Laboratory for Physiology of the Cardiovascular and Lymphatic Systems, I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
Bull Exp Biol Med. 2020 Mar;168(5):597-601. doi: 10.1007/s10517-020-04759-z. Epub 2020 Apr 6.
The study examined the effect of HS on the tone of cerebral arteries in rats after global cerebral ischemia/reperfusion injury and cooperation between NO and HS in the control over cerebral circulation during the postischemic period. In control sham-operated and in experimental rats with ischemia/reperfusion injury, the diameter of pial arteries was repeatedly measured in vivo under a light microscope after removal of parietal bone and dura mater in 1 h and in 7 days after the surgery. The study established that HS is an important signaling molecule in pial arteries, where it is responsible for vasodilation. Interaction of HS and NO augmented dilation of pial arteries; in these arteries, HS up-regulated the effect of NO/cGMP/sGC/PKG signaling pathways. Partially, the dilating effect of HS is realized via activation of ATP-sensitive K channels in plasmalemma of smooth muscle cells. In the brain, ischemia/reperfusion injury degrades the ability of pial arteries to dilate via inhibition of NO-mediated signaling pathway.
本研究探讨了高渗盐水（HS）对全脑缺血/再灌注损伤后大鼠大脑动脉张力的影响，以及在缺血后期间控制脑循环中 NO 和 HS 之间的相互作用。在对照假手术和缺血/再灌注损伤的实验大鼠中，在去除颅骨和硬脑膜后 1 小时和手术后 7 天，在活体下通过光显微镜反复测量软脑膜动脉的直径。研究表明，HS 是软脑膜动脉中的一种重要信号分子，负责血管扩张。HS 和 NO 的相互作用增强了软脑膜动脉的扩张；在这些动脉中，HS 增强了 NO/cGMP/sGC/PKG 信号通路的作用。部分情况下，HS 的舒张作用是通过激活平滑肌细胞膜质膜上的 ATP 敏感性 K 通道来实现的。在大脑中，缺血/再灌注损伤通过抑制 NO 介导的信号通路，降低了软脑膜动脉的扩张能力。
