Ischemic preconditioning attenuates cardiac sympathetic nerve injury via ATP-Sensitive potassium channels during myocardial ischemia

Citation
T. Miura et al., Ischemic preconditioning attenuates cardiac sympathetic nerve injury via ATP-Sensitive potassium channels during myocardial ischemia, CIRCULATION, 104(9), 2001, pp. 1053-1058
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
0009-7322 → ACNP
Volume
104
Issue
9
Year of publication
2001
Pages
1053 - 1058
Database
ISI
SICI code
0009-7322(20010828)104:9<1053:IPACSN>2.0.ZU;2-I
Abstract
Background-During myocardial ischemia, massive norepinephrine (NE) is relea sed from the cardiac sympathetic nerve terminals, reflecting the sympatheti c nerve injury. A brief preceding ischemia can reduce infarct size; this is known as ischemic preconditioning (PC). The effect of PC on sympathetic ne rves, however, including, its underlying mechanisms in dog hearts, has rema ined unclear. Thus, this study was designed to elucidate whether the activa tion of ATP-sensitive potassium (K-ATP) channels is involved in the mechani sm of cardiac sympathetic nerve protection conferred by PC. Methods and Results-Interstitial NE concentration was measured by the in si tu cardiac microdialysis method in 45 anesthetized dogs. Five minutes of is chemia followed by 5 minutes of reperfusion was performed as PC. In the con trols, the dialysate NE concentration (dNE) increased 15-fold after the 40- minute ischemia. PC decreased dNE at 40-minute ischemia by 59% (P < 0.01), which was reversed by glibenclamide. A K-ATP channel opener, nicorandil (25 <mu>g.kg(-1).min(-1) IV), decreased dNE at 40 minutes of ischemia by 76% ( P < 0.01), which was also reversed by glibenclamide. During the PC procedur e, no significant increase in dNE was detected, even with the uptake-1 inhi bitor desipramine. Conclusions-Cardiac sympathetic nerve injury during myocardial ischemia was attenuated by PC via the activation of K-ATP channels, but the trigger of the PC effect is unlikely to be NE release in dog hearts.