Circulation, Vol 84, 1732-1740, Copyright © 1991 by American Heart Association
V Molina-Viamonte, EP Anyukhovsky and MR Rosen
BACKGROUND. We used standard microelectrode techniques to study delayed
afterdepolarizations and triggered activity induced by alpha 1- adrenergic
stimulation in canine Purkinje fibers in the setting of simulated ischemia
and reperfusion. METHODS AND RESULTS. The ischemic environment included
10.8 mM [Ca2+]o, 10 mM [K+]o, 40-50 mm Hg PO2, 20 mM lactate (pH 6.7), and
1 x 10(-7) M phenylephrine. During ischemia, there was the variable
occurrence of abnormal automaticity, early afterdepolarizations, and
delayed afterdepolarizations. During reperfusion, 100% of preparations
manifested delayed afterdepolarizations and 40% manifested triggered
activity. Decreasing PO2 to less than 20 mm Hg markedly reduced the
incidence of delayed afterdepolarizations and triggered activity, as did
increasing PO2 to values of more than 90 mm Hg. WB 4101, an alpha
1-subtype-selective competitive blocker that antagonizes the effects of
alpha 1-agonists to induce phosphoinositide metabolism and increase
[Ca2+]i, significantly reduced the incidence of delayed
afterdepolarizations and triggered activity. In contrast, the alpha
1-subtype-selective blocker chloroethylclonidine, an alkylating agent, had
no effect on afterdepolarizations or triggered activity. CONCLUSIONS. Our
results indicate that a specific alpha 1-adrenergic pathway is involved in
the induction of triggered activity in the setting of ischemia and
reperfusion and suggest that interventions used to block this specific
pathway have the potential to be antiarrhythmic. They also emphasize the
importance of the magnitude of hypoxia in the expression of the
arrhythmias.
ARTICLES
An alpha-1-adrenergic receptor subtype is responsible for delayed afterdepolarizations and triggered activity during simulated ischemia and reperfusion of isolated canine Purkinje fibers
Department of Pharmacology, Columbia University, New York, NY 10032.
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