Carbachol Prolongs Ventricular Repolarisation through Nitric Oxide Release in an Intact Heart

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Abstract

Summary. Aims: The primary aim of the study was to investigate the effect of carbachol on ventricular repolarisation in an intact animal heart. Methods: In five sheep, carbachol was administered to the left circumflex coronary artery (LCX) at 1.0 and 2.5 'mol/ml/min respectively for 3 min. Multiple unipolar ECGs were acquired from the epicardium of LCX territory. Activation-recovery interval (ARI) was analysed from these ECGs. Administration of carbachol at 2.5 'mol/ml/min was also repeated after pre-treatment with nitro-L-arginine (20 mg/kg), a nitric oxide synthase inhibitor. Results: Carbachol at 1.0 or 2.5 'mol/ml/min resulted in a T wave inversion and ARI prolongation in the LCX territory. The increase in ARI at 1.0 and 2.5 'mol/ml/min was 38±17 and 58±14 ms respectively (p<0.05). T wave inversion and ARI prolongation at 2.5 'mol/ml/min was diminished by pre-treatment with nitro-L-arginine. Conclusions: Carbachol results in a dose-dependent prolongation in ventricular repolarisation in this open-chest animal model. This effect is partially mediated by endogenous nitric oxide.
Original languageEnglish
Pages (from-to)367-370
Number of pages4
JournalCardiovascular Drugs and Therapy
Volume17
Issue number4
Publication statusPublished - 2003

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