Improvement in thermoelectric properties of n-type Si₉₅Ge₅ alloys by heavy multi-dopants

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• 作者：Ya-dong Xu ; Gui-ying Xu ; Chang-chun Ge
• 关键词：Thermoelectric materials ; Si₉₅Ge₅ alloys ; Multi-dopants
• 刊名：Scripta Materialia
• 出版年：2008
• 期刊代码：157_13596462
• 类别：et
• 出版时间：June 2008
• 卷：58
• 期：12
• 页码：1070-1073
• 文件大小：358 K

摘要

The aim of the present study was to investigate the mechanisms underlying the vasorelaxation induced by the selective phosphodiesterase 5 (PDE5) inhibitor vardenafil in rat penile small arteries. Segments of the rat dorsal penile artery were mounted in microvascular myographs for isometric tension recording. Concentration–response curves for vardenafil (1 nM–3 μM) and other PDE inhibitors (sildenafil, rolipram and milrinone) were constructed by adding cummulative concentrations of the drugs to arteries precontracted with phenylephrine. The effect of mechanical endothelial cell removal and of selective blockers of the nitric oxide (NO)/cGMP pathway and K⁺ channels were evaluated on the vardenafil relaxant responses. Vardenafil was the most potent of the four PDE inhibitors tested that maximally relaxed penile arteries, pD₂ and maximum relaxation being 6.96 ± 0.08 and 97 ± 1%(n = 48), respectively. Blockade of guanylate cyclase with ODQ (5 μM), mechanical removal of the endothelium or inhibition of NO synthase with l-NOARG (100 μM) markedly reduced vardenafil-induced relaxations, without altering maximum response. Inhibitors of both the cGMP-dependent (PKG) and the cAMP-dependent (PKA) protein kinases, Rp-8-Br-PET-cGMPS (5 μM) and Rp-8-CPT-cAMPS (50 μM), respectively, both reduced vardenafil relaxant responses and the later abolished that of rolipram. Vardenafil-elicited relaxation was reduced by the selective inhibitor of the large-conductance Ca²⁺-activated K⁺ channels (BK_Ca), iberiotoxin (30 nM) and also by the ATP-sensitive K⁺ channel (K_ATP) inhibitor, glibenclamide (1 μM). Vardenafil induces a potent vasodilatation in rat penile arteries that is partially dependent on the endothelium and the NO/cGMP pathway and involves activation of both BK_Ca and K_ATP channels.