Su Xianming, Zhi Xiaowen, Cui Ting, Zheng Qiaowei, Wang Shixiang, Cao Yongxiao, Cui Changcong, Feng Weiyi
*First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, China; †Shaanxi General Hospital of Chinese People's Armed Police Forces, Xi'an, China; ‡China Resources Sanjiu Medical & Pharmaceutical Co. Ltd, Shenzhen, China; §College of Life Science, Northwest University, Xi'an, China; and ¶Medical College of Xi'an Jiaotong University, Xi'an, China.
J Cardiovasc Pharmacol. 2015 Jan;65(1):62-71. doi: 10.1097/FJC.0000000000000164.
Previous studies have found that Danhong injection (DHI), an extensively used herbal extract preparation in China, might be a powerful vasodilator. The aims of this study were to determine the vascular activity of DHI and its effects on arteries of different sizes. The results showed that DHI significantly inhibited rat-hindquarters and rabbit-ear vasoconstriction elicited by norepinephrine (NE) perfusion and markedly relaxed KCl-contracted and NE-contracted rat abdominal aortic and mesenteric artery rings. The endothelium made only a minor contribution to the vasorelaxant effect of DHI on artery segments. The vasorelaxant effect of DHI varied with the artery size, with larger arteries exhibiting a more sensitive and potent vasodilator response. DHI relaxed NE-induced vasoconstriction probably through inhibition of the intracellular Ca2+ release through the inositol triphosphate receptor system in the abdominal aorta and mesenteric artery, along with blockage of extracellular Ca2+ influx through the receptor-linked Ca2+ channels in the mesenteric artery. In addition, DHI completely relaxed KCl-induced contraction in both of the arteries, suggesting that inhibition of Ca2+ influx through voltage-gated Ca2+ channels is involved in the vasorelaxant effect of DHI. This elucidation of the vascular effects of DHI and the underlying mechanisms could lead to improved clinical applications.
以往研究发现，在中国广泛使用的中药提取物制剂丹红注射液（DHI）可能是一种强效血管扩张剂。本研究旨在确定DHI的血管活性及其对不同大小动脉的影响。结果显示，DHI显著抑制去甲肾上腺素（NE）灌注引起的大鼠后肢和兔耳血管收缩，并明显舒张氯化钾收缩和NE收缩的大鼠腹主动脉和肠系膜动脉环。内皮对DHI对动脉段的血管舒张作用贡献较小。DHI的血管舒张作用随动脉大小而异，较大动脉表现出更敏感和更强效的血管扩张反应。DHI舒张NE诱导的血管收缩可能是通过抑制腹主动脉和肠系膜动脉中通过肌醇三磷酸受体系统的细胞内Ca2+释放，以及阻断肠系膜动脉中通过受体偶联Ca2+通道的细胞外Ca2+内流。此外，DHI完全舒张了两条动脉中氯化钾诱导的收缩，表明抑制通过电压门控Ca2+通道的Ca2+内流参与了DHI的血管舒张作用。对DHI血管效应及其潜在机制的这一阐释可能会改善其临床应用。
