中文摘要：

目的：硫化氢（hydrogen sulfide，H2S）为一种假定的血管内皮衍生超极化因子（endothelium—derived hyperpolarizing factor，EDHF），本研究探讨外源性H2S，即外源性假定的EDHF对脑缺血再灌注损伤的影响。方法：采用线栓法复制大鼠局灶性脑缺血（MCAO）再灌注损伤模型，测定动物行为功能、脑组织梗死体积、脑组织含水量、血清乳酸脱氢酶（LDH）活性及丙二醛（MDA）含量，用HE染色法观察脑组织学改变。结果：H2S供体硫氢化钠（NaHS，i．v．）0．195、0．390、0．780mg／kg能明显改善神经功能状态，降低缺血再灌注后脑梗死体积百分比，降低脑含水量，显著地抑制局灶性脑缺血再灌注损伤大鼠血清MDA含量和LDH活性，并不同程度地改善大鼠脑病理组织学的变化。结论：NaHS可明显改善大鼠脑缺血再灌注性损伤，提示外源性ED—HF（H2S）有抗脑缺血再灌损伤作用。

英文摘要：

AIM. Hydrogen sulfide （H2S） is one of the supposed endothelium-dependent hyperpolarizing factor （EDHF）, the protective effects of exogenous H2 S, namely exogenous supposed EDHF on cerebral ischemia reperfu- sion （I/R） injury was observed in present study. METHODS： Sodium hydrosulfide （NariS） was taken as a donor of He S. Focal cerebral I/R injury was caused by occluding the right middle cerebral artery （MCAO） in rats. The numerical data, which were from infarct volume, neurological deficit, brain water content, malondial- dehyde （MDA） level and lactate dehydrogenase （LDH） activities in serum, were evaluated. HE staining was used to observe brain pathologic changes. RESULTS：0. 195, 0. 390, 0. 780 mg/kg Naris markedly ameliorated the neurological deficit, decreased the percentage of infarct vol- ume, reduced the brain water content, and dra- matically inhibited the cerebral I/R injurer-in- duced increases of LDH activity and MDA con- tent in serum, improved brain pathologic chan- ges in different degrees. CONCLUSION. NariS significantly improved the cerebral I/R injury in rats, this suggests exogenous supposed EDHF （H2S） has a significant protective effect against cerebral I/R injury.