Abstract:
:Isolated rabbit hearts undergo ventricular depolarization when exposed to 0.5 mM K--Krebs during 30 to 45 min. A ventricular tachyarrhythmia develops when these hearts are allowed to repolarize in 1.5 mM K--Krebs. Ventricular fibrillation usually follows. These arrhythmias do not cease spontaneously. Initially, perfusion with 0.5 mM K hyperpolarized the membrane to -100 +/- 1.2 mV (means +/- SEM), decreased the plateau level, greatly increased the action potential duration, and slowed down intraventricular conduction, despite the level of membrane polarization and a high rate of rise of the upstroke. After a delay of 15 to 30 min, a progressive depolarization occurred and a stable potential level of -61 +/- 1.9 mV was reached. The arrhythmia elicited by perfusion with 1.5 mM K was of ventricular origin but did not appear when the previous exposure to 0.5 mM K was reduced to 10 min. Addition of verapamil (1.0 microM) to the 1.5 mM K medium did not prevent the early appearance of the arrhythmia, but restored driven electrical activity after variable delays despite the persistence of alterations in the action potential configuration. Verapamil also abolished the slow depolarizing phase of the upstroke. It is proposed that the abnormal electrical activity arose in a partly depolarized Purkinje network and it may have been triggered by the electrical nonhomogeneity created by the repolarization of ventricular cells in an extracellular K+ concentration of 1.5 mM.
journal_name
Can J Physiol Pharmacoljournal_title
Canadian journal of physiology and pharmacologyauthors
Ruiz-Ceretti E,Ponce-Zumino A,Blaney R,Chartier Ddoi
10.1139/y82-226subject
Has Abstractpub_date
1982-12-01 00:00:00pages
1533-40issue
12eissn
0008-4212issn
1205-7541journal_volume
60pub_type
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