Aims: To examine endogenous acetylcholine (ACh) release in the rabbit left ventricle during acute ischemia, ischemic preconditioning and electrical vagal stimulation. Main methods: We measured myocardial interstitial ACh levels in the rabbit left ventricle using a cardiac microdialysis technique. In Protocol 1 (n = 6), the left circumflex coronary artery (LCX) was occluded for 30 min and reperfused for 30 min. In Protocol 2 (n = 5), the LCX was temporarily occluded for 5 min. Ten minutes later, the LCX was occluded for 30 min and reperfused for 30 min. In Protocol 3 (n = 5), bilateral efferent vagal nerves were stimulated at 20 Hz and 40 Hz (10 V, 1-ms pulse duration). Key findings: In Protocol 1, a 30-min coronary occlusion increased the ACh level from 0.39 ± 0.15 to 7.0 ± 2.2 nM (mean ± SE, P < 0.01). In Protocol 2, a 5-min coronary occlusion increased the ACh level from 0.33 ± 0.07 to 0.75 ± 0.11 nM (P < 0.05). The ACh level returned to 0.48 ± 0.10 nM during the interval. After that, a 30-min coronary occlusion increased the ACh level to 2.4 ± 0.49 nM (P < 0.01). In Protocol 3, vagal stimulation at 20 Hz and 40 Hz increased the ACh level from 0.29 ± 0.06 to 1.23 ± 0.48 (P < 0.05) and 2.44 ± 1.13 nM (P < 0.01), respectively. Significance: Acute ischemia significantly increased the ACh levels in the rabbit left ventricle, which appeared to exceed the vagal stimulation-induced ACh release. Brief ischemia as short as 5 min can also increase the ACh level, suggesting that endogenous ACh release can be a trigger for ischemic preconditioning.
- Cardiac microdialysis
- Coronary artery occlusion
- Vagal stimulation
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)