Sufentanil attenuates impairment of the endothelium-dependent vasodilation induced by hypoxia–reoxygenation in the rat coronary artery
| Autor: | Hao Wu, Zhi-Wu Chen, Xinqi Cheng, Shan-Shan Gao, Youmei Zuo, Jun-yan Zhang, Erwei Gu |
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| Rok vydání: | 2016 |
| Předmět: |
Male
Sufentanil Physiology Sodium chemistry.chemical_element Vasodilation 030204 cardiovascular system & hematology Pharmacology Rats Sprague-Dawley 03 medical and health sciences Organ Culture Techniques 0302 clinical medicine 030202 anesthesiology Physiology (medical) Animals Medicine Channel blocker Large-Conductance Calcium-Activated Potassium Channels Dose-Response Relationship Drug biology business.industry General Medicine Iberiotoxin Coronary Vessels Cell Hypoxia Rats Nitric oxide synthase chemistry Anesthesia biology.protein Endothelium Vascular Sodium nitroprusside business Acetylcholine medicine.drug |
| Zdroj: | Canadian Journal of Physiology and Pharmacology. 94:1309-1314 |
| ISSN: | 1205-7541 0008-4212 |
| DOI: | 10.1139/cjpp-2016-0037 |
| Popis: | Sufentanil has been used broadly in cardiac surgery, but the mechanisms by which it modulates coronary vascular tone after ischemia–reperfusion injury are largely unknown. Effects of sufentanil on coronary tone and on the relaxation of rat coronary arteries (CAs) in response to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) relaxing agents in the presence of hypoxia–reoxygenation (H/R) was studied in an in vitro organ chamber setup. Sufentanil (10−7–10−4 mol/L) relaxed rat CA rings in endothelium-dependent and endothelium-independent manners. In endothelium-intact rings, preincubation of H/R-treated CAs with sufentanil (10−5 mol/L) significantly increased the acetylcholine response, but did not augment sodium nitroprusside-induced relaxation. Sufentanil-mediated potentiation of acetylcholine-induced relaxation was not affected by a nitric oxide synthase inhibitor or by intermediate- or small-conductance Ca2+-activated K+ channel blockers. However, potentiation was abolished by iberiotoxin (100 nmol/L), a selective inhibitor of large-conductance Ca2+-activated K+ channels, as well as Rp-cAMPS (30 μmol/L), a cyclic AMP-dependent protein kinase (PKA) inhibitor. Sufentanil induced endothelium-dependent and endothelium-independent relaxation and attenuated H/R-induced impairment of endothelium-dependent vasodilation in the rat CAs. The potentiating effect of sufentanil may involve activation of large-conductance Ca2+-activated K+ channels via cAMP-dependent mechanisms. |
| Databáze: | OpenAIRE |
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