractile deficit was voltage dependent and the
gain of excitation-contraction coupling was selectively depressed
for contractions initiated negative to -40 mV.
@article{Sjaa_2005_45,
abstract = {A{IM}: We examined the cellular basis for depressed cardiac contractility
in rats with congestive heart failure (CHF) secondary to myocardial
infarction. METHODS: Six weeks after ligation of the left coronary
artery, CHF was confirmed by haemodynamic measures and echocardiographic
demonstration of reduced myocardial contractility in vivo. Papillary
muscles from CHF animals developed less force than those from sham
operated (SHAM) animals. Cell shortening was measured in isolated
ventricular myocytes voltage-clamped with high resistance electrodes.
{C}a$^{2+}$ transients were measured in fluo-4 loaded myocytes. RESULTS:
Contractions triggered by depolarizing test steps from a post conditioning
potential of -70 mV were significantly smaller and had significantly
reduced velocity of shortening in CHF compared with SHAM myocytes.
However, contractions initiated from -40 mV, were similar in amplitude
and velocity of shortening in CHF and SHAM cells. L-type {C}a$^{2+}$
current was not significantly different between CHF and SHAM cells,
whether activated from -70 or -40 mV. Therefore, in SHAM cells, excitation-contraction
coupling exhibited higher gain when contractions were initiated from
negative (-70 mV), as compared with depolarized potentials (-40 mV).
However, in CHF myocytes, excitation-contraction coupling gain was
selectively depressed with steps from -70 mV. This depression of
gain in CHF was not accompanied by a significant reduction in sarcoplasmic
reticulum {C}a$^{2+}$ content. Isoproterenol increased {C}a$^{2+}$
transients less in CHF than SHAM myocytes. CONCLUSION: In this post-infarction
model of CHF, the contractile deficit was voltage dependent and the
gain of excitation-contraction coupling was selectively depressed
for contractions initiated negative to -40 mV.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Sjaastad, I. and Birkeland, J. A. and Ferrier, G. and Howlett, S. and Skomedal, T. and Bj�rnerheim, R. and Wasserstrom, J. A. and Sejersted, O. M.},
biburl = {https://www.bibsonomy.org/bibtex/280a7014a5c5ec8c9017412e9f8b4f1bb/hake},
description = {The whole bibliography file I use.},
doi = {10.1111/j.1365-201X.2005.01431.x},
file = {Sjaa_2005_45.pdf:Sjaa_2005_45.pdf:PDF},
interhash = {52d9886379173285c51cf9be29c1c154},
intrahash = {80a7014a5c5ec8c9017412e9f8b4f1bb},
journal = {Acta Physiol. Scand.},
key = 20,
keywords = {, 15847643},
month = May,
number = 1,
pages = {45-58},
pii = {APS1431},
timestamp = {2009-06-03T11:21:30.000+0200},
title = {Defective excitation-contraction coupling in hearts of rats with
congestive heart failure.},
url = {http://dx.doi.org/10.1111/j.1365-201X.2005.01431.x},
volume = 184,
year = 2005
}