Detection of endogenous acetylcholine release during brief ischemia in the rabbit ventricle

A possible trigger for ischemic preconditioning

Toru Kawada, Tsuyoshi Akiyama, Shuji Shimizu, Atsunori Kamiya, Kazunori Uemura, Meihua Li, Mikiyasu Shirai, Masaru Sugimachi

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)597-601
Number of pages5
JournalLife Sciences
Volume85
Issue number15-16
DOIs
Publication statusPublished - Oct 7 2009
Externally publishedYes

Fingerprint

Ischemic Preconditioning
Acetylcholine
Ischemia
Rabbits
Coronary Occlusion
Heart Ventricles
Microdialysis
Electric Stimulation
Coronary Vessels

Keywords

  • Acetylcholine
  • Cardiac microdialysis
  • Coronary artery occlusion
  • Rabbits
  • Vagal stimulation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Detection of endogenous acetylcholine release during brief ischemia in the rabbit ventricle : A possible trigger for ischemic preconditioning. / Kawada, Toru; Akiyama, Tsuyoshi; Shimizu, Shuji; Kamiya, Atsunori; Uemura, Kazunori; Li, Meihua; Shirai, Mikiyasu; Sugimachi, Masaru.

In: Life Sciences, Vol. 85, No. 15-16, 07.10.2009, p. 597-601.

Research output: Contribution to journalArticle

Kawada, Toru ; Akiyama, Tsuyoshi ; Shimizu, Shuji ; Kamiya, Atsunori ; Uemura, Kazunori ; Li, Meihua ; Shirai, Mikiyasu ; Sugimachi, Masaru. / Detection of endogenous acetylcholine release during brief ischemia in the rabbit ventricle : A possible trigger for ischemic preconditioning. In: Life Sciences. 2009 ; Vol. 85, No. 15-16. pp. 597-601.
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T1 - Detection of endogenous acetylcholine release during brief ischemia in the rabbit ventricle

T2 - A possible trigger for ischemic preconditioning

AU - Kawada, Toru

AU - Akiyama, Tsuyoshi

AU - Shimizu, Shuji

AU - Kamiya, Atsunori

AU - Uemura, Kazunori

AU - Li, Meihua

AU - Shirai, Mikiyasu

AU - Sugimachi, Masaru

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N2 - 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.

AB - 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.

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KW - Cardiac microdialysis

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KW - Rabbits

KW - Vagal stimulation

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