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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Sufentanil attenuates impairment of the endothelium-dependent vasodilation induced by hypoxia-reoxygenation in the rat coronary artery
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Sufentanil attenuates impairment of the endothelium-dependent vasodilation induced by hypoxia-reoxygenation in the rat coronary artery

机译：舒芬太尼减轻大鼠冠状动脉缺氧-复氧所致内皮依赖性血管舒张功能的损害

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摘要

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 mu mol/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.
机译：舒芬太尼已广泛用于心脏外科手术，但在缺血再灌注损伤后其调节冠状血管张力的机制尚不清楚。研究了在缺氧-复氧（H / R）存在下舒芬太尼对内皮依赖性（乙酰胆碱）和内皮依赖性（硝普钠）松弛剂的应答，对冠状动脉张力和大鼠冠状动脉（CAs）松弛的影响在体外器官腔室设置中。 Sufentanil（10（-7）-10（-4）mol / L）以内皮依赖性和非内皮依赖性方式松弛大鼠CA环。在内皮完整环中，用舒芬太尼（10（-5）mol / L）进行H / R处理的CAs的预孵育显着增加了乙酰胆碱反应，但没有增加硝普钠钠引起的松弛。舒芬太尼介导的乙酰胆碱诱导的舒张增强不受一氧化氮合酶抑制剂或中或小电导Ca2 +激活的K +通道阻滞剂的影响。然而，增强作用被大分子Ca2 +激活的K +通道的选择性抑制剂iberiotoxin（100 nmol / L）以及环状AMP依赖性蛋白激酶Rp-cAMPS（30μmol / L）废除了。 ）抑制剂。舒芬太尼诱导大鼠CAs内皮依赖性和内皮依赖性松弛，并减弱H / R诱导的内皮依赖性血管舒张损害。舒芬太尼的增强作用可能涉及通过cAMP依赖性机制激活大电导的Ca2 +激活的K +通道。

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