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.
Keywords: H2S; NO; dilation; ischemia/reperfusion; pial arteries.