Carbachol prolongs ventricular repolarisation through nitric oxide release in an intact heart.

Abstract:

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.

journal_name

Cardiovasc Drugs Ther

authors

Wang L

doi

10.1023/a:1027324412869

subject

Has Abstract

pub_date

2003-07-01 00:00:00

pages

367-70

issue

4

eissn

0920-3206

issn

1573-7241

journal_volume

17

pub_type

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