Mrsić-Pelcić Jasenka, Pelcić Goran, Vitezić Dinko, Antoncić Igor, Filipović Tatjana, Simonić Ante, Zupan Gordana
Department of Pharmacology, School of Medicine, University of Rijeka, Brace Branchetta 20/I 51000 Rijeka, Croatia.
Neurochem Int. 2004 Jun;44(8):585-94. doi: 10.1016/j.neuint.2003.10.004.
The influence of hyperbaric oxygen (HBO) treatment on the activities of superoxide dismutase (SOD) and Na(+),K(+)-ATPase was determined during different time periods of reperfusion in rats exposed to global cerebral ischemia. Ischemic animals were either sacrificed or exposed to the first HBO treatment 2, 24, 48 or 168 h after ischemic insult (for SOD activities measurement) or immediately, 0.5, 1, 2, 6, 24, 48, 72 or 168 h after ischemic procedure (for Na(+),K(+)-ATPase activities measurement). Hyperbaric oxygenation procedure was repeated for seven consecutive days. The results of presented experiments demonstrated the statistically significant increase in the hippocampal SOD activity 24 and 48 h after global cerebral ischemia followed by a decrease in the enzymatic activity 168 h after ischemic insult. In the ischemic rats treated with HBO the level of hippocampal SOD activity was significantly higher after 168 h of reperfusion in comparison to the ischemic, non HBO-treated animals. In addition, it was found that global cerebral ischemia induced a statistically significant decrease of the hippocampal Na(+),K(+)-ATPase activity starting from 1 to 168 h of reperfusion. Maximal enzymatic inhibition was obtained 24 h after the ischemic damage. Decline in Na(+),K(+)-ATPase activity was prevented in the animals exposed to HBO treatment within the first 24 h of reperfusion. Our results suggest that global cerebral ischemia induces significant alterations in the hippocampal SOD and Na(+),K(+)-ATPase activities during different periods of reperfusion. Enhanced SOD activity and preserved Na(+),K(+)-ATPase activity within particular periods of reperfusion, could be indicators of a possible beneficial role of HBO treatment in severe brain ischemia.
在全脑缺血的大鼠再灌注的不同时间段,测定了高压氧(HBO)治疗对超氧化物歧化酶(SOD)和钠钾ATP酶活性的影响。缺血动物在缺血损伤后2、24、48或168小时(用于测量SOD活性)处死或接受首次HBO治疗,或在缺血手术后立即、0.5、1、2、6、24、48、72或168小时(用于测量钠钾ATP酶活性)接受治疗。高压氧治疗连续重复7天。实验结果表明,全脑缺血后24和48小时海马SOD活性有统计学意义的增加,随后在缺血损伤168小时后酶活性下降。与未接受HBO治疗的缺血动物相比,接受HBO治疗的缺血大鼠在再灌注168小时后海马SOD活性水平显著更高。此外,发现全脑缺血从再灌注1至168小时开始导致海马钠钾ATP酶活性有统计学意义的下降。缺血损伤后24小时获得最大酶抑制。在再灌注的前24小时接受HBO治疗的动物中,钠钾ATP酶活性的下降得到了预防。我们的结果表明,全脑缺血在再灌注的不同时期诱导海马SOD和钠钾ATP酶活性发生显著改变。在特定的再灌注时期增强的SOD活性和保留的钠钾ATP酶活性,可能是HBO治疗在严重脑缺血中可能发挥有益作用的指标。