摘要
本文采用家兔失血性休克模型,使血压下降至30mmHg维持30min后再灌流,让血压回升到正常范围。观察缺血再灌流期 SCBF和 SEP变化。缺血期平均动脉压 30~40mmHg,脊髓 T12及Ll节段灰质血流量减少57%~64%,白质血流量减少32%~50%;SMEP的潜伏期明显延长(P<0.001),各波的波幅降低并有25%~67%的波幅消失。再灌流期当血压回升到90~130mmHg时,灰质血流量仍低于伤前(P<0.01),白质血流量无显著差异.SMEP潜伏期仍明显延长(P<0.05),除Pl波波幅下降有统计意义外,其它各波幅无差异,波幅消失占25%~33.3%。光镜下见脊髓存在损伤性病理变化,显示缺血再灌流后脊髓组织仍然存在继发缺血性病理损害和神经功能障碍。
In hemorrhage shock rabbits model, the mean arterial pressure (MAP) was reduced to 30 mmHg for 30 min, and recovered to normal level by reperfusion. At 30-40 mmHg of MAP, the gray and white spinal cord blood flow (SCBF) reduced by 57%-64% and 32%- 50% respectively. The peak latencies of spinal motor evoked potentials (SMEP) delayed significantly (P<0. 01) and amplitude decreased by 25%-67%. After reperfusion, the MAP returned to normal, the SCBF and SMEP didn' t recover. The pathological changes of spinal cord demonstrated that ischemia-reperfusion producing the secondary ischemic injury and. neural disfuction.
出处
《中国脊柱脊髓杂志》
CAS
CSCD
1992年第6期261-264,共4页
Chinese Journal of Spine and Spinal Cord
关键词
缺血
诱发电位
脊髓
再灌注损伤
Ischemia
Reperfusion injury
Spinal cord blood flow
Spinal motor evoked potentials
Mean arteral pressure