Jacobs T P, Kempski O, McKinley D, Dutka A J, Hallenbeck J M, Feuerstein G
National Institutes of Health, Bethesda, Md.
Stroke. 1992 Mar;23(3):367-73. doi: 10.1161/01.str.23.3.367.
Delayed deterioration of neurological function after central nervous system ischemia is a well-documented clinical problem. The purpose of our study was to elucidate the role of spinal cord blood flow and spinal cord-blood barrier integrity in the evolution of delayed neurological deterioration after transient spinal cord ischemia in rabbits.
Anesthetized rabbits were subjected to lumbar spinal cord ischemia (25 minutes) and variable periods of reperfusion (30 minutes to 48 hours after ischemia). Regional spinal cord blood flow was monitored by carbon-14-labeled iodoantipyrine autoradiography; vascular permeability was assessed by quantitative microhistofluorescence of Evans blue-albumin in frozen sections of spinal cord. Hindlimb motor function was assessed by standard scoring system and tissue edema by wet/dry weight method.
Hindlimb motor function indicated complete paralysis during ischemia and partial gradual recovery upon reperfusion (up to 8 hours), followed by progressive deterioration to severe deficits over 48 hours. Severe vascular permeability disruption was noticed early (30 minutes) after reperfusion, but almost complete recovery reestablished at 8 hours was followed by a secondary progressive increase in vascular permeability. Blood flow was reduced by 20-30% (p less than 0.01) 4 hours after ischemia in the gray matter, but hyperemia (200-300%, p less than 0.01) was observed 12-24 hours after ischemia. Spinal cord water content increased by 5.7% (p less than 0.05) 24 hours after ischemia.
This study demonstrates that delayed neurological and motor deterioration after spinal cord ischemia is associated with severe progressive breakdown of spinal cord-blood barrier integrity that develops late (hours) after the injury. Our data suggest that no ischemic insult in early or late reperfusion is associated with delayed motor deterioration.
中枢神经系统缺血后神经功能的延迟恶化是一个有充分文献记载的临床问题。我们研究的目的是阐明脊髓血流和脊髓血脑屏障完整性在兔短暂性脊髓缺血后延迟神经功能恶化演变过程中的作用。
对麻醉的兔进行腰段脊髓缺血（25分钟）及不同时长的再灌注（缺血后30分钟至48小时）。通过碳-14标记的碘安替比林放射自显影术监测脊髓局部血流；通过对脊髓冰冻切片中伊文思蓝-白蛋白进行定量显微组织荧光分析评估血管通透性。采用标准评分系统评估后肢运动功能，通过湿/干重法评估组织水肿情况。
后肢运动功能显示在缺血期间完全麻痹，再灌注时（长达8小时）部分逐渐恢复，随后在48小时内逐渐恶化至严重功能缺损。再灌注后早期（30分钟）即出现严重的血管通透性破坏，但在8小时时几乎完全恢复，随后血管通透性再次逐渐增加。缺血4小时后灰质血流减少20%-30%（p<0.01），但缺血12-24小时后出现充血（200%-300%，p<0.01）。缺血24小时后脊髓含水量增加5.7%（p<0.05）。
本研究表明，脊髓缺血后延迟的神经和运动功能恶化与脊髓血脑屏障完整性的严重进行性破坏有关，这种破坏在损伤后较晚时间（数小时）出现。我们的数据表明，早期或晚期再灌注时的缺血性损伤均与延迟的运动功能恶化无关。
