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Published on: April 21, 2014
Carbachol prolongs ventricular repolarisation through nitric oxide release in an intact heart
1School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia. lwang@csu.edu.au
Aims:
The primary ain of this 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 micromol/ml/min respectively for 3 min. Multiple unipolar ECGs were acquired from the epicardium of LCX territory. Administration of carbachol at 2.5 micromol/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 micromol/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 micromol/ml/min was 38 +/- 17 and 58 +/- 14 ms respectively (p<0.05). T wave inversion and ARI prolongation at 2.5 micromol/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.
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