尼卡地平控制性降压对家犬脊髓诱发电位的影响

目的观察尼卡地平控制性降压对家犬脊髓诱发电位（SCEPs）的影响，探讨脊柱手术麻醉中尼卡地平控制性降压的安全性。方法成年杂种犬6只，体重12．0～15．5kg，用2．5o,4硫喷妥钠行麻醉诱导并维持麻醉。股动脉置管监测MAP。以尼卡地平8μg·kg^-1·min^-1持续静脉注射进行控制性降压，降压标准为基础MAP的40％。以日本光电诱发电位监测仪测定SCEPs。结果MAP平均下降幅度为42．9％，控制性降压后体感诱发电位（SEP）波幅及运动诱发电位（MEP）波幅差异无统计学意义。结论尼卡地平控制性降压对SCEPs影响较小，可安全用于脊髓手术。     

脊髓急性牵拉损伤动物模型机理研究

目的对犬脊髓(神经根)急性牵拉损伤的病理机制进行初步探讨。方法12只健康成年杂种犬，随机分为对照组和不同程度牵拉损伤组。前后路联合手术离断脊柱后施加纵向牵拉损伤，对牵拉应变率、体感诱发电位(SEP)、神经源性脊髓运动诱发电位(NMEP)、硬膜下压力(SP)、硬膜血流量(EBF)等进行持续观察。伤后取脊髓及神经根标本进行HE、髓鞘神经中丝(NF)及胶原纤维酸性蛋白(GFAP)抗体免疫组织化学染色及电镜超微结构观察。结果牵拉损伤涉及牵拉节段和其上下脊髓及神经根的损伤。牵拉后出现硬膜下压力的显著增高和硬膜血流的显著降低。SEP异常的出现较NMEP更早。结论牵拉后脊髓内压力的增加导致脊髓血流减少。以及直接的机械性牵拉损伤可能是脊髓牵拉损伤的重要机制。     

脊髓损伤后早期减压对诱发电位影响的实验研究

[目的]观察脊髓损伤后早期减压对体感诱发电位及经颅磁刺激运动诱发电位的影响，以探讨诱发电位在判断手术时机及预后中的应用价值。[方法]日本大耳兔32只随机分4组。A组为对照组，不造成脊髓损伤。B、C、D组为脊髓损伤组。对每组动物于不同时间分别检测SEP、MEP。分析波形的潜伏期、峰问波幅。用后肢的Tarlov分级法作伤后运动功能评分。取脊髓标本，行组织学观察。[结果]随着脊髓压迫时间的延长，SEP、MEP的潜伏期逐渐延长，波幅逐渐减小．波幅变化较潜伏期更为敏感。在恢复过程中，脊髓受压时间越短，诱发电位恢复越早。潜伏期恢复早于波幅，而且SEP恢复早于MEP，MEP的恢复早于功能评分。[结论]SEP与TMS-MEP对脊髓损伤十分敏感，能较早反映脊髓损伤程度，可用于指导临床手术治疗和判断预后。     

兔脊髓分级缺血-再灌注损伤对体感诱发电位的影响

目的 了解不同程度脊髓缺血-再灌注损伤与体感诱发电位（SEP）、神经功能评分及脊髓病理改变的关系。方法 将40只新西兰大耳白兔随机均分为4组，假手术组、缺血30min组、缺血45min组和缺血60min组。采用腹主动脉阻断法建立兔脊髓缺血-再灌注损伤模型，分别于缺血前、缺血5、10min、再灌注15、30min、1、2、24和48h监测SEP。于再灌注6、12、24和48h进行神经功能评分，再灌注48h进行脊髓病理学观察。结果 阻断腹主动脉血流30、45和60min后开放分别表现为轻、中、重度缺血-再灌注损伤脊髓的病理学改变特点。脊髓轻度缺血-再灌注损伤中SEP波幅和潜伏期分别于再灌注15和30min时恢复至缺血前水平（P〉0．05）；脊髓中度缺血-再灌注损伤中SEP波幅和潜伏期分别于再灌注30min和再灌注1h恢复至缺血前水平（P〉0．05）；脊髓重度缺血-再灌注损伤中SEP波幅和潜伏期分别明显下降和延长，与其他各组组间比较差异有统计学意义（P〈0.01）。各组神经功能评分组间比较差异均有统计学意义（P〈0. 01）。结论 脊髓缺血-再灌注损伤中SEP波幅较潜伏期恢复迅速。术中SEP监测能够敏感而准确地反映缺血-再灌注损伤中脊髓功能的变化，可为临床应用提供实验依据。     

体感诱发电位在椎管内占位显微手术中的监测

目的 评价体感诱发电位(SEP)在神经外科脊髓疾病显微手术中的监测作用，避免或减少医源性脊髓损伤。方法 28例病人行术前、术中EP全程监测，包括脊髓EP(SSEP）及皮层SEP(SSEP)，术中及时把监测信息反馈给术者。并将术中监测结果与术后疗效对照分析。结果 椎管内占位手术在行髓内肿瘤切除时最易引发EP波幅降低及潜时延长。术中监测按Frankel分级D、E级患者波幅较基准电位下降不超过50％，潜伏期延长不超过7％；B、C级患者波幅较基准电位下降不超过40％；潜伏期延长不超过5％。术后不会引起脊髓功能不可逆损害。结论 脊髓手术时行EP和SSEP联合监测可及时反映出脊髓功能的变化，提高术者术中操作的安全性，避免或减少术后并发症。     

兔颈髓牵张性损伤早期脊髓血流变化及其对运动诱发电位的影响

目的 :观察颈髓牵张性损伤早期脊髓血流的变化 ,并探讨其对运动诱发电位 (motorevokedpotentials ,MEP)的影响。方法 :构建兔颈髓牵张性损伤模型 ,应用激光多普勒血流仪监测C5～ 6段脊髓血流 (spinecordbloodflow ,SCBF) ,并同时观察运动诱发电位的变化。结果 :随着颈髓牵张程度的不断加重 ,血流呈进行性下降 ,而当脊髓微血管自我调节能力丧失时则SCBF不能恢复。颈髓牵张性损伤后MEP波幅及潜伏时均有明显的变化。结论 :颈髓血流量的下降与牵张程度呈正相关 ,是继发性脊髓神经功能障碍的基础 ,是脊髓牵张性损伤的早期指标。MEP能反映脊髓运动神经功能的改变 ,与SCBF的下降和脊髓病理学改变呈一致性     

牵张性脊髓损伤脊髓SCEP监护作用的实验研究

目的：探讨脊髓皮层诱发电位对牵张性脊髓损伤的监护作用。方法：选用４０只健康大白兔，随机分成对照组（Ａ组）、体感皮层诱发电位（ＳＣＥＰ）波幅下降３０％组（Ｂ组）、ＳＣＥＰ波幅下降５０％５ｍｉｎ组（Ｃ组）和１０ｍｉｎ组（Ｄ组）。通过对脊髓ＳＣＥＰ监测、动物脊髓功能评定、组织形态学观察以及脊髓微血管铸型扫描电镜观察来研究牵张性脊髓损伤。结果：随着牵开负荷增大和作用时间的延长，脊髓微血管发生充盈缺损、痉挛直至破裂出血；Ｃ组及Ｄ组脊髓功能下降，与Ａ组相比有显著性差异。结论：ＳＣＥＰ波幅变化能较客观地反映脊髓功能状况，波幅下降５０％持续１０ｍｉｎ脊髓将出现不可逆损害     

颈胸椎手术中体感诱发电位监护的影响因素分析及准确性观察

目的探讨体感诱发电位监护在颈、胸椎手术中的应用价值,对其准确性及影响因素进行分析。方法颈、胸椎疾病患者采用皮层体感诱发电位（CSEP）及皮层下体感诱发电位（Sub-CSEP）术中监测,根据麻醉前、后及不同手术阶段体感诱发电位的变化与术后功能相结合,判断体感诱发电位（SEP）的准确性。结果麻醉因素引起的SEP波幅降低主要影响CSEP,双侧刺激均改变,但基本未达到手术预警标准值,而Sub-SEP变化不明显。手术高危操作侵及脊髓,SEP波幅降低主要影响高危操作的同侧,表现为同侧CSEP及Sub—CSEP波幅同时降低,并且降低幅度较大,达到预警标准值,而对侧CSEP及Sub-CSEP波幅变化不甚明显。其他非手术原因如低体温、局部冷盐水冲洗脊髓,引起SEP潜伏期延长,波幅变化不明显。失血过多致平均动脉压降低可引起SEP波幅降低,潜伏期变化不明显。局部低温及低血压引起的SEP改变,均未达到预警标准值。结论颈、胸椎手术中采用体感诱发电位监测排除各种干扰,可较准确地反映脊髓的生理或病理状况。     

体感诱发电位在建立双节段脊髓压迫模型中的作用

目的通过研究兔胸椎管形态结合体感诱发电位(SEP)建立一种胸椎双节段脊髓慢性压迫模型。方法首先对兔新鲜胸椎标本作详细的解剖学研究,选定2F Fogarty球囊导管作为压迫模型所用的球囊。成年新西兰大白兔30只,随机分为对照组(球囊不扩张)、40μl压迫组、50μl压迫组。通过T_6、T_7椎板的小孔,将导管置入硬膜外腔,再分别向头尾端插入到T_3、T_(10)水平。通过皮层SEP、Tarlov's评分、X线片及CT检查、脊髓HE染色评价该模型的可靠性。结果 40μl压迫组T_3脊髓压迫率为(42.81±5.54)%,T10脊髓压迫率为(44.74±5.85)%。50μl压迫组T3脊髓压迫率为(62.52±1.91)%,T_(10)脊髓压迫率为(63.77±2.06)%。球囊扩张后7 d 40μl压迫组SEP开始逐渐恢复,至术后28 d趋于稳定,与压迫后即刻比较SEP的潜伏期明显缩短,波幅增高,差异有统计学意义(P0.05);50μl压迫组术后SEP改变差异无统计学意义(P0.05)。40μl压迫组、50μl压迫组的SEP波幅较对照组明显降低,潜伏期明显延长,差异有统计学意义(P0.05);但40μl压迫组与50μl压迫组间差异无统计学意义(P0.05)。结论 SEP对早期脊髓损伤诊断具有敏感性和特异性,并且能反应脊髓损伤程度。脊髓压迫率为62%~64%的压迫模型的SEP更稳定,模型更可靠。     

脊髓及神经根监测技术在脊柱外科手术中的应用

[目的]应用体感诱发电位（somatosensory evoked potential，SEP）行颈、胸椎手术脊髓监护及应用自发肌电图行腰椎手术神经根监护，对2种电生理检查的方法学、准确性及影响因素进行分析。[方法]颈、胸椎手术采用SEP监测，根据不同阶段SEP的变化与术后功能相结合，判断SEP的准确性。腰椎手术采用自发肌电图监测神经根功能，以判断神经根在术中是否受到牵拉、激惹及刺激。并观察手术中SEP及自发肌电图的影响因素，减少监测假阳性及假阴性的发生。[结果]颈、胸椎手术128例病人中，监护未达到预警标准116例，术后无神经症状加重表现。术中SEP变化达到预警标准8例，及时提醒手术医生，暂停手术操作，7例患者SEP波幅渐恢复，术后无神经症状加重。1例患者因SEP波幅降低时间超过10min未恢复，术后神经症状加重。非手术原因如麻醉、低血压及局部低温对SEP的影响均未达到预警标准。假阴性3例，假阳性1例。腰椎手术40例，12例术中出现肌电反应，及时提醒手术医生，避免过多的刺激及牵拉，术后均未出现神经根损伤症状。[结论]颈、胸椎手术，采用SEP监测，排除各种干扰因素，体感诱发电位可较准确地反应脊髓的生理或病理状况。腰椎手术采用自发性肌电图，在严格控制肌松剂使用下，可准确及时地反应神经根的功能，避免神经根的损伤。     

脊髓纵向压缩过程中脊髓诱发电位,血流量和微循环变化

根据临床上脊往后凸畸形矫正过程中，脊柱截骨缩短后的脊髓受力情况，采用脊柱立体定位仪来调节脊髓的压缩量，设计了大鼠脊髓纵向压缩动物模型，模拟脊往后凸畸形矫正的病理变化．使用末梢循环血流仪（氢清除法）、奥林巴氏生物显微镜及显示系统、 ＳＥＮ３２０１刺激器、 ＡＰＰＬＥⅡ机诱发电位检测系统（硬膜外记录），分别观测了脊髓压缩部位及邻近节段不同压缩量脊髓灰白质血流量、动态微循环、运动诱发电位（ＭＥＰ）、感觉诱发电位（ＳＥＰ），并常规光镜检查．结果表明；大鼠脊髓不可逆性压缩的临界值为６．０ｍｍ，脊髓回缩率为１／２６— ｌ／２３；脊髓监护时ＭＥＰ较ＳＥＰ更敏感地反映脊髓功能，是较理想的监护手段；脊髓压缩过程中主要为瘀血性缺血改变，与目前脊髓牵拉压迫过程中报道的变化有所不同。     

The influence of induced hypotension and spine distraction on canine spinal cord blood flow

Deliberate hypotension is used in scoliosis surgery to reduce the need for blood transfusion and to improve operating conditions. There are concerns, however, that hypotension may decrease spinal cord blood flow (SCBF) and thereby predispose the spinal cord to ischemic injury, particularly when it is distracted during Harrington instrumentation. In a canine model, the mean arterial pressure (MAP) was reduced to 50% of the normotensive value with sodium nitroprusside and halothane to study its effects, with and without spinal distraction, on spinal cord blood flow measured by the hydrogen clearance technique. The induction of systemic hypotension resulted in a significant decrease in spinal cord blood flow from 15.7 +/- 1.1 ml/min/100 g (control) to 10.7 +/- 4.7 ml/min/100 g. This initial decrease in spinal cord blood flow returned to normotensive values by 35 minutes following the induction of hypotension, suggesting an autoregulatory effect. This indicates that the induction of deliberate hypotension to half its normotensive mean arterial pressure is associated with a significant decrease in spinal cord blood flow that returns to normotensive levels by 35 minutes. One and two centimeters of longitudinal distraction applied during systemic hypotension did not reduce spinal cord blood flow when it was applied at least 45 minutes after the hypotension was induced. Thus, when longitudinal stretch of a magnitude approximating that used clinically during Harrington instrumentation is applied in the presence of systemic hypotension, the normal SCBF is not reduced when the autoregulating system is functioning.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effet de l''administration continue de nimodipine à la phase aiguë d''un traumatisme médullaire chez le babouin

This study was carried out to assess the putative improvement of spinal cord blood flow obtained with a calcium channel blocker after acute spinal cord injury in ten baboons. The injury was generated by compressing the cord at L1 level for 5 seconds with a balloon catheter inflated to 2 bars with Ringer's solution. Subsequently, five monkeys received a saline infusion, and five others a nimodipine infusion (0.04 mg.kg-1 x h-1), for seven days. Spinal cord blood flow (SCBF) was measured using a scanographic technique with stable xenon. Somatosensory evoked potentials (SEP), magnetic resonance imaging (MRI) and a histological study of the spine were carried out a different times of the study. SCBF and SEP were recorded before injury. Thereafter SCBF was measured every thirty minutes during the four hours following the injury, as well as on day 7. SEP and MRI were recorded on days 1 and 7. The histological study was carried out on the eighth day. Three spinal cord and vertebral segments were collected, fixed, sliced and stained. SCBF before injury was not significantly different in either group (39.8 +/- 15.9 ml x 100 g-1 x min-1 for the treatment group 40.9 +/- 16.3 ml x 100 g-1 x min-1 for the control group). During the injury, there were major variations between animals. The results were expressed as percentages of each animal's control SCBF (before injury). Immediately after injury, SCBF increased in both groups. However, in the control group, SCBF decreased more than in the treatment group on the seventh day after injury (80 to 90% vs 25 to 50%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

TRH对大鼠脊髓损伤后SCBF和SEP的影响

脊髓损伤（ＳＣＩ）后内源性阿片肽释放，并参与脊髓的继发损伤机制。ＴＲＨ可阻断阿片肽的自主神经效应，而不影响痛觉。本实验探讨大剂量ＴＲＨ（２ｍｇ／ｋｇ／ｈ）治疗对大鼠脊髓打击伤（Ａｌｌｅｎｓ法１０ｇｘ５ｃｍ）后脊髓血流量（ＳＣＢＦ）和脊髓诱发电位（ＳＥＰ）的影响。脊髓损伤后１ｈ，ＳＣＢＦ开始显著下降，持续至伤后２４ｈ，ＳＥＰ峰潜时呈进行性延长趋势；伤后即刻静脉注射ＴＲＨ（２ｍｇ／ｋｇ／ｈ，共５次），可使伤后即刻和２４ｈ的ＳＣＢＦ显著升高，并使伤后ＳＣＢＦ下降时间延迟３ｈ，同时ＳＥＰ峰潜时有不同程度改善。结果表明，ＴＲＨ对受伤脊髓早期有一定的防治作用，并具有一定的后发效应；同时也可促进脊髓的神经传导功能。本文亦对ＴＲＨ治疗ＳＣＩ的病理生物学机制进行了讨论。     

The influence of trimethaphan (Arfonad)-induced hypotension with and without spine distraction on canine spinal cord blood flow

Controlled hypotension is used in scoliosis surgery to reduce the need for transfusion and to improve operating conditions, but there is concern that deliberate hypotension may decrease spinal cord blood flow (SCBF) and predispose the spinal cord to injury, particularly when it is distracted during Harrington instrumentation. To study the effect of deliberate hypotension on SCBF, the mean arterial pressure (MAP) was reduced to 50% of its normotensive value with trimethaphan (Arfonad) in dogs and the SCBF measured using the hydrogen washout technique with and without spine distraction. The SCBF was significantly reduced to half its normotensive value of 23.2 ml/min/100 gm to 11.4 ml/min/100 gm after hypotension was established. The SCBF remained significantly decreased compared with controls when measured at 30, 45, and 60 minutes following the induction of hypotension and also when hypotension was terminated. SCBF was not further reduced when 2 cm of spine distraction was added. These results show that induction of hypotension with trimethaphan is associated with a similar decrease in SCBF, which is maintained as long as the drug is used and that this effect continues after the drug is terminated and the MAP increases. Cautiously extrapolating these findings clinically would suggest that trimethaphan may not be the drug of choice for controlled hypotension during scoliosis surgery, despite its apparently favorable hemodynamic and hormonal responses.     

Successful improvement of blood pressure, cardiac output, and spinal cord blood flow after experimental spinal cord injury

Thirty-seven rats were anesthetized and ventilated and had continuous monitoring of mean systemic arterial pressure (MSAP) and central venous pressure (CVP). The animals underwent a 60-g clip compression injury at T-1 for 1 minute. Fifteen minutes after injury, microspheres were used to measure cardiac output (CO) and spinal cord blood flow (SCBF). Each animal was then randomized into one of five groups. Four groups received intravenous infusions for 1 hour each of 5% albumin, autologous packed cells, low molecular weight dextran, or autologous whole blood to maintain the MSAP. The fifth group served as a control group and received an infusion of normal saline. Seventy-five minutes after injury, CO and SCBF were measured. The posttraumatic reduction in CO was significantly improved by all four treatment infusions. However, only autologous whole blood and dextran successfully reversed the posttraumatic hypotension. Dextran significantly elevated the CVP (P less than 0.01) and reduced the hematocrit (P less than 0.01). Whole blood improved SCBF in all segments of the spinal cord by nearly 100% (P less than 0.05), and dextran increased SCBF by 200% (P less than 0.01). Thus, the most marked improvements in MSAP, CO, and SCBF were produced by hypervolemia and hemodilution associated with dextran infusion. The therapeutic implications of this reversal of local and systemic changes in acute spinal cord injury are discussed.     

Further studies of nimodipine in experimental spinal cord injury in the rat.

Previously in our laboratory, nimodipine was effective in reversing posttraumatic ischemia and promoting electrophysiologic recovery in a rat spinal cord injury (SCI) model. However, these beneficial effects were achieved when nimodipine was combined with adjuvant therapy to reverse posttraumatic hypotension, by either volume expansion or vasopressor therapy. The present experiments determined if nimodipine alone can increase spinal cord blood flow (SCBF) and improve function after SCI. The hydrogen clearance technique was used to measure SCBF, and motor and somatosensory evoked potentials (MEP and SSEP) were used to quantitate electrophysiologic function. SCBF, MEP, and SSEP were recorded before and after a 52 g clip compression injury at the T1 segment and then repeated after a 35 minute infusion of nimodipine. Twenty-five rats were allocated randomly to five equal groups, each of which received 35 minute infusions of one of the following doses of nimodipine: (1) 0 mg/kg, (2) 0.005 mg/kg, (3) 0.01 mg/kg, (4) 0.025 mg/kg, or (5) 0.05 mg/kg. SCBF decreased after injury in all groups, and there was no increase in SCBF after nimodipine infusion in any group. MEP and SSEP were abolished by the injury in all rats, and there was no recovery of the evoked potentials in any group. It is concluded that adjuvant therapy for posttraumatic hypotension may be necessary for nimodipine to improve SCBF and promote recovery of function in the injured spinal cord.     

钙调素拮抗剂对大鼠脊髓损伤的作用及意义

目的观察钙调素（ＣａＭ）特异性拮抗剂三氟啦嗪（ＴＦＰ）对脊髓损伤（ＳＣＩ）的影响,探讨ＣａＭ在ＳＣＩ病理机制中的作用。方法采用氢清除法、斜板试验和电生理技术,以６４只大鼠为实验对象观察ＴＦＰ对ＳＣＩ后脊髓血流量（ＳＣＢＦ）、运动功能和诱发电位（ＭＥＰ）的影响。结果在肾上腺素维持系统动脉压的条件下,ＴＦＰ可明显改善ＳＣＩ后ＳＣＢＦ、ＭＥＰ和运动功能。结论ＣａＭ拮抗剂对ＳＣＩ具有保护作用,ＣａＭ可能是参与ＳＣＩ病理机制的重要因素     

Effect of hemorrhagic shock upon spinal cord blood flow and evoked potentials

Although somatosensory evoked potentials are being used in the evaluation of spinal cord injury and the monitoring of cord function during surgical procedures, their limitations in the face of fluctuations in blood pressure await further clarification. To study the effect of hypotension upon spinal cord blood flow (SCBF) and spinal evoked potentials (SEPs), we subjected five anesthetized lambs to graded hypotension to a mean arterial pressure (MAP) of 80, 60, 40, and less than or equal to 30 mm Hg. Five animals served as controls. Maximal hypotension was associated with a significant decrease in renal and sciatic nerve blood flow of 83% and 77%, respectively. SCBF, on the other hand, showed no decrease with hypotension down to a MAP of 40 mm Hg. As hypotension progressed, a gradual but significant slowing in nerve conduction velocity was noted without alteration in the cord conduction velocity from L7 to L1. Control animals demonstrated a decline in sciatic nerve blood flow of 48%, without any change in latency or amplitude of nerve action potentials. These findings suggest that, in hypotension, the peripheral nerve (lacking autoregulation) becomes ischemic, resulting in slowing of nerve conduction velocity with an increase in latency and decrease in amplitude of SEPs. Cord conduction velocity, on the other hand, remains unchanged. Caution is advised in relying upon SEPs generated by peripheral nerve stimulation to monitor cord function in situations where profound hypotension is anticipated. Variations in SEPs may reflect alterations in the peripheral nerve and not the spinal cord.