ArticleBritish journal of pharmacology1999
KATP channels and 'border zone' arrhythmias: role of the repolarization dispersion between normal and ischaemic ventricular regions.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 34 citations in OpenAlex.
- Pro-arrhythmic Effects of Hydrogen Sulfide in Healthy and Ischemic Cardiac Tissues: Insight From a Simulation Study.Frontiers in physiology · 2019Article
- Metformin prevents ischaemic ventricular fibrillation in metabolically normal pigs.Diabetologia · 2017Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Cardiac Events Theoretically Cannot Be Produced By Non-Ischemic And/Or Iso-Ischemic Myocardium: Challenging Postulations And Vitality Of The Concept Of "Ischemia-Dependent Conflictogenic Arrhythmias".Journal of atrial fibrillation · 2013Review
- Rabbit ventricular myocardium undergoing simulated ischemia and reperfusion in a double compartment tissue bath: a model to investigate both antiarrhythmic and arrhythmogenic likelihood.International journal of physiology, pathophysiology and pharmacology · 2013Article
- Role of KATP channel in electrical depression and asystole during long-duration ventricular fibrillation in ex vivo canine heart.American journal of physiology. Heart and circulatory physiology · 2012Article
- Mitochondrial KATP channel inhibition blunts arrhythmia protection in ischemic exercised hearts.American journal of physiology. Heart and circulatory physiology · 2010Article
- Thiazolidinedione drugs block cardiac KATP channels and may increase propensity for ischaemic ventricular fibrillation in pigs.Diabetologia · 2008Article
- The mitochondrial origin of postischemic arrhythmias.The Journal of clinical investigation · 2005Article
- Thrombin receptor and ventricular arrhythmias after acute myocardial infarction.Molecular medicine (Cambridge, Mass.)Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. In order to investigate the role of KATP channel activation and repolarization dispersion on the 'border zone' arrhythmias induced by ischaemia-reperfusion, the effects of glibenclamide and bimakalim, agents modifying action potential (AP) duration, were studied in an in vitro model of myocardial 'border zone'. 2. The electrophysiological effects of 10 microM glibenclamide and 1 microM bimakalim (n=8 each), respectively KATP channel blocker and activator, were investigated on guinea-pig ventricular strips submitted partly to normal conditions (normal zone, NZ) and partly to simulated ischaemic then reperfused conditions (altered zone, AZ). 3. By preventing the ischaemia-induced AP shortening (P<0.0001), glibenclamide reduced the dispersion of AP duration 90% (APD90) between NZ and AZ (P<0.0001), and concomitantly inhibited the 'border zone' arrhythmias induced by an extrastimulus (ES), their absence being significantly related to the lessened APD90 dispersion (chi2=8.28, P<0.01). 4. Bimakalim, which also reduced the APD90 dispersion (P<0.005) due to differential AP shortening in normal and ischaemic tissues, decreased the incidence of myocardial conduction blocks (25% of preparations versus 83% in control, n=12, P<0.05) and favoured 'border zone' spontaneous arrhythmias (75% of preparations versus 25% in control, P<0.05). 5. During reperfusion, unlike bimakalim, glibenclamide inhibited the ES-induced arrhythmias and reduced the incidence of the spontaneous ones (12% of preparations versus 92% in control, P<0.05), this latter effect being significantly related (chi2=6.13, P<0.02) to the lessened ischaemia-induced AP shortening in the presence of glibenclamide (P<0.0001). 6. These results suggest that KATP blockade may protect the ischaemic-reperfused myocardium from 'border zone' arrhythmias concomitantly with a reduction of APD90 dispersion between normal and ischaemic regions. Conversely, KATP channel activation may modify the incidence of conduction blocks and exacerbate the ischaemia-induced 'border zone' arrhythmias.
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