© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Myocardial interstitial norepinephrine and dihydroxyphenylglycol levels during ischemia and reperfusion
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan
* Corresponding author. Tel.: +81-6-6833-5012; fax: +81-6-6872-8092 takiyama{at}ri.ncvc.go.jp
Objective: The aim was to elucidate the relation between norepinephrine (NE) release and intraneuronal NE kinetics in the ischemic region of the in vivo heart. Methods: Using dialysis technique in the heart of anesthetized cats, we sampled dialysate from the ischemic region during 120-min coronary occlusion and reperfusion. Dialysate NE and dihydroxyphenylglycol (DHPG) contents were measured as indexes of myocardial interstitial NE and DHPG levels. Results: Within 20 min of occlusion, interstitial NE levels increased while DHPG levels decreased. This NE increase was suppressed by 
-conotoxin GVIA and enhanced by desipramine. These data suggest that axoplasmic NE levels increased by neuronal reuptake following exocytotic release, while intraneuronal DHPG production was suppressed due to the reduced monoamine oxidase activity. After 20 min of occlusion, interstitial NE levels increased markedly, accompanied by increased DHPG levels. This NE increase was suppressed by desipramine. These findings imply that NE mobilization from stored vesicles to axoplasma exceeded outward NE transport through uptake1 carrier in the amount of NE, and that a substantial increase in axoplasmic NE levels compensated for the reduced monoamine oxidase activity. After reperfusion, interstitial NE levels rapidly decreased while DHPG levels increased further. Both responses in NE and DHPG were suppressed by desipramine, indicating the involvement of recovered neuronal reuptake function. Conclusions: In the ischemic region, intraneuronal DHPG production was affected by alterations in monoamine oxidase activity, NE mobilization from stored vesicles, and carrier-mediated NE transport. The involvement of these factors in intraneuronal NE kinetics varied with the time of occlusion and reperfusion.
KEYWORDS Autonomic nervous system; Ca-channel; Ischemia; Neurotransmitters; Reperfusion
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  Y. Kuroko, T. Yamazaki, N. Tokunaga, T. Akiyama, H. Kitagawa, K. Ishino, S. Sano, and H. Mori Cardiac epinephrine synthesis and ischemia-induced myocardial epinephrine release Cardiovasc Res, June 1, 2007; 74(3): 438 - 444. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Fujii, T. Yamazaki, T. Akiyama, S. Sano, and H. Mori Extraneuronal enzymatic degradation of myocardial interstitial norepinephrine in the ischemic region Cardiovasc Res, October 1, 2004; 64(1): 125 - 131. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Eisenhofer, I. J. Kopin, and D. S. Goldstein Catecholamine Metabolism: A Contemporary View with Implications for Physiology and Medicine Pharmacol. Rev., September 1, 2004; 56(3): 331 - 349. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Koyama, N. Seyedi, W.-P. Fung-Leung, T. W. Lovenberg, and R. Levi Norepinephrine Release from the Ischemic Heart Is Greatly Enhanced in Mice Lacking Histamine H3 Receptors Mol. Pharmacol., February 1, 2003; 63(2): 378 - 382. [Abstract] [Full Text] [PDF]
|
|