Blockade of central histaminergic H2 receptors aggravates ischemic neuronal damage in gerbil hippocampus.
作者： Naoto Adachi , Frank J. Seyfried , Tatsuru Arai
DOI: 10.1097/00003246-200106000-00021
关键词: Hippocampus 、 Anesthesia 、 Microdialysis 、 Glutamate receptor 、 Histaminergic 、 Gerbil 、 Medicine 、 Internal medicine 、 Ischemia 、 Adenosine 、 Ranitidine 、 Endocrinology
摘要: Objective: Histaminergic H 2 antagonists have been reported to provoke central nervous system dysfunction in humans. They also aggravate ischemic neuronal damage experimental animals. Because energy failure and glutamate release are crucial factors damage, the effects of ranitidine on state extracellular concentration were investigated gerbil brain. Design: Prospective, randomized, controlled animal study. Setting: University laboratory. Subjects: Male Mongolian gerbils. Interventions: The changes direct-current potential shift hippocampal CA1 area produced by transient forebrain ischemia for 2.5 mins compared gerbils pretreated with saline or (10 nmol) intracerebroventricularly. histologic outcome was evaluated 7 days after observing delayed death these In a second study, brain concentrations adenosine 5'-triphosphate various durations decapitation determined, effect evaluated. third experiment, excitatory amino acids during examined microdialysis orocedure. Measurements Main Results: sudden membrane 62 ± 5 secs (mean SD, n = 6) start ischemia. preischemic administration facilitated onset depolarization (38 8 secs; p <.01). aggravated (p Decapitation reduced rapidly. Ranitidine reduction 5'-triphosphate, value 1 min 55% that corresponding group enhanced increase concentration, peak 316% <.05). Conclusion: deleterious may involve facilitation depletion an anaerobic state.
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