应用激光多普勒血流仪监测兔急性脊髓缺血损伤后腰髓血流动力学变化及病理学观察的研究

Hemodynamic and Pathological Changes after Acute Ischemic Spinal Cord Injury in Lumbar Spinal Cord in the Rabbit

目的：应用激光多普勒血流仪监测兔脊髓缺血再灌流后腰髓血流的动态性变化，讨论腰髓血流的动力学特点。方法：通过阻断腹主动脉，造成脊髓腰尾段缺血。按缺血和再灌流各时间段分别连续测定腰髓血流变化。取缺血前、缺血４０分钟、再灌流４小时局部脊髓行组织病理和透射电镜检查。结果：在缺血４０分钟腰髓局部血灌流量迅速下降至基线值的－８１．５７％（Ｐ值＝２．０１Ｅ－１７）。再灌流时，局部血流迅速增高并超过基线水平。再灌流１０分钟，局部血灌流量与基线的百分比变化值为５７．９８％（Ｐ值＝３．３Ｅ－０７）。随后逐渐降低，再灌流１小时后，局部血灌流量基本恢复基线水平（３．９７％，Ｐ值＝０．５５７８９９）。以后血灌流量低于基线水平，出现缺血后延迟性低灌流。直至再灌流４小时（－２３．５％，Ｐ值＝１．８４Ｅ－０３）低灌流保持相对稳定，血流未见恢复。缺血４０分钟，有明确病理学改变；再灌流４小时后，病理学改变明显进一步加重。结论：上述结果对于脊髓缺血性损伤后继发性功能障碍提供了理论依据。

Objective: Hemodynamic changes in the lumbal spinal cord caused by ischemia_reperfusion were measured in anesthetized rabbits by Laser_Doppler flowmetry, and the hemodynamic features of lumbar spinal cord blood flow (SCBF) were clarified. Method: Occlusion of the abdominal aorta produces lumbosacral spinal cord ischemia. Hemodynamic changes in the lumbal spinal cord were measured according to events of ischemia_reperfusion. The lumbo_sacral cord tissue block was rapidly dissected for the examination of histopathology and transmission electron microscopy according to preischemia, 40 min of ischemia and 4h of reperfusion respectively. Results: The lumbar local SCBF decreased rapidly to - 81.57% (P=2.01E- 17), percentage changes of the mean baseline value, after 40 min of ischemia. The onset of reperfusion, the SCBF increased rapidly and exceed the baseline level. The SCBF was 57.98% (P=3.3E- 07) of baseline at 10 min of reperfusion. And the local blood perfusion basically recovered baseline level after 1 hour of perfusion (3.97% of baseline, P=0.557899). Afterwards, the SCBF decreased gradually. Up to 4h of reperfusion (- 23.5% of baseline, P=1.84E- 03), the SCBF did not returned to the baseline level. It was found that there were definite injuried changes in pathology after 40 min of ischemia, and the damage went a step further after 4h of reperfusion. Conclusion: The results from this study provide theoretical certification for the secondary dysfunction after the spinal cord ischemic injury.