Hargadine J R, Branston N M, Symon L
Stroke. 1980 Nov-Dec;11(6):637-42. doi: 10.1161/01.str.11.6.637.
The relationship between central conduction time (CCT) and levels of regional blood flow were studied in 9 primates. Flows were recorded in both hemispheres using the method of hydrogen (2 min) clearance. The somatosensory evoked potentials were recorded over the contralateral cortex and the dorsal columns, following median nerve stimulation. The CCT, a measure of the brain's electrical conduction, was determined by the difference in latencies between N10, (the arrival of the afferent volley at the sensory cortex) and N7 (its arrival at the dorsal column). Ischemia was produced by transorbital occlusion of the right middle cerebral artery. In the acute ischemic phase within 5 minute of occlusion, there was a significant correlation between the change in CCT and the decrease in flow. In the later occlusive phase, the CCT was unaltered with flows above 15 ml/100g/min. Below that level smaller decreases in flow resulted in progressively larger changes in CCT until a flow was reached where the N10 disappeared or the entire cortex was electrically silent. Focal ischemia had no effect on the first positive deflection recorded from the cortex (P8) or the first negative peak response from the cervical region (N7). However, the latency of P8 was increased or it was absent with the introduction of hypotension, while N8 was unaltered. From our measurements, it appears that prolongation of CCT can be related to developing ischemia, and that the thresholds for change are not dissimilar to those already recorded for somatosensory evoked responses to the basis of amplitude alterations in the cortex. Below these levels, prolongation of CCT appears to bear a parametric relationship to alteration in blood flow. While the measurement displays only one of the many alterations which are induced by ischemia in the brain, its attraction lies in its simplicity and in the fact that it may be applied with relative ease in the clinical situation. Under these circumstances, it appears to be an adequately sensitive monitor of developing brain ischemia, and deserves further study.
在9只灵长类动物中研究了中枢传导时间(CCT)与局部血流量水平之间的关系。使用氢清除法(2分钟)记录了双侧半球的血流量。在正中神经刺激后,在对侧皮层和背柱记录体感诱发电位。CCT是衡量大脑电传导的指标,由N10(传入冲动到达感觉皮层)和N7(到达背柱)潜伏期的差异确定。通过经眶阻断右大脑中动脉产生局部缺血。在阻断后5分钟内的急性缺血期,CCT的变化与血流量的减少之间存在显著相关性。在后期阻塞阶段,当血流量高于15 ml/100g/min时,CCT未发生改变。低于该水平,血流量的较小减少会导致CCT逐渐发生更大的变化,直到达到N10消失或整个皮层电静息的血流量水平。局灶性缺血对从皮层记录的第一个正向偏转(P8)或颈部区域的第一个负向峰值反应(N7)没有影响。然而,引入低血压后P8的潜伏期延长或消失,而N8未改变。根据我们的测量结果,似乎CCT的延长可能与缺血的发展有关,并且变化阈值与基于皮层振幅改变的体感诱发电反应中已经记录的阈值没有差异。低于这些水平,CCT的延长似乎与血流量的改变呈参数关系。虽然该测量仅显示大脑缺血诱导的众多变化之一,但它的吸引力在于其简单性以及可以相对容易地应用于临床情况这一事实。在这些情况下,它似乎是发展中的脑缺血的一个足够敏感的监测指标,值得进一步研究。