目的探讨组胺对海马脑片缺血诱导细胞水肿及活性降低的作用,以及与受体亚型的关系。方法大鼠海马脑片以缺氧缺糖(OGD)诱导缺血损伤后,实时检测CA1区透光度变化评价细胞水肿;并测定2,3,5-三苯基氯化四氮唑(TTC)产物甲腊,评价脑片活性。观察不同浓度组胺的作用,以及组胺受体拮抗剂对组胺作用的影响。结果组胺(0.01—10μmol·L^-1)明显抑制OGD诱导的海马脑片透光度增加,并提高脑片活性。H1受体拮抗剂苯海拉明(0.1—10μLmol·L^-1)不影响组胺的作用,H2受体拈抗剂西咪替丁(0.1~10μLmol·L^-1)则部分拮抗组胺的保护作用。结论组胺对大鼠海马脑片缺血诱导细胞水肿及活性降低有保护作用,该作用与H2受体有关。
Aim To determine the effect of histamine on ischemia-induced cellular edema and viability reduction in rat hippocampal slices, and the involved subtypes of histamine receptor in this effect. Methods In vitro ischemic injury of hippocampal slices was induced by oxygen-glucose deprivation (OGD). The slice injury was determined by real-timely measuring the changes of light transmittance (LT) for the cellular edema in CA1 region of the hippocampal slice, and by detecting the product of 2,3,5- triphenyhetrazolium chloride (TTC) , formazan, for the slice viability. The effect of histamine at various concentrations on the slice injury was observed, and the blockage by antagonists of histamine receptors was also investigated. Results Histamine (0. 01 - 10 μmol · L^-1 ) inhibited the peak value of LT during OGD in hippocampal slices and improved the reduced viability after OGD. Diphenhydramine (0. 1 - 10 μLmol·L^-1 ), an H2 receptor antagonist, did not affect the effect of histamine, while cimetidine (0. 1 - 10 μLmol·L^-1) , an H2 receptor antagonist, partly abolished the protective effect of histamine. Conclusion Histamine protects hippocampal slices against ischemia-induced cellular edema and viability reduction; this effect might be mediated via, at least partly, H2 receptor.