%0 Journal Article %1 Litw_2000_1040 %A Litwin, S. E. %A Zhang, D. %A Bridge, J. H. %D 2000 %J Circ. Res. %K 11090539 Action Adrenergic Animal, Animals, Calcium Calcium, Channels, Disease Dysfunction, Gov't, Infarction, Isoproterenol, L-Type, Left, Male, Models, Myocardial Myocardium, Non-P.H.S., Non-U.S. P.H.S., Patch-Clamp Potentials, Processes, Rabbits, Research Reticulum, Sarcoplasmic Signaling, Stochastic Support, Techniques, U.S. Ventricular beta-Agonists, %N 11 %P 1040--1047 %T Dyssynchronous Ca$^2+$ sparks in myocytes from infarcted hearts. %U http://circres.ahajournals.org/cgi/content/full/87/11/1040 %V 87 %X The kinetics of contractions and Ca$^2+$ transients are slowed in myocytes from failing hearts. The mechanisms accounting for these abnormalities remain unclear. Myocardial infarction (MI) was produced by ligation of the circumflex artery in rabbits. We used confocal microscopy to record spatially resolved Ca$^2+$ transients during field stimulation in left ventricular (LV) myocytes from control and infarcted hearts (3 weeks). Compared with controls, Ca$^2+$ transients in myocytes adjacent to the infarct had lower peak amplitudes and prolonged time courses. Control myocytes showed relatively uniform changes in Ca$^2+$ throughout the cell after electrical stimulation. In contrast, in MI myocytes Ca$^2+$ increased inhomogeneously and localized increases in Ca$^2+$ occurred throughout the rising and falling phases of the Ca$^2+$ transient. Ca$^2+$ content of the sarcoplasmic reticulum did not differ between MI and control myocytes. Peak L-type Ca$^2+$ current density was reduced in MI myocytes. The macroscopic gain function was not different in control and MI myocytes when calculated as the amplitude of the Ca$^2+$ transient/peak I:(Ca). However, when calculated as the peak rate of rise of the Ca$^2+$ transient/peak I:(Ca), the gain function was modestly decreased in the MI myocytes. Application of isoproterenol (100 nmol/L) improved the synchronization of Ca$^2+$ release in MI myocytes at both 0.5 and 1 Hz. The poorly coordinated production of Ca$^2+$ sparks in myocytes from infarcted rabbit hearts likely contributes to the diminished and slowed macroscopic Ca$^2+$ transient. These abnormalities can be largely overcome when phosphorylation of Ca$^2+$ cycling proteins is enhanced by ss-adrenergic stimulation.

@article{Litw_2000_1040, abstract = {The kinetics of contractions and {C}a$^{2+}$ transients are slowed in myocytes from failing hearts. The mechanisms accounting for these abnormalities remain unclear. Myocardial infarction (MI) was produced by ligation of the circumflex artery in rabbits. We used confocal microscopy to record spatially resolved {C}a$^{2+}$ transients during field stimulation in left ventricular (LV) myocytes from control and infarcted hearts (3 weeks). Compared with controls, {C}a$^{2+}$ transients in myocytes adjacent to the infarct had lower peak amplitudes and prolonged time courses. Control myocytes showed relatively uniform changes in [{C}a$^{2+}$] throughout the cell after electrical stimulation. In contrast, in MI myocytes [{C}a$^{2+}$] increased inhomogeneously and localized increases in [{C}a$^{2+}$] occurred throughout the rising and falling phases of the {C}a$^{2+}$ transient. {C}a$^{2+}$ content of the sarcoplasmic reticulum did not differ between MI and control myocytes. Peak L-type {C}a$^{2+}$ current density was reduced in MI myocytes. The macroscopic gain function was not different in control and MI myocytes when calculated as the amplitude of the {C}a$^{2+}$ transient/peak I:(Ca). However, when calculated as the peak rate of rise of the {C}a$^{2+}$ transient/peak I:(Ca), the gain function was modestly decreased in the MI myocytes. Application of isoproterenol (100 nmol/L) improved the synchronization of {C}a$^{2+}$ release in MI myocytes at both 0.5 and 1 Hz. The poorly coordinated production of {C}a$^{2+}$ sparks in myocytes from infarcted rabbit hearts likely contributes to the diminished and slowed macroscopic {C}a$^{2+}$ transient. These abnormalities can be largely overcome when phosphorylation of {C}a$^{2+}$ cycling proteins is enhanced by ss-adrenergic stimulation.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Litwin, S. E. and Zhang, D. and Bridge, J. H.}, biburl = {https://www.bibsonomy.org/bibtex/266f861a179b1eab370be27213627bf6f/hake}, description = {The whole bibliography file I use.}, file = {Litw_2000_1040.pdf:Litw_2000_1040.pdf:PDF}, interhash = {26fb0d81659fa29bce40a1881a267e2f}, intrahash = {66f861a179b1eab370be27213627bf6f}, journal = {Circ. Res.}, key = 290, keywords = {11090539 Action Adrenergic Animal, Animals, Calcium Calcium, Channels, Disease Dysfunction, Gov't, Infarction, Isoproterenol, L-Type, Left, Male, Models, Myocardial Myocardium, Non-P.H.S., Non-U.S. P.H.S., Patch-Clamp Potentials, Processes, Rabbits, Research Reticulum, Sarcoplasmic Signaling, Stochastic Support, Techniques, U.S. Ventricular beta-Agonists,}, month = Nov, number = 11, pages = {1040--1047}, pmid = {11090539}, timestamp = {2009-06-03T11:21:20.000+0200}, title = {Dyssynchronous {C}a$^{2+}$ sparks in myocytes from infarcted hearts.}, url = {http://circres.ahajournals.org/cgi/content/full/87/11/1040}, volume = 87, year = 2000 }