Dyste G N, Hitchon P W, Girton R A, Chapman M
Department of Surgery, University of Iowa Hospitals and Clinics, Iowa City.
Neurosurgery. 1989 Feb;24(2):228-35. doi: 10.1227/00006123-198902000-00012.
Anesthetized lambs were subjected to epidural cord compression at T13 by means of an epidural balloon distended to 200 mmHg for 80 minutes. Determinations of spinal cord blood flow (SCBF) were made by labelled microspheres prior to and during compression, and then 1/2, 1 1/2, and 2 1/2 hours after compression. Twelve control animals received saline (80 ml/h). Nine animals received hetastarch (a 20 ml/kg bolus followed by an 80 ml/h infusion) and 8 animals received mannitol (a 1 g/kg bolus followed by 1 g/kg/hr). An additional 10 animals received phenylephrine to raise mean arterial pressure by 20 to 40%. Somatosensory evoked potentials (SEPs) were recorded following each determination of SCBF. Animals were killed following determination of the 2 1/2 hour postcompressive flow. The animals treated with either hetastarch or phenylephrine had a postcompressive mean arterial pressure that was significantly greater than that of the controls (P less than 0.01). During treatment, cardiac output in the hetastarch and mannitol animals was significantly greater and hematocrit significantly less than in the controls (P less than 0.05). In spite of these changes, postcompressive SCBF was significantly increased only in those animals treated with phenylephrine (P less than 0.05). Statistical analysis of the relationship between mean arterial pressure and postcompressive SCBF revealed that autoregulation is indeed lost with this experimental model of spinal cord injury. Histological examination of the injured site failed to demonstrate any difference in the area of hemorrhagic necrosis among the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
将麻醉后的羔羊在T13水平通过硬膜外球囊扩张至200 mmHg并维持80分钟，造成硬膜外脊髓压迫。在压迫前、压迫期间以及压迫后1/2小时、1个半小时和2个半小时，用标记微球测定脊髓血流量（SCBF）。12只对照动物接受生理盐水（80 ml/h）。9只动物接受羟乙基淀粉（先静脉推注20 ml/kg，然后以80 ml/h输注），8只动物接受甘露醇（先静脉推注1 g/kg，然后以1 g/kg/h输注）。另外10只动物接受去氧肾上腺素，使平均动脉压升高20%至40%。每次测定SCBF后记录体感诱发电位（SEP）。在测定压迫后2个半小时的血流量后处死动物。接受羟乙基淀粉或去氧肾上腺素治疗的动物，其压迫后的平均动脉压显著高于对照组（P< 0.01）。治疗期间，接受羟乙基淀粉和甘露醇治疗的动物的心输出量显著高于对照组，血细胞比容显著低于对照组（P< 0.05）。尽管有这些变化，但仅接受去氧肾上腺素治疗的动物其压迫后的SCBF显著增加（P< 0.05）。对平均动脉压与压迫后SCBF之间关系的统计分析表明，在这种脊髓损伤实验模型中，自动调节功能确实丧失。对损伤部位的组织学检查未能显示四组之间出血性坏死面积有任何差异。（摘要截断于250字）
