4-chloro-cyclohexa-1,4-dienecarboxylic acid | 98550-86-8

• 分子结构分类: 有机化合物 - 有机卤素化合物 - 乙烯基卤化物
• 英文名称: 4-chloro-cyclohexa-1,4-dienecarboxylic acid
• 英文别名: 4-Chlor-cyclohexa-1,4-diencarbonsaeure；4-Chlorocyclohexa-1,4-diene-1-carboxylic acid
• CAS: 98550-86-8
• 化学式: C₇H₇ClO₂
• 分子量: 158.584
• InChiKey: GOURJERNMLEBTR-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.8
• 重原子数：
  10
• 可旋转键数：
  1
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.29
• 拓扑面积：
  37.3
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为产物：
  描述：

  2-氯-1.3-丁二烯 、 丙炔酸 在 对苯二酚 、 甲苯 作用下， 生成 4-chloro-cyclohexa-1,4-dienecarboxylic acid
  参考文献：
  名称：

  Small amounts of venous gas embolism cause delayed impairment of endothelial function and increase polymorphonuclear neutrophil infiltration

  摘要：

  Gas bubbles from decompression and gas embolization lead to endothelial dysfunction and mechanical injury in the pig. rabbit and lamb. In the study presented here, 0.01 ml air/min/kg was infused through a catheter into the jugular vein in 12 rabbits for 60 min. The endothelial response was measured using tension measurements in the blood vessel wall, and morphological changes where quantified using light microscopy and image processing. Percent lung water content was calculated and used to estimate the severity of pulmonary oedema. The infusion led to a significant decrease in the acetylcholine-mediated endothelial-dependent vasodilatation in the pulmonary artery 6 h after the infusion (6-h group, n = 6). A decrease in substance-P-mediated endothelial-dependent vasodilatation was also detected. No changes where seen in a group of rabbits examined I h after infusion (1-h group, n=6). The impaired endothelial-dependent vasodilatation caused by the bubbles is probably biochemical in origin, since no visible changes were seen in the endothelial layer. A significant increase in polymorphonuclear neutrophils was observed in the 6-h group compared to the 1-h group. This study demonstrates that small numbers of bubbles, corresponding to ''silent bubbles'', lead to an impairment of the endothelial-dependent vasoactive response.

  DOI：

  10.1007/s00421-001-0531-y