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

The study examined the effect of H₂S on the tone of cerebral arteries in rats after global cerebral ischemia/reperfusion injury and cooperation between NO and H₂S 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 H₂S is an important signaling molecule in pial arteries, where it is responsible for vasodilation. Interaction of H₂S and NO augmented dilation of pial arteries; in these arteries, H₂S up-regulated the effect of NO/cGMP/sGC/PKG signaling pathways. Partially, the dilating effect of H₂S 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.