Intravenous adenosine reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+channel
| Autor: | Jing-Lin Zhao, Ji-Lin Chen, Yu-Hua Sun, Run-Lin Go, Wei-Dong Pei, Yue-Jin Yang |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
medicine.medical_specialty
Adenosine Necrosis Swine Vasodilator Agents Myocardial Infarction Radioimmunoassay Myocardial Reperfusion Injury Anterior Descending Coronary Artery Glibenclamide Random Allocation KATP Channels Coronary Circulation Internal medicine medicine Animals Channel blocker Myocardial infarction Endothelin-1 business.industry Myocardium General Medicine medicine.disease Endothelin 1 Disease Models Animal Treatment Outcome Endocrinology Echocardiography Injections Intravenous Cardiology Swine Miniature medicine.symptom Cardiology and Cardiovascular Medicine business Ligation medicine.drug |
| Zdroj: | Acta Cardiologica. 63:355-359 |
| ISSN: | 0001-5385 |
| DOI: | 10.2143/ac.63.3.1020313 |
| Popis: | UNLABELLED It has been verified that adenosine can attenuate myocardial no-reflow. However, the effects of adenosine on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown. METHODS Forty mini-swines were randomized into 5 study groups: 8 in the control group, 8 in the adenosine pretreatment group, 8 in the glibenclamide (K(ATP) channel blocker)-treated group, 8 in the adenosine and glibenclamide-pretreated group and 8 in the sham-operated group. An acute myocardial infarction and reperfusion model was created with three-hour occlusion of the left anterior descending coronary artery followed by a one-hour reperfusion. RESULTS Compared with the control group, adenosine significantly decreased the area of no-reflow (myocardial contrast echocardiography: from 78.5 +/- 4.5% to 20.7 +/- 4.1%, pathological means: from 82.3 +/- 1.9% to 21.5 +/- 4.3% of ligation area, respectively; all P < 0.01), reduced necrosis size from 98.5 +/- 1.3% to 75 +/- 4.7% of ligation area, P < 0.05). It also decreased plasma ET-1 and myocardial tissue ET-1. However, glibenclamide abrogated the protective effect of adenosine. CONCLUSION The beneficial effect of adenosine on myocardial no-reflow could be due to its effect on ET-1 via the activation of K(ATP) channel. |
| Databáze: | OpenAIRE |
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