Saito R, Kawase T, Toya S, Koga K, Miura I
Department of Neurosurgery, Keio University, School of Medicine, Tokyo, Japan.
Neurol Res. 1992 Dec;14(5):411-6. doi: 10.1080/01616412.1992.11740095.
We have previously developed a reproducible model of transient forebrain ischaemia in rats by bilateral carotid artery occlusion combined with temporary increase of ICP. With this model, reversibility of the energy metabolism and intracellular pH (pHi) was investigated by 31P-MRS during 120 min of recirculation in three groups of, respectively, 30, 60, and 120 min of ischaemia. With the induction of ischaemia, ATP and phosphocreatine (PCr) disappeared, and measurement of pHi showed severe acidosis in all rats. In the 30 min ischaemia group, both energy metabolism and pHi recovered almost completely. In the 60 min ischaemia group, ATP recovered to 74% of control values, but pHi showed full recovery. In the 120 min ischaemia group, ATP recovered to about 50% of control values, and recovery of pHi was variable. Showing logarithmical changes during recirculation in ATP and PCr, the rate of metabolic recovery was fast during 60 min of recirculation, but it decreased and reached plateau thereafter in all groups. Recovery of pHi was affected by ATP levels, and was precipitously accelerated as ATP levels exceeded 50% of pre-ischaemic values. These results suggest that prolongation of the duration of ischaemia limits the restoration of the energy state, and the quality of pHi recovery after cerebral ischaemia is affected by the degree of ATP recovery during 60 min of recirculation.
我们之前通过双侧颈动脉闭塞并临时增加颅内压,建立了一种可重复的大鼠短暂性前脑缺血模型。利用该模型,在三组分别经历30分钟、60分钟和120分钟缺血的大鼠再灌注120分钟期间,通过31P - MRS研究了能量代谢和细胞内pH值(pHi)的可逆性。随着缺血的诱导,ATP和磷酸肌酸(PCr)消失,并且pHi测量显示所有大鼠均出现严重酸中毒。在30分钟缺血组中,能量代谢和pHi几乎完全恢复。在60分钟缺血组中,ATP恢复至对照值的74%,但pHi显示完全恢复。在120分钟缺血组中,ATP恢复至对照值的约50%,pHi的恢复情况各不相同。ATP和PCr在再灌注期间呈对数变化,所有组在再灌注60分钟期间代谢恢复速率很快,但此后下降并达到平台期。pHi的恢复受ATP水平影响,当ATP水平超过缺血前值的50%时,pHi恢复急剧加速。这些结果表明,缺血持续时间的延长限制了能量状态的恢复,并且脑缺血后pHi恢复的质量受再灌注60分钟期间ATP恢复程度的影响。