Contribution of Hydrogen Sulfide to Dilation of Rat Cerebral Arteries after Ischemia/Reperfusion Injury

• Published in: Bulletin of experimental biology and medicine 2020-03, Vol.168 (5), p.597-601
• Main Authors: Lobov, G. I., Sokolova, I. B., Gorshkova, O. P., Shvetsova, M. E., Dvoretskii, D. P.
• Format: Article
• Language: English
• Subjects: Animals; Arteries; Biomedical and Life Sciences; Biomedicine; Blood vessels; Brain injury; Brain Ischemia - metabolism; Brain Ischemia - pathology; Brain Ischemia - physiopathology; Cell Biology; Cerebral Arteries - drug effects; Cerebral Arteries - physiopathology; Cerebral blood flow; Cerebrovascular Circulation - drug effects; Cyclic GMP; Dilatation; Dura mater; Hydrogen sulfide; Hydrogen Sulfide - metabolism; Hydrogen Sulfide - pharmacology; Internal Medicine; Ischemia; Laboratory Medicine; Male; Nitric Oxide - metabolism; Parietal bone; Pathology; Physiology; Pial artery; Plasma membranes; Rats; Rats, Wistar; Reperfusion; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Reperfusion Injury - physiopathology; Signal Transduction; Smooth muscle; Surgery; Vasodilation; Vasodilation - drug effects; Vasodilation - physiology
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-020-04759-z

The study examined the effect of H 2 S on the tone of cerebral arteries in rats after global cerebral ischemia/reperfusion injury and cooperation between NO and H 2 S 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 H 2 S is an important signaling molecule in pial arteries, where it is responsible for vasodilation. Interaction of H 2 S and NO augmented dilation of pial arteries; in these arteries, H 2 S up-regulated the effect of NO/cGMP/sGC/PKG signaling pathways. Partially, the dilating effect of H 2 S 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.