scholarly journals Antiarrhythmic properties of specific inhibitors of sarcoplasmic reticulum calcium ATPase in the isolated perfused rat heart after coronary artery ligation

1994 ◽  
Vol 23 (6) ◽  
pp. 1505-1510 ◽  
Author(s):  
Eugene Francois du Toit ◽  
Lionel Henry Opie
Keyword(s):  
Coronary Artery ◽  
Sarcoplasmic Reticulum ◽  
Rat Heart ◽  
Calcium Atpase ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Sarcoplasmic Reticulum Calcium ◽  
Specific Inhibitors

Reduction of tissue noradrenaline content in the isolated perfused rat heart during ischemia: importance of monoamine oxidation

1991 ◽  
Vol 69 (8) ◽  
pp. 1190-1195 ◽  
Author(s):  
Daniel Lamontagne ◽  
Nobuharu Yamaguchi ◽  
Christophe Ribuot ◽  
Jacques de Champlain ◽  
Réginald Nadeau
Keyword(s):  
Monoamine Oxidase ◽  
Rat Heart ◽  
Interventricular Septum ◽  
Isolated Rat Heart ◽  
Coronary Artery Ligation ◽  
Noradrenaline Content ◽  
Artery Ligation ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Noradrenaline Concentration

The effect of ischemia on myocardial noradrenaline concentration and endogenous noradrenaline output was studied in the isolated perfused rat heart. Following a 15-min stabilization period, regional ischemia was produced by coronary artery ligation. After 60 min of ischemia, noradrenaline concentrations were significantly reduced in the interventricular septum and left ventricle but not in the right ventricle. The reduction in tissue noradrenaline concentration was not prevented when the 60-min ischemia was replaced by a 10-min ischemia followed by a 50-min perfusion. No modification in noradrenaline output was observed during a 60-min ischemia. In contrast, reperfusion was accompanied by a washout of noradrenaline in the coronary effluent, corresponding to only 2% of the amount lost by the tissue. The effect of monoamine oxidase inhibition during the whole ischemic period was studied by perfusing the preparation with pargyline starting 10 min before the artery ligation. Although the administration of pargyline did not alter the noradrenaline output, it did prevent a reduction in myocardial noradrenaline concentration. It was concluded that monoamine oxidase may contribute to the elimination of the noradrenaline lost by the cardiac tissue during ischemia.Key words: tissue noradrenaline, myocardial ischemia, monoamine oxidase, isolated rat heart.

Noradrenaline turnover after left coronary artery ligation in rat heart

1987 ◽  
Vol 143 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Masafumi Inoue ◽  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Coronary Artery ◽  
Rat Heart ◽  
Left Coronary Artery ◽  
Coronary Artery Ligation ◽  
Noradrenaline Turnover ◽  
Artery Ligation

Normal contractions triggered by I Ca,L in ventricular myocytes from rats with postinfarction CHF

2002 ◽  
Vol 283 (3) ◽  
pp. H1225-H1236 ◽  
Author(s):  
Ivar Sjaastad ◽  
Janny Bøkenes ◽  
Fredrik Swift ◽  
J. Andrew Wasserstrom ◽  
Ole M. Sejersted
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Fractional Shortening

Attenuated L-type Ca2+ 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°C and 9.4 ± 0.5 vs. 8.4 ± 0.5 pApF−1 at 37°C), the bell-shaped voltage-contraction relationship 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) and the sigmoidal voltage-contraction relationship in K+ solutions. Caffeine-induced Ca2+ release and sarcoplasmic reticulum Ca2+-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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