Titova E, Ostrowski R P, Zhang J H, Tang J
Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA 92354, USA.
Acta Neurochir Suppl. 2008;105:119-21. doi: 10.1007/978-3-211-09469-3_24.
Recent studies have shown that amantadine, an uncompetitive N-methyl-d-aspartate receptor antagonist and dopamine agonist, is effective for the treatment of various cerebral disorders and causes relatively mild side effects. In this study, we investigated whether administration of amantadine will provide a neuroprotective effect in the intracerebral hemorrhage (ICH) rat model. A total of 15 male Sprague Dawley rats (300-380 g) were divided into sham, ICH-untreated, and ICH-treated with amantadine sulphate groups. ICH was induced by collagenase injection. Total dose 6 mg/kg of amantadine sulphate was divided into 3 injections and administered intraperitoneally at 1, 8, and 16 h after ICH. Brain injury was evaluated by investigating neurological function and brain edema at 24 h after ICH. Our data demonstrates that ICH caused significant neurological deficit associated with marked brain edema. Amantadine did not reduce brain injury after ICH; neurological function and brain edema in the treated group were not different from those of the untreated group. We conclude that amantadine sulphate does not offer neuroprotection in acute stage of experimental ICH-induced brain injury.
近期研究表明，金刚烷胺作为一种非竞争性N-甲基-D-天冬氨酸受体拮抗剂及多巴胺激动剂，对多种脑部疾病的治疗有效，且副作用相对较轻。在本研究中，我们调查了给予金刚烷胺是否会在脑出血（ICH）大鼠模型中产生神经保护作用。总共15只雄性斯普拉格-道利大鼠（300 - 380克）被分为假手术组、ICH未治疗组和硫酸金刚烷胺治疗的ICH组。通过注射胶原酶诱导脑出血。硫酸金刚烷胺的总剂量6毫克/千克分为3次注射，在脑出血后1、8和16小时腹腔注射。在脑出血后24小时，通过调查神经功能和脑水肿来评估脑损伤。我们的数据表明，脑出血导致了与明显脑水肿相关的显著神经功能缺损。金刚烷胺并未减轻脑出血后的脑损伤；治疗组的神经功能和脑水肿与未治疗组并无差异。我们得出结论，硫酸金刚烷胺在实验性脑出血诱导的脑损伤急性期不提供神经保护作用。
