Boscán P L, Piña-Crespo J C, Daló N L
Decanato de Ciecias Veterinarias, Universidad Centroccidental Lisandro Alvarado, Barquisimeto, Venezuela.
Invest Clin. 1996 Jun;37(2):129-35.
Injection of large doses of ammonia (1.2g/kg, i.p.) was used to induce acute toxicity in mice which was characterized by hyperresponsiveness, taquipnea, clonic and tonic seizures and death. Pretreatment with 20, 40, or 80 mg/Kg, i.p., of ketamine increased 30 to 55% survival rate. This pretreatment significantly retarded the beginning of the first tonic convulsion attenuating its intensity and delayed the time of the animal death; but did not alter the onset of the first clonic seizures. These experiments may be an evidence that support the hypothesis that seizures due to hyperammonemia involve activation of excitatory amino acid receptors.
注射大剂量氨（1.2克/千克，腹腔注射）用于诱导小鼠急性毒性，其特征为反应过度、呼吸急促、阵挛性和强直性惊厥以及死亡。用20、40或80毫克/千克腹腔注射氯胺酮进行预处理可使存活率提高30%至55%。这种预处理显著延迟了首次强直性惊厥的开始，减弱了其强度，并延长了动物死亡时间；但未改变首次阵挛性惊厥的发作时间。这些实验可能支持这样一种假说，即高氨血症引起的惊厥涉及兴奋性氨基酸受体的激活。
