Bari F, Lazics K, Domoki F, Agárdi S, Pelikán S, Vásárhelyi B, Temesvári P
Department of Physiology, Faculty of Medicine, University of Szeged, Dóm tér 10, Szeged 6720, Hungary.
Neurosci Lett. 2002 Aug 30;329(2):189-92. doi: 10.1016/s0304-3940(02)00643-2.
We examined whether hypoxic/ischemic (H/I) stress decreased the cerebral Na(+),K(+)-ATPase enzyme activity (NEA) of newborn pigs. The effects of global ischemia (10 min), asphyxia (10 min), and incomplete forebrain ischemia (45 min) were analyzed in ten different brain regions. The lengths of the reperfusion periods varied between 15 min and 3 h. NEA was determined as the ouabain-sensitive fraction of the total ATPase activity of the sample. Marked regional differences in NEA were observed in all experimental groups, whereas NEA was not significantly affected in any of the brain structures investigated. The present results suggest that damaged brain Na(+),K(+)-ATPase may not be the cause of the neuronal-vascular impairment following H/I stress.
我们研究了缺氧/缺血（H/I）应激是否会降低新生猪大脑的钠钾ATP酶活性（NEA）。分析了全脑缺血（10分钟）、窒息（10分钟）和不完全性前脑缺血（45分钟）对十个不同脑区的影响。再灌注时间在15分钟至3小时之间变化。NEA被确定为样品总ATP酶活性中对哇巴因敏感的部分。在所有实验组中均观察到NEA存在明显的区域差异，而在所研究的任何脑结构中，NEA均未受到显著影响。目前的结果表明，受损的脑钠钾ATP酶可能不是H/I应激后神经元-血管损伤的原因。
