These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Ischaemia-induced and reperfusion-induced arrhythmias differ in their sensitivity to potassium: implications for mechanisms of initiation and maintenance of ventricular fibrillation.
    Author: Curtis MJ, Hearse DJ.
    Journal: J Mol Cell Cardiol; 1989 Jan; 21(1):21-40. PubMed ID: 2716065.
    Abstract:
    The effects of four different K+ concentrations (2, 4, 6 or 8 mM) on arrhythmias resulting from ischaemia, and from reperfusion (after 3, 5, 7, 10, 15 or 30 min of ischaemia), in isolated perfused rat hearts were examined. A randomized experimental design with blind analysis was used. Regional myocardial ischaemia was produced by occlusion of the left main coronary artery. The incidence of ischaemia-induced ventricular fibrillation (VF) was inhibited by elevating K+ concentration, as reported previously. Furthermore, this effect was linearly and inversely related to the log of the K+ concentration (r = 0.99, P less than 0.001), a finding which has not been reported previously. This finding implies that the antiarrhythmic effect may result from depolarization in the non-ischaemic tissue, since resting membrane potential is also linearly related to the log of the K+ concentration. The maintenance of ischaemia-induced VF (its tendency to sustain) was also influenced by K+, in that a significantly higher incidence of sustained VF (defined as VF still present at the end of the period of ischaemia) was seen with 2 mM K+ compared with higher K+ concentrations (P less than 0.05). In contrast with its effect on the incidence of ischaemia-induced VF, K+ was without effect on the incidence of reperfusion-induced VF, indicating that reperfusion initiates VF independently of the K+ concentration in the perfusion fluid. However, the maintenance of reperfusion-induced VF was K+-dependent (in a similar manner to the maintenance of ischaemia-induced VF). In summary, the effects of K+ on ischaemia-induced VF were different from its effects on reperfusion-induced VF. We conclude that ischaemia-induced VF and reperfusion-induced VF are unlikely to be initiated by a common electrophysiological mechanism since only the former was influenced by K+. The mechanisms of maintenance of ischaemia-induced VF and reperfusion-induced VF might, however, be common, since the tendency for spontaneous defibrillation to occur (as reflected by the incidence of sustained VF) was equally sensitive to K+ in both settings. Finally, the nature of the time course of susceptibility to ischaemia-induced VF compared with that of reperfusion-induced VF raises the possibility that the reperfusion-induced VF may be clinically relevant as a cause of sudden death only when ischaemia-induced VF is suppressed.
    [Abstract] [Full Text] [Related] [New Search]