Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat.
Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat.
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分析大鼠对 H2S 供体 Na2S 和 NaHS 的心血管反应。
DOI：
10.1152/ajpheart.00171.2015
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Kadowitz,PhilipJ
中科院分区：
文献类型：
--
作者：
Yoo,Daniel;Jupiter,RyanC;Pankey,EdwardA;Reddy,VishwaradhG;Edward,JustinA;Swan,KevinW;Peak,TaylorC;Mostany,Ricardo;Kadowitz,PhilipJ
硫化氢(H_2S)是血管组织中由L-半胱氨酸形成的内源性气体分子。本研究观察了麻醉大鼠对硫化氢供体Na2S和NaHS的心血管反应。静脉注射Na2S和NaHS 0.03-0.5 mg/kg可使体循环动脉压和心率呈剂量依赖性降低，较高剂量时降低心输出量、肺动脉压和体循环血管阻力。硫化氢输注研究表明，全身动脉压、心率、心输出量和全身血管阻力的下降得到很好的维持，对Na2S的反应是可逆的。心率减慢不能被阿托品阻断，这表明心动过缓不依赖于副交感神经的激活，并且是通过对窦房结的影响来调节的。六甲铵、格列本脲、NW-硝基-L-精氨酸甲酯盐酸盐、甲氯芬酸钠、ODQ、咪康唑、5-羟基癸酸或四乙基铵不能减轻体动脉压的降低，提示ATP敏感性钾通道、一氧化氮、花生四烯酸代谢物、环GMP、P450环氧合酶代谢物或大电导钙激活钾通道不参与介导大鼠对硫化氢供体的降压反应，这种反应不是中枢调节的。目前的数据表明，供体体动脉压的降低可以通过血管阻力和心输出量的减少来调节，供体对窦房结的影响不依赖于副交感神经系统。目前的数据表明，在正常大鼠中，外周介导的对硫化氢供体的降压反应的机制尚不确定。
Hydrogen sulfide (H2S) is an endogenous gaseous molecule formed from L-cysteine in vascular tissue. In the present study, cardiovascular responses to the H2S donors Na2S and NaHS were investigated in the anesthetized rat. The intravenous injections of Na2S and NaHS 0.03–0.5 mg/kg produced dose-related decreases in systemic arterial pressure and heart rate, and at higher doses decreases in cardiac output, pulmonary arterial pressure, and systemic vascular resistance. H2S infusion studies show that decreases in systemic arterial pressure, heart rate, cardiac output, and systemic vascular resistance are well-maintained, and responses to Na2S are reversible. Decreases in heart rate were not blocked by atropine, suggesting that the bradycardia was independent of parasympathetic activation and was mediated by an effect on the sinus node. The decreases in systemic arterial pressure were not attenuated by hexamethonium, glybenclamide,Nw-nitro-l-arginine methyl ester hydrochloride, sodium meclofenamate, ODQ, miconazole, 5-hydroxydecanoate, or tetraethylammonium, suggesting that ATP-sensitive potassium channels, nitric oxide, arachidonic acid metabolites, cyclic GMP, p450 epoxygenase metabolites, or large conductance calcium-activated potassium channels are not involved in mediating hypotensive responses to the H2S donors in the rat and that responses are not centrally mediated. The present data indicate that decreases in systemic arterial pressure in response to the H2S donors can be mediated by decreases in vascular resistance and cardiac output and that the donors have an effect on the sinus node independent of the parasympathetic system. The present data indicate that the mechanism of the peripherally mediated hypotensive response to the H2S donors is uncertain in the intact rat.
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