Lantos J, Temes G, Török B
Acta Physiol Hung. 1986;67(1):141-53.
Changes in the time lag until a steep increase in cerebral extracellular potassium ion concentration occurring during total ischaemia caused by clamping of the aorta were investigated in dogs. The results indicate that during two subsequent clamping of the aorta in the same animal the time lag between the start of ischaemia and the steep increase in potassium ion concentration (1) hardly changed during nitrous oxide anaesthesia, i.e. from 2.09 +/- 0.31 to 2.22 +/- 0.51 min; (2) as a response to the administration of hexobarbital-sodium the steep increase took place 0.50 +/- 0.37 min later, i.e. 2.89 +/- 0.74 min after the administration of the drug and then, at the second clamping, 2.39 +/- 0.71 min; (3) during a 1 degree C decrease in body temperature the steep increase took place 0.29 +/- 0.05 min later. From the values of cerebral extracellular potassium ion concentration during ischaemia the conclusion might be drawn that hypothermia serves as the principal factor in the protection of the ischaemic brain tissue; meanwhile, also hexobarbital-sodium has a significant though somewhat smaller protective effect.
研究了在狗身上因主动脉夹闭导致全脑缺血期间,直至脑细胞外钾离子浓度急剧升高的时间延迟变化。结果表明,在同一动物连续两次夹闭主动脉的过程中,缺血开始至钾离子浓度急剧升高之间的时间延迟:(1)在氧化亚氮麻醉期间几乎没有变化,即从2.09±0.31分钟变为2.22±0.51分钟;(2)作为对戊巴比妥钠给药的反应,急剧升高发生在给药后0.50±0.37分钟,即给药后2.89±0.74分钟,然后在第二次夹闭时为2.39±0.71分钟;(3)体温每降低1℃,急剧升高发生的时间延迟0.29±0.05分钟。从缺血期间脑细胞外钾离子浓度的值可以得出结论,低温是保护缺血性脑组织的主要因素;同时,戊巴比妥钠也有显著但稍小的保护作用。