Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine.
- Author:
Jing-lin ZHAO
1
;
Yue-jin YANG
;
Shi-jie YOU
;
Zhi-cheng JING
;
Yong-jian WU
;
Wei-xian YANG
;
Ji-lin CHEN
;
Run-lin GAO
;
Zai-jia CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adenosine; pharmacology; therapeutic use; Animals; Disease Models, Animal; Endothelin-1; genetics; metabolism; Female; Male; Myocardial Infarction; drug therapy; physiopathology; Myocardial Reperfusion; Swine; Swine, Miniature
- From: Acta Academiae Medicinae Sinicae 2006;28(2):225-229
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the effect of adenosine on endothelin-1 (ET-1) after acute myocardial infarction (AMI) and reperfusion and explore the possible mechanism of no-reflow.
METHODSTwenty-four mini-swine were randomized into three study groups: control group (n=8), adenosine treated group (n=8), and sham-operated group (n=8). The mini-swine in the groups were subjected to 3 hours of coronary occlusion, followed by 60 minutes of reperfusion except those in the sham-operated group. The levels of ET-1 in blood sample, normal, infracted reflow and no-reflow myocardium were evaluated by radioimmuno-assay (RIA). The gene expressions of ET-1 in normal, infracted reflow and no-reflow myocardium were quantified by reverse transcription-polymerase chain reaction.
RESULTSIn both control group and adenosine group, compared with that at the baseline, ET-1 in blood sample significantly increased at 5 minutes and 180 minutes of left anterior descending coronary artery occlusion, as well as 5 and 60 minutes of reperfusion (all P < 0.01). In adenosine group, the levels of ET-1 were significantly lower than those in the control group (P < 0.05, P < 0.01). In both control group and adenosine group, compared with that in normal myocardium, ET-1 levels in both infarcted reflow and no-reflow myocardium significantly increased (both P < 0.01), with the level of ET-1 in no-reflow myocardium significantly higher than that in infarcted reflow myocardium (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). In both control and adenosine groups, compared with that in normal myocardium, the gene expression of ET-1 in infarcted reflow myocardium was significantly up-regulated (P < 0.01), while that of ET-1 in. no-reflow myocardium significantly down-regulated (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01).
CONCLUSIONThe endothelium injury may be one of the important mechanisms for no-reflow phenomenon. Adenosine cay prevent endothelium from injury to reduce no-reflow.