缺血和再灌流对脊髓血流量及运动诱发电位的影响

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。

Effects of ischemia and reperfusion of spinal cord blood flow and spinal motor evoked potentials in rabbits

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.