(2-chloro-ethyl)-(1-chloro-vinyl)-sulfide | 742104-99-0

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: (2-chloro-ethyl)-(1-chloro-vinyl)-sulfide
• 英文别名: (2-Chlor-aethyl)-(1-chlor-vinyl)-sulfid；(β-Chlor-aethyl)-(α-chlor-vinyl)-sulfid；1-Chloro-1-(2-chloroethylsulfanyl)ethene
• CAS: 742104-99-0
• 化学式: C₄H₆Cl₂S
• mdl: MFCD19232616
• 分子量: 157.064
• InChiKey: UGOSKOADRQGJGM-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.8
• 重原子数：
  7
• 可旋转键数：
  3
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  25.3
• 氢给体数：
  0
• 氢受体数：
  1

反应信息

• 作为反应物：
  描述：

  (2-chloro-ethyl)-(1-chloro-vinyl)-sulfide 在 四氯化碳 、 氯 作用下， 生成 (2-chloro-ethyl)-(1,2-dichloro-vinyl)-sulfide
  参考文献：
  名称：

  Dawson; Lawson, Journal of the American Chemical Society, 1927, vol. 49, p. 3128

  摘要：

  DOI：
• 作为产物：
  描述：

  (2-chloro-ethyl)-(1,2-dichloro-ethyl)-sulfide 生成 (2-chloro-ethyl)-(2-chloro-vinyl)-sulfide 、 (2-chloro-ethyl)-(1-chloro-vinyl)-sulfide
  参考文献：
  名称：

  Mechanical and electrophysiological effects of endothelin-1 on guinea-pig isolated lower oesophageal sphincter circular smooth muscle

  摘要：

  研究了内皮素-1 (ET-1)对豚鼠下食管括约肌 (LOS)环形平滑肌的影响，采用细胞内微电极和等张张力记录技术。ET-1引起双相机械反应：初始的短暂松弛，随后是持续的收缩。初始松弛不受河豚毒素 (TTX, 1 μM) 或 L-N^G-硝基精氨酸 (L-NOARG, 100 μM) 抑制。持续性收缩则显著减弱于尼非地平 (1 μM)。ET-1 (1–30 nM) 诱导浓度依赖性的超极化，不受 TTX 或 L-NOARG 影响。ET_A受体拮抗剂 BQ123 (0.3 μM) 消除了 ET-1 诱导的超极化，而 ET_B受体拮抗剂 BQ788 (0.3 μM)则无明显影响。Sarafotoxin S6c (10 nM)未改变膜电位。ET-1 诱导的超极化被阿帕霉素 (0.1 μM) 消除。有趣的是，阿帕霉素不仅消除了 ET-1诱导的短暂松弛，还增强了持续性收缩。在无 Ca²⁺的 Krebs 溶液中，ET-1 诱导的超极化显著减弱，当组织再次用含 Ca²⁺的 Krebs 溶液灌注时，超极化恢复到对照值。ET-1 诱导的超极化对尼非地平不敏感，但对受体介导 Ca²⁺内流的抑制剂 SK&F 96365 (50 μM) 敏感。ET-1 诱导的超极化的残留部分对 Thapsigargin (1 μM) 敏感。这些结果表明，在豚鼠 LOS 环形平滑肌中，ET-1 通过激活阿帕霉素敏感的 K⁺通道引起膜超极化，主要是由于受体介导的 Ca²⁺内流，部分由内源性 Ca²⁺库的释放引起。此次超极化触发了初始的短暂松弛，这作用于抑制持续性收缩。 British Journal of Pharmacology (2002) 135, 197–205; doi:10.1038/sj.bjp.0704426

  DOI：

  10.1038/sj.bjp.0704426

文献信息

• HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells<b><i>in vitro</i></b>: a comparative study using different statins
  作者：Franz Wiesbauer、Christoph Kaun、Gerlinde Zorn、Gerald Maurer、Kurt Huber、Johann Wojta

  DOI：10.1038/sj.bjp.0704454

  日期：2002.1

  The results of several clinical studies investigating the effect of statin therapy on the fibrinolytic system in vivo are inconclusive. We compared the effect of six different statins (atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, simvastatin) on components of the fibrinolytic system expressed by human vascular endothelial cells and smooth muscle cells and by the human hepatoma cell line HepG2. All statins used except pravastatin significantly decreased PAI‐1 production in human endothelial and smooth muscle cells. This effect was also seen in the presence of IL‐1α and TNF‐α. All statins except pravastatin increased t‐PA production in human smooth muscle cells. On a molar basis cerivastatin was the most effective HMG CoA reductase inhibitor used. Only simvastatin and lovastatin increased t‐PA production in endothelial cells. The effects on the fibrinolytic system were reversed by mevalonate. Statins decreased mRNA levels for PAI‐1 in endothelial and smooth muscle cells and increased mRNA levels for t‐PA in smooth muscle cells. Statins did not affect PAI‐1 expression in HepG2 cells. Cell viability was not influenced by statins in endothelial cells and HepG2 cells whereas in smooth muscle cells a cytotoxic effect was seen at high concentrations. If the effects on the fibrinolytic system of vascular cells in vitro shown in this study are also operative in vivo one could speculate that by increasing t‐PA and decreasing PAI‐1 at sites of vascular lesions statins might reduce fibrin formation and thrombus development. Such an effect might contribute to the clinically proven benefits of statin therapy. British Journal of Pharmacology (2002) 135, 284–292; doi:10.1038/sj.bjp.0704454

  多项临床研究调查了他汀类药物疗法对纤维蛋白溶解系统的影响，但结果尚无定论。我们比较了六种不同他汀类药物（阿托伐他汀、西立伐他汀、氟伐他汀、洛伐他汀、普伐他汀、辛伐他汀）对人血管内皮细胞和平滑肌细胞以及人肝癌细胞系HepG2所表达的纤维蛋白溶解系统成分的影响。 除普伐他汀外，所有使用的他汀类药物均显著减少了人内皮细胞和平滑肌细胞中的PAI-1产生。这一效应在IL-1α和TNF-α存在时亦观察到。除普伐他汀外的所有他汀类药物均增加了人平滑肌细胞中的t-PA产生。从摩尔浓度来看，西立伐他汀是最有效的HMG CoA还原酶抑制剂。仅辛伐他汀和洛伐他汀增加了内皮细胞中的t-PA产生。他汀类药物对纤维蛋白溶解系统的作用可被甲戊二酸逆转。他汀类药物降低了内皮细胞和平滑肌细胞中PAI-1的mRNA水平，并增加了平滑肌细胞中t-PA的mRNA水平。他汀类药物不影响HepG2细胞中的PAI-1表达。在内皮细胞和HepG2细胞中，他汀类药物不影响细胞活力，而在平滑肌细胞中，高浓度下观察到了细胞毒性作用。 如果本研究中血管细胞上他汀类药物对纤维蛋白溶解系统的作用在环境中同样适用，那么可以推测，通过在血管病变部位增加t-PA并减少PAI-1，他汀类药物可能会减少纤维蛋白形成和血栓的发展。这种效果可能有助于解释他汀类药物临床证实的益处。 British Journal of Pharmacology (2002) 135, 284–292; doi:10.1038/sj.bjp.0704454
• US4097526A
  申请人：——

  公开号：US4097526A

  公开（公告）日：1978-06-27
• US4248795A
  申请人：——

  公开号：US4248795A

  公开（公告）日：1981-02-03
• Dawson; Lawson, Journal of the American Chemical Society, 1927, vol. 49, p. 3128
  作者：Dawson、Lawson

  DOI：——

  日期：——
• Mechanical and electrophysiological effects of endothelin-1 on guinea-pig isolated lower oesophageal sphincter circular smooth muscle
  作者：Kenro Imaeda、Stephen J Trout、Thomas C Cunnane

  DOI：10.1038/sj.bjp.0704426

  日期：2002.1

  The effects of endothelin‐1 (ET‐1) on guinea‐pig lower oesophageal sphincter (LOS) circular smooth muscle were investigated by using intracellular microelectrodes and isometric tension recording techniques. ET‐1 produced biphasic mechanical responses; an initial transient relaxation followed by a sustained contraction. The initial relaxation was not inhibited by either tetrodotoxin (TTX, 1 μM) or L‐NG‐nitroarginine (L‐NOARG, 100 μM). The sustained contraction was greatly attenuated by nifedipine (1 μM). ET‐1 (1 – 30 nM) induced a concentration‐dependent hyperpolarisation that was unaffected by TTX or L‐NOARG. The ETA receptor antagonist, BQ123 (0.3 μM) abolished the ET‐1‐induced hyperpolarisation, whereas the ETB receptor antagonist, BQ788 (0.3 μM) had no detectable effect. Sarafotoxin S6c (10 nM) did not change the membrane potential. The ET‐1‐induced hyperpolarisation was abolished by apamin (0.1 μM). Interestingly, apamin abolished the ET‐1‐induced transient relaxation but potentiated the sustained contraction. In Ca2+‐free Krebs solution, the ET‐1‐induced hyperpolarisation was greatly attenuated and returned to the control value when the tissue was reperfused with Krebs solution containing Ca2+. The ET‐1‐induced hyperpolarisation was insensitive to nifedipine but was attenuated by SK&F 96365 (1 ‐ β‐[3‐(4 ‐ methoxy ‐ phenyl)propoxy] ‐ 4 ‐ methoxyphenethyl} ‐ 1H‐imidazole hydrochloride, 50 μM), an inhibitor of receptor‐mediated Ca2+ entry. The residual component of the ET‐1‐induced hyperpolarisation was sensitive to thapsigargin (1 μM). These results demonstrate that, in guinea‐pig LOS circular smooth muscle, ET‐1 hyperpolarizes the membrane by activating apamin‐sensitive K+ channels, mainly as a result of receptor‐mediated Ca2+ entry and partly by Ca2+ release from intracellular stores. The hyperpolarisation triggers the initial transient relaxation, which acts to oppose the sustained contraction. British Journal of Pharmacology (2002) 135, 197–205; doi:10.1038/sj.bjp.0704426

  研究了内皮素-1 (ET-1)对豚鼠下食管括约肌 (LOS)环形平滑肌的影响，采用细胞内微电极和等张张力记录技术。ET-1引起双相机械反应：初始的短暂松弛，随后是持续的收缩。初始松弛不受河豚毒素 (TTX, 1 μM) 或 L-N^G-硝基精氨酸 (L-NOARG, 100 μM) 抑制。持续性收缩则显著减弱于尼非地平 (1 μM)。ET-1 (1–30 nM) 诱导浓度依赖性的超极化，不受 TTX 或 L-NOARG 影响。ET_A受体拮抗剂 BQ123 (0.3 μM) 消除了 ET-1 诱导的超极化，而 ET_B受体拮抗剂 BQ788 (0.3 μM)则无明显影响。Sarafotoxin S6c (10 nM)未改变膜电位。ET-1 诱导的超极化被阿帕霉素 (0.1 μM) 消除。有趣的是，阿帕霉素不仅消除了 ET-1诱导的短暂松弛，还增强了持续性收缩。在无 Ca²⁺的 Krebs 溶液中，ET-1 诱导的超极化显著减弱，当组织再次用含 Ca²⁺的 Krebs 溶液灌注时，超极化恢复到对照值。ET-1 诱导的超极化对尼非地平不敏感，但对受体介导 Ca²⁺内流的抑制剂 SK&F 96365 (50 μM) 敏感。ET-1 诱导的超极化的残留部分对 Thapsigargin (1 μM) 敏感。这些结果表明，在豚鼠 LOS 环形平滑肌中，ET-1 通过激活阿帕霉素敏感的 K⁺通道引起膜超极化，主要是由于受体介导的 Ca²⁺内流，部分由内源性 Ca²⁺库的释放引起。此次超极化触发了初始的短暂松弛，这作用于抑制持续性收缩。 British Journal of Pharmacology (2002) 135, 197–205; doi:10.1038/sj.bjp.0704426