Effects of diltiazem on early ischemic ventricular arrhythmias

Dennis, Steven C.; Coetzee, W.A.; Keding, B

doi:10.1016/s0022-2828(87)80060-3

Journal of Molecular and Cellular Cardiology

1987

DOI: 10.1016/s0022-2828(87)80060-3

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Effects of diltiazem on early ischemic ventricular arrhythmias

Steven C. Dennis¹,

W.A. Coetzee²,

B Keding³

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1990

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“…In this model of global ischemia, ventricular arrhythmias are consistently observed. 19 In both models of ischemia, the epicardial electrogram was monitored on an oscilloscope (model 5110, Tektronix, Beaverton, Oregon) and recorded on magnetic tape or a chart recorder for analysis of arrhythmias.…”

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Reduction of ischemic K+ loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea.

Kantor

Coetzee

Carmeliet

et al. 1990

Circulation Research

205

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Glibenclamide, one of the antidiabetic sulfonylureas, is known to block ATP-dependent K' channels. We used this drug to determine to what extent K' loss from acutely ischemic myocardium is mediated via these channels. We also investigated whether glibenclamide would influence ischemic arrhythmias. Isolated rat hearts rendered globally ischemic showed no correlation between early lactate and K' efflux rates. Cumulative K' loss during 11 minutes of global ischemia (0.5 ml min' g-') was reduced, from 3.2±0.3 to 2.5±0.1 ,ieq/g (p<0.025) by 1 ,uM glibenclamide and from 3.3±0.2 to 1.9±0.2 ,ueq/g (p<0.005) by 10 ,uM glibenclamide, while lactate efflux was unaltered by the drug. Glibenclamide also exhibited potent antifibrillatory activity, abolishing irreversible ventricular fibrillation during regional ischemia (0/6 vs. 5/6 controls; p <0.02) and during global ischemia (0/7 vs. 9/9 controls; p <0.01). Heart rate, coronary flow rate, peak systolic pressure, and myocardial oxygen consumption were unaltered by the drug (1 ,uM). Similarly, glibenclamide (1 ,M) did not alter myocardial ATP, phosphocreatine or lactate content, or glucose utilization. Ventricular fibrillation threshold during normoxia was also unaltered by glibenclamide (1 ,uM). We conclude that K' loss during acute myocardial ischemia is mediated partly by ATP-dependent K' channels, and not by a tightly coupled co-efflux with anionic lactate. (Circulation Research 1990;66:478-485) T he loss of K' ions from myocardial tissue is an early response to the interruption of oxygenated blood flow.1,2 The mechanism of this K' efflux is uncertain, and several explanations have been proposed.3 In particular, the hypothesis that K' efflux is an ionic shift in response to electrogenic anion loss in the form of anionic lactate from ischemic tissues has enjoyed some prominence.3-5 More recently, ATP-regulated potassium channels have been demonstrated in pancreatic cells6 and isolated cardiac myocytes7,8 and may provide an alternative explanation for the increased K' conductance and efflux seen during hypoxia7,9'10 and metabolic inhibition.1" We tested the hypothesis that K' loss in acute myocardial ischemia may be partly regulated by these channels by using glibenclamide, a sulfonylurea that blocks ATP-dependent potassium channels in Published previously as a preliminary report in abstract form (Circulation 1987;76[suppl IV]:IV-17

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confidence: 99%

Reduction of ischemic K+ loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea.

Kantor

Coetzee

Carmeliet

et al. 1990

Circulation Research

205

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Effects of diltiazem on early ischemic ventricular arrhythmias

Cited by 1 publication

References 0 publications

Reduction of ischemic K+ loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea.

Reduction of ischemic K+ loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea.

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