The Lambeth Conventions: guidelines for the study of arrhythmias in ischaemia, infarction, and reperfusion

Walker, Michael J.; Curtis, Michael J.; Hearse, David J.; Campbell, Robert W.; Janse, Michiel J.; Yellon, Derek M.; Cobbe, S M; Coker, Susan J.; Harness, J.B.; Harron, D. W. G.

doi:10.1093/cvr/22.7.447

Cited by 1,019 publications

(488 citation statements)

References 27 publications

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“…Diazoxide could induce translocation of PKC-epsilon as an upstream signaling molecule for mitochondrial K ATP channels [22,23] . Although propofol causes an increase in PKC activity in rat ventricular myocytes, it caused translocation of PKC-epsilon to sites not associated with mitochondria [16] . Thus, the mechanisms involved in opening of mitochondrial K ATP channels are not identical between propofol and diazoxide and need further study.…”

Section: Discussionmentioning

confidence: 89%

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Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

et al. 2012

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Aim: To investigate the potential of propofol in suppressing ventricular arrhythmias and to examine whether mitochondrial ATP-sensitive potassium channels are involved. Methods: Male Sprague-Dawley rats were pretreated with intravenous infusion of propofol (Prop), a selective mitochondrial KATP channel inhibitor 5-hydroxydecanoate (5-HD), propofol plus 5-HD (Prop+5-HD), a potent mitochondrial K ATP channel opener diazoxide (DZ) or NS, respectively. The dosage of each drug was 10 mg/kg. The animals then underwent a 30 min-ligation of the left anterior descending artery. The severity of arrhythmias, the incidence of ventricular fibrillation (VF), and the time of the first run of ventricular arrhythmias were documented using an arrhythmia scoring system. Mitochondrial membrane potential (ΔΨm) was measured in freshly isolated rat cardiomyocytes with a fluorescence microscope. Results: The arrhythmia scores in the Prop and DZ group were 2.6(0-5) and 2.4(0-5), respectively, which were significantly lower than that in the control group [4.9(2-8)]. VF was not observed in both Prop and DZ groups. The first run of ventricular arrhythmias was significantly postponed in the Prop group (10.5±2.2 vs 7.3±1.9 min). Bracketing of propofol with 5-HD eliminated the anti-arrhythmic effect of propofol. In isolated rat cardiomyocytes, propofol (50 μmol/L) significantly decreased ΔΨm, but when propofol was co-administered with 5-HD, the effect on ΔΨm was reversed. Conclusion: Propofol preconditioning suppresses ischemia-induced ventricular arrhythmias in the rat heart, which are proposed to be caused by opening of mitochondrial K ATP channels.

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Section: Discussionmentioning

confidence: 89%

“…Arrhythmia study All types of arrhythmias were classified according to the Lambeth Conventions [16] standard (Figure 2). An arrhythmia scoring system [17] was used for quantitative comparison.…”

Section: Experiments Protocolsmentioning

confidence: 99%

Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

et al. 2012

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“…1237/ PO/c/2008/CPCSEA, dated 23.11.2012) and Lambeth Convention [14]. Adult male wistar rats weighing 180-200 g were used for the study.…”

Section: Animal Husbandry and Maintenancementioning

confidence: 99%

QT prolongation by ranitidine in hypokalemia and arrhythmogen provoked rat heart

Karmakar¹,

Ali²,

Bera³

et al. 2017

Vascul Dis Ther

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Drugs with low arrhythmogenic tendencies fail to overcome the threshold to prolong QT interval and are ruled as safe. However, at provoked conditions these drugs might have the possibility to precipitate arrhythmia. Although small yet QT prolongation capability of such drugs must be investigated. The threshold required to prolong QT was attenuated using chronic dose of furosemide and clarithromycin. Once attenuated, QT prolongation capability of ranitidine was explored. Furosemide 10mg.kg -1 IP on co-administration with Clarithromycin 70mg.kg -1 orally for seven day manifested QTc interval at par with that of self-control group. A significant drop in serum potassium level was observed. In test groups, Furosemide 10mg.kg -1 + Clarithromycin 70 mg.kg -1 & Ranitidine 25 mg.kg -1 (once daily) and Furosemide 10mg.kg -1 + Clarithromycin 70 mg.kg -1 & Ranitidine 25 mg.kg -1 (Twice daily) the QTc prolongation compared to self control group was +28.0 % and +55.3 %, respectively. In the later group, the QT interval was observed to increase more than half the RR interval on ECG, a clinical indicator of cardiac emergency. Marked change in serum potassium level was also observed in the test groups. When Ranitidine alone was administered twice daily for seven days, no significant change in QTc interval was observed. Attenuation of the QT interval prolongation threshold exacerbates slightest QT prolongation tendencies and hence determine arrhythmogenic tendency of test drug. This model may be implied in the assessment of cardio-safety of drugs.

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“…The incidences of the main categories of arrhythmia (VPBs, bigeminy, salvos, VT, and VF) must be analyzed separately. Whether the incidences of subcategories of VTand VF are analyzed is a matter of personal preference (Walker et al 1988).ECG scoring system criteria was in accordance with following formula: Score: (log10 PVCs) + (log10 episodes VT) + 2 [(log10 episodes of VF) + (log10 total duration of VF)] (Miller et al 2012).…”

Section: Evaluation Of Ischemic-reperfusion Induced Ventricular Arrhymentioning

confidence: 99%

The Effect of PM 10 on Ischemia- Reperfusion Induced Arrhythmias in Rats

Radmanesh

Dianat

Badavi

et al. 2016

Braz. arch. biol. technol.

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The Lambeth Conventions: guidelines for the study of arrhythmias in ischaemia, infarction, and reperfusion

Cited by 1,019 publications

References 27 publications

Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

QT prolongation by ranitidine in hypokalemia and arrhythmogen provoked rat heart

The Effect of PM 10 on Ischemia- Reperfusion Induced Arrhythmias in Rats

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