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Cardiovascular Research 1998 40(3):492-501; doi:10.1016/S0008-6363(98)00200-4
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Regional electrophysiological effects of hypokalaemia, hypomagnesaemia and hyponatraemia in isolated rabbit hearts in normal and ischaemic conditions

Robert Wolkb, Kathleen A Kaneb, Stuart M Cobbea and Martin N Hicksa,*

aDepartment of Medical Cardiology, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK
bDepartment of Physiology and Pharmacology, University of Strathclyde, Royal College, 204 George Street, Glasgow G1 1XW, UK

* Corresponding author. Tel.: +44-(141)-211-0461; fax: +44-(141)-552-4683.

Objective: The aims of this study were to establish an isolated working heart model for electrophysiological recordings from the epicardium and endocardium and to examine regional effects of changes in ion concentrations in normal and ischaemic conditions. Methods: Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured simultaneously in the epicardium and endocardium of rabbit hearts paced at 3.3 Hz, subjected to 30 min of regional ischaemia and 15 min of reperfusion. The hearts were exposed before and throughout ischaemia and reperfusion to hypokalaemia (K+=2 mM), hypomagnesaemia (Mg2+=0.5 mM) or hyponatraemia (Na+=110 mM). Results: In the control hearts, no regional electrophysiological differences were seen before ischaemia, but ischaemia-induced MAPD90 shortening and postrepolarisation refractoriness were greater in the epicardium than in the endocardium and conduction delay increased only in the epicardium. Hypokalaemia shortened ERP in the epicardium (but not endocardium) and increased conduction delay in all areas before ischaemia, but it had no effects during ischaemia. During reperfusion hypokalaemia increased the incidence of recurrent tachyarrhythmias. Hypomagnesaemia had no effect before ischaemia, increased epicardial (but not endocardial) MAPD90 shortening during ischaemia, although it had no pro-arrhythmic action. Hyponatraemia increased conduction delay in all areas before ischaemia and produced asystole or severe bradycardia in all hearts. During ischaemia, hyponatraemia decreased ERP shortening and inducibility of arrhythmias in the epicardium (but not endocardium). Conclusions: We conclude that the more pronounced effect of ischaemia upon the epicardium than the endocardium can be explained by the contact of the endocardium with intracavitary perfusate. We also conclude that changes in ion concentrations may have differential regional electrical effects in normal or ischaemic conditions.

KEYWORDS Hypokalaemia; Hypomagnesaemia; Hyponatraemia; Epicardium; Endocardium; Ischaemia; Rabbit


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