Olmarker K
University of Göteborg, Department of Anatomy, Sweden.
Acta Orthop Scand Suppl. 1991;242:1-27.
A model for experimental studies of acute, graded compression of the cauda equina in pigs was presented (Olmarker et al. 1991a). Detailed analyses of the neural and vascular anatomy demonstrated a close resemblance to the human cauda equina. There were structural and vascular differences between spinal nerve roots and peripheral nerves that could contribute to differences in compression susceptibility between these two parts of the nervous system. The pressure transmission from the balloon to the nerve roots showed to have a high accuracy. The occlusion-pressures for the arterioles, capillaries and venules of the cauda equina were determined (Olmarker et al. 1989a). Arteriolar blood flow was stopped at a pressure close to the mean arterial blood pressure. Capillary blood flow was found to be dependent upon flow in the connected venules. The blood flow in some venules was found to be stopped at 5-10 mm Hg. However, venular occlusion pressures ranged from 5 to 60 mm Hg. Compression up to 200 mm Hg for 2 hours did not induce a "no-reflow" phenomenon when the compression was ended. However, a transient hyperemia was noted at all pressure/time relations studied, indicating nutritional deficit in the compressed segment during compression. Signs of edema were seen in nerve roots exposed to compression for 2 hours at either 50 or 200 mm Hg. The nutritional supply to the cauda equina was found to be impaired at low pressure levels (less than 10 mm Hg; Olmarker et al. 1990a). Diffusion from adjacent tissues with a better nutritional supply, including the cerebrospinal fluid, could thus not compensate completely for compression-induced effects on the transport of nutrients. However, a certain nutritional supply to the compressed segment was present even at 200 mm Hg compression. There were more pronounced effects on the nutritional supply induced by a rapid (0.05-0.1 sec.) than a slow (20 sec.) compression onset rate. Nutritional impairment was noted both within and outside the compressed nerve segment. An increase in vascular permeability was induced by compression at 50 mm Hg for 2 minutes (Olmarker et al. 1989b). The magnitude of this permeability increase was dependent on both the magnitude and the duration of compression. The permeability increase was more pronounced for the rapid than for the slow compression onset rate at all pressure/time relations studied. Reduction of muscle action potential (MAP) amplitude in tail muscles, after stimulation cranial to the compression zone, was induced by compression at 100 and 200 mm Hg for 2 hours (Olmarker et al. 1990b).(ABSTRACT TRUNCATED AT 400 WORDS)
介绍了一种用于猪马尾急性分级压迫实验研究的模型（奥尔马克等人，1991a）。对神经和血管解剖结构的详细分析表明，其与人类马尾非常相似。脊神经根和周围神经在结构和血管方面存在差异，这可能导致神经系统这两个部分在压迫易感性上存在差异。从球囊到神经根的压力传递显示具有很高的准确性。确定了马尾小动脉、毛细血管和小静脉的闭塞压力（奥尔马克等人，1989a）。小动脉血流在接近平均动脉血压的压力下停止。发现毛细血管血流依赖于相连小静脉中的血流。发现一些小静脉中的血流在5 - 10毫米汞柱时停止。然而，小静脉闭塞压力范围为5至60毫米汞柱。当压迫结束时，高达200毫米汞柱持续2小时的压迫并未诱发“无复流”现象。然而，在所研究的所有压力/时间关系中均观察到短暂性充血，表明压迫期间受压节段存在营养缺乏。在50或200毫米汞柱下暴露于压迫2小时的神经根中可见水肿迹象。发现低压力水平（低于10毫米汞柱；奥尔马克等人，1990a）时马尾的营养供应受损。因此，来自营养供应较好的相邻组织（包括脑脊液）的扩散不能完全补偿压迫对营养物质运输的影响。然而，即使在200毫米汞柱的压迫下，受压节段仍存在一定的营养供应。快速（0.05 - 0.1秒）压迫起始速率比缓慢（20秒）压迫起始速率对营养供应的影响更明显。在受压神经节段内外均观察到营养损害。在50毫米汞柱下压迫2分钟可诱导血管通透性增加（奥尔马克等人，1989b）。这种通透性增加的幅度取决于压迫的幅度和持续时间。在所研究的所有压力/时间关系中，快速压迫起始速率比缓慢压迫起始速率引起的通透性增加更明显。在压迫区颅侧进行刺激后，100和200毫米汞柱压迫2小时可诱导尾部肌肉动作电位（MAP）幅度降低（奥尔马克等人，1990b）。（摘要截断于400字）
