Why the study?
Does diltiazem pretreatment improve electrical properties and conduction velocity in isolated canine cardiac Purkinje fibers under conditions simulating acute myocardial ischemia?
Does diltiazem pretreatment improve electrical properties and conduction velocity in isolated canine cardiac Purkinje fibers under conditions simulating acute myocardial ischemia?
Diltiazem pretreatment reduces ischemia-induced increases in longitudinal resistance in canine Purkinje fibers, potentially explaining its ability to improve conduction delay during acute myocardial ischemia.
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Diltiazem may preserve conduction in ischemic Purkinje fibers; leaves open clinical translation from this animal model.
The effect of a calcium channel blocker diltiazem on the electrical properties of canine Purkinje fibers superfused in a milieu similar to that occurring in acute myocardial ischaemia was studied. Action potential parameters, passive electrical properties, and conduction velocity were measured using conventional microelectrode techniques. Superfusion with glucose-free Tyrode's solution containing 9 mM K+, gassed with 100% N2 at pH = 6.5 ('ischemic solution') significantly reduced the maximal diastolic potential, action potential duration, maximal upstroke velocity, conduction velocity and length constant, while input resistance and longitudinal resistance were elevated and membrane resistance remained unchanged. Diltiazem (1 microM) alone reduced only the action potential duration, while all other parameters were unaffected. Pretreatment with diltiazem did not fully prevent the effects of ischemic superfusion; however, the ischaemia-induced decrease in length constant was not significant in the presence of diltiazem. In addition, the increase in longitudinal resistance during ischaemia was significantly reduced following diltiazem pretreatment. This decrease in longitudinal resistance may contribute to the improvement of ischaemia-induced conduction delay observed in intact animals and may be related to a reduction of ischaemia-induced increase in intracellular free Ca2+.
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Nánási et al. (1992) studied this question.
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