Premium
Resting and Action Potentials of Nonischemic and Chronically Ischemic Human Ventricular Muscle
Author(s) -
MUBAGWA KANIGULA,
FLAMENG WILLEM,
CARMELIET EDWARD
Publication year - 1994
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.1540-8167.1994.tb01189.x
Subject(s) - medicine , cardiology , action (physics) , physics , quantum mechanics
Membrane Potentials in Human Ventricle. Introduction: The effect of chronic ischemia on the electrical properties of human cardiac tissue is not well understood. Methods and Results: Membrane potentials were studied using microelectrode techniques in isolated human ventricular tissues obtained from nonischemic (n = 17) or chronically ischemic (n = 71 myocardium. In normal Tyrode's solution, resting potential (V r ) was lower in ischemic (−70.1 · 2.12 mV) than in nonischemic muscles (−77.6 · 0.93 mV; mean · SKM; P < 0.051. In high [K] 0 (> 10 mM) media, V, was of similar magnitude in both types of tissue (in 21.6 mM [K] 0 V r was −53.1 · 2.24 mV in nonischcmic and −49.6 · 2.03 mV in ischemic preparations; n = 7 each; P > 0.05). Lowering [K] 0 . caused persistent Hyperpolarization in nonischemic muscles, but caused depolarization in chronically ischemic preparations (in 2,7 mM [K] 0 V r was −84.9 · 2.74 mV and –61.7 · 7.72 mV, respectively; n = 7; P < 0.05). Pinacidil (100 μM) normalized the response of chronically ischemic preparations to [K] 0 . Action potentials (APs) from nonischemic tissues varied in shape and could show aberrations. Kpinephrine (1.5 μM) and 4‐aminopyridine (3 mM) increased the AP duration, while butanedione monoxime (20 mM) and tetrodotoxin (1 μM) shortened it. In chronically ischemic muscles, the AP was characterized by the absence of a plateau and the presence of a slow phase of final repolarization. Conclusion: The differential effect of tow [K] 0 on the resting membrane potential of nonischemic and chronically ischemic tissues suggests a change in the properties or the regulation of background K + channels during chronic ischemia.