Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation

1  Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1096; and 2  Department of Emergency Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107 This study tests the hypothesis that cardioprotection exer...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 1997-10, Vol.273 (4), p.H1677
Main Authors: Zhao, Zhi-Qing, Todd, James C, Sato, Hiroki, Ma, Xin-Liang, Vinten-Johansen, J
Format: Article
Language:English
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:1  Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1096; and 2  Department of Emergency Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107 This study tests the hypothesis that cardioprotection exerted by adenosine A 2 -receptor activation and neutrophil-related events involves stimulation of ATP-sensitive potassium (K ATP ) channels on neutrophils during reperfusion. The adenosine A 2 agonist CGS-21680 (CGS) inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from 17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs ( P  
ISSN:0363-6135
1522-1539