Khan S H, Wright Sandra Lea, Banigesh Ali, Miyashita Hiro, Todd Kathryn, Hemmings Susan Jean, Wishart Tom, Shuaib Ashfaq
Stroke Research Unit, University of Saskatchewan, Saskatoon, SK, Canada.
Neurochem Res. 2003 Aug;28(8):1235-9. doi: 10.1023/a:1024288730853.
The mechanisms of action of the anticonvulsant topiramate (TPM) are indicative of a potential benefit during cerebral ischemia. TPM was studied in a transient global forebrain ischemia (TGFI) model in gerbils in which 40 mg/kg was administered before or after TGFI. Control groups were administered 0.9% normal saline similarly. The evaluation consisted of neurochemical, histological, and functional analyses. The data obtained indicates that unlike the focal cerebral ischemia model, TPM is not neuroprotective in TGFI. The difference in effect, which may be due to the difference in species or the type of ischemia, points to the need for caution when extrapolating animal data from this drug to humans.
抗惊厥药物托吡酯(TPM)的作用机制表明其在脑缺血期间可能具有益处。在沙土鼠短暂性全脑缺血(TGFI)模型中对TPM进行了研究,在TGFI之前或之后给予40mg/kg的TPM。对照组同样给予0.9%的生理盐水。评估包括神经化学、组织学和功能分析。获得的数据表明,与局灶性脑缺血模型不同,TPM在TGFI中没有神经保护作用。这种效应差异可能是由于物种差异或缺血类型不同,这表明在将该药物的动物数据外推至人类时需要谨慎。