Editorials |
From the Department of Pharmacology, Center for Molecular Therapeutics (P.A.B., H.E.D.J.t.K.), Columbia University, New York, NY; and the Department of Medicine, Physiology, and Biophysics (H.E.D.J.t.K.), University of Calgary, Alberta, Canada.
Correspondence to Dr Penelope A. Boyden, Dept of Pharmacology, Columbia College of Physicians and Surgeons, 630 West 168th St., New York, NY 10032. E-mail pab4@columbia.edu
Key Words: action potentials Cai transients APD restitution
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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At that time we did not discuss the role of Ca2+ cycling in the maintenance or conversion of stable tachycardias to VF. However, in consideration of the new data on the role of APD restitution in the initiation of VF (increase in wavebreaks; eg, see Garfinkel et al2), we turn our attention now to the role Ca2+ cycling in the myocyte and its impact on APD restitution relations in the isolated rabbit ventricular cell.3 Goldhaber et al consider the role of Ca2+ using different types of APD restitution protocols to emphasize the dynamic nature of intracellular Ca2+ changes and its subsequent impact on the myocyte APD.
In their study APD alternans is coupled to Ca2+ cycling, which in itself is not new since others have observed that APD alternans demonstrates a hystersis and is inhibited with BAPTA-AM buffering.4 Some have suggested that repolarization alternans is more closely associated with Ca2+ than APD restitution.57 In fact there has been a large body of work implying that APD alternans and Ca2+ cycling are intimately linked (eg, see8,9). However caution must be raised because Chudin et al10 have reported that the dynamics of Cai are altered even
Related Article:
Circ. Res. 2005 96: 459-466.
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