Premium
Inhibition of Na,K‐ATPase by External Electrical Cardioversion in a Sheep Model of Atrial Fibrillation
Author(s) -
MAIXENT JEANMICHEL,
BARBEY ODILE,
PIERRE SANDRINE,
DURAN MARIEJOSÉE,
SENNOUNE SOUAD,
BOURDEAUX MADELEINE,
RICARD PHILIPPE,
LÉVY SAMUEL
Publication year - 2000
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2000.tb00340.x
Subject(s) - ouabain , medicine , homeostasis , endocrinology , cardioversion , atrial fibrillation , atpase , cardiology , sodium , biochemistry , chemistry , enzyme , organic chemistry
Na,K‐ATPase and Cardioversion. Introduction : Electrical external cardioversion commonly used to treat atrial fibrillation (AF) is associated with myocardial membrane damage and disturbances in ionic homeostasis (hemodynamically unstable). The present study was designed to investigate whether alterations in ionic homeostasis observed were due in part to changes in the myocardial activity of Na,K‐ATPase. Methods and Results : AF was induced by pacing in ten anesthetized sheep divided into two groups. Group I (n = 4) received a single external countershock of 360 J after three episodes of AF lasting 10 minutes. Group II (n = 6) served as controls. Activity, responsiveness to ouabain, and membrane expression of catalytic α and β subunits of Na,K‐ATPase in sarcolemmal myocardial membrane fractions were investigated. Membrane fluidity and fatty acid composition, and plasma levels of atrial natriuretic factor (ANF) also were measured. One shock after episodes of AF significantly decreased ventricular Na,K‐ATPase activity up to 50% IP < 0.001) without modification of atrial activity at the membrane level. Sites with low affinity to ouabain showed a fivefold lower affinity for ouabain in the cardioversion group than in the control group (IC 50 = 7.9 μmol/L vs 40 μmol/L ouabain, P < 0.05). Plasma levels of ANF were significantly increased in the cardioversion group compared with the control group. These changes were independent of membrane modulation in terms of expression of Na,K‐ATPase, membrane fluidity, and fatty acid composition. Conclusion : This study suggests that left ventricular perturbation of ionic homeostasis subsequent to transthoracic cardioversion could result from inactivation of Na,K‐ATPase activity.