Affiliation:
1. Krannert Institute of Cardiology, Indianapolis, Indiana 46202
Abstract
Sudden increases in heart rate cause accumulation of K+ in the extracellular space. However, the exact relationship between rate and extracellular K+ concentration ([K+]o) in vivo is unknown. We measured [K+]o in right atria of anesthetized dogs by using K+-sensitive electrodes. Peak increase in [K+]o ranged from 0.18 ± 0.04 mM [means ± SE; cycle length (CL) = 350 ms] to 0.80 ± 0.09 mM (CL = 250 ms) above baseline (3.50 ± 0.08 mM at CL = 380 ms; n = 5). During rapid pacing-induced atrial fibrillation, peak increase in [K+]oaveraged 0.80 ± 0.07 mM ( n = 5). Whole cell current-clamp measurements in single right atrial myocytes ( n = 5) showed that raising [K+]o from 3 to 5 mM in 1-mM steps progressively depolarized resting membrane potential and reduced both phase 0 action potential amplitude and maximal upstroke velocity. Multisite epicardial mapping ( n = 4) demonstrated that sudden rate increases changed longitudinal conduction velocity (CVL) by −3.6 ± 1.8% to −5.9 ± 1.2% over a CL range of 330 to 250 ms. Our observations suggest that rate-related [K+]o accumulation in vivo is of sufficient magnitude to modulate those cellular electrophysiological properties that determine atrial CVL.
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
13 articles.
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