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     

Failure of naloxone to improve spinal cord blood flow and cardiac output after spinal cord injury

It has been reported that the narcotic antagonist, naloxone, can improve spinal cord blood flow (SCBF) and clinical recovery after experimental spinal cord injury produced by the weight-dropping technique. The purpose of the present study was to determine the effect of naloxone on SCBF, cardiac output (CO) and blood flow to other organs following clip compression injury. Rats were anesthetized, paralyzed and ventilated, with mean systemic arterial pressure (MSAP) recorded continuously. After a C-7-T-1 laminectomy and a 1-minute acute compression injury with a 50-g clip at T-1, rats were given injections of radioactive microspheres for measurement of SCBF, CO, and blood flow to other organs. The first determination was made 15 minutes after injury and a second was made after a 1-hour treatment with naloxone. Treated animals each received an intravenous bolus injection of naloxone (10 mg/kg) followed by a 1-hour intravenous infusion (2 mg/kg/hour). Naloxone failed to improve posttraumatic SCBF in the injured spinal cord. In addition, naloxone did not prevent posttraumatic hypotension or the progressive decline in CO seen between 15 and 75 minutes after injury. Thus, this study does not support the previous claims of a beneficial effect of naloxone on posttraumatic SCBF and MSAP.     

缺血和再灌流对脊髓血流量及运动诱发电位的影响

本文采用家兔失血性休克模型，使血压下降至３０ｍｍＨｇ维持３０ｍｉｎ后再灌流，让血压回升到正常范围。观察缺血再灌流期 ＳＣＢＦ和 ＳＥＰ变化。缺血期平均动脉压 ３０～４０ｍｍＨｇ，脊髓 Ｔ１２及Ｌｌ节段灰质血流量减少５７％～６４％，白质血流量减少３２％～５０％；ＳＭＥＰ的潜伏期明显延长（Ｐ＜０．００１），各波的波幅降低并有２５％～６７％的波幅消失。再灌流期当血压回升到９０～１３０ｍｍＨｇ时，灰质血流量仍低于伤前（Ｐ＜０．０１），白质血流量无显著差异．ＳＭＥＰ潜伏期仍明显延长（Ｐ＜０．０５），除Ｐｌ波波幅下降有统计意义外，其它各波幅无差异，波幅消失占２５％～３３．３％。光镜下见脊髓存在损伤性病理变化，显示缺血再灌流后脊髓组织仍然存在继发缺血性病理损害和神经功能障碍。     

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.     

Relation between spinal cord blood flow and functional recovery after blocking weight-induced spinal cord injury in rats

Spinal cord blood flow (SCBF) and motor performance on the inclined plane were measured up to 9 days after a reversible spinal cord compression injury in 49 Sprague-Dawley rats. A load of 35 g on 11 mm2 of the thoracic spinal cord for 5 minutes caused transient paraparesis with a decrease in the capacity angle on the inclined plane from 62 +/- 1 degree (mean +/- SEM) before injury to 33 +/- 1 degree on Day 1, 45 +/- 2 degrees on Day 4, d and 54 +/- 3 degrees on Day 9. SCBF was measured by the [14C]iodoantipyrine method, and in gray matter there was a decrease from 78.4 +/- 2.3 ml/min/100 g of tissue in uninjured animals to 33.7 +/- 1.5 ml/min/100 g of tissue on Day 1 after injury, increasing to 50.1 +/- 2.0 on Day 4 and to 70.5 +/- 2.7 ml/min/100 g of tissue on Day 9. At the corresponding times, the SCBF values in white matter were 14.5 +/- 0.5, 6.7 +/- 0.5, 10.2 +/- 0.6, and 13.4 +/- 0.6 ml/min/100 g of tissue, respectively. The animals in another group were loaded with 25 g for 5 minutes and on Day 1 exhibited a capacity angle of 43 +/- 2 degrees while the SCBF values for gray and white matter were 55.1 +/- 2.0 and 11.1 +/- 0.4 ml/min/100 g of tissue, respectively; thus, the results in this group were similar to the values on Day 4 in the animals loaded with 35 g.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased locoregional blood flow in brain tumors after cervical spinal cord stimulation

OBJECT: Patients with high-grade gliomas have poor prognoses following standard treatment. Generally, malignant brain tumors have a decreased blood flow that results in increased resistance to radiation and reduced delivery of chemotherapeutic agents and oxygen. The aim of the present study was to assess the effect of spinal cord stimulation (SCS) on locoregional blood flow in high-grade tumors in the brain. METHODS: Fifteen patients (11 with Grade III and four with Grade IV brain tumors) had SCS devices inserted prior to scheduled radiotherapy. Both before and after SCS, the patients underwent the following procedures: 1) single-photon emission computerized tomography (SPECT) scanning; 2) middle cerebral artery (MCA) blood flow velocity measurements (centimeters/second) with the aid of transcranial Doppler (TCD) ultrasonography; and 3) common carotid artery (CCA) blood flow volume quantification (milliliters/minute) based on time-domain processing by using color Doppler ultrasonography. The indices demonstrated on SPECT scanning before SCS were significantly lower (p < 0.001) in tumor sites compared with those in peritumoral sites (32%) and healthy contralateral areas (41%). Poststimulation results revealed the following: 1) a mean increase of 15% in tumor blood flow in 75% of patients (p = 0.033), as demonstrated on SPECT scanning: 2) a mean increase of greater than 18% in systolic and diastolic blood flow velocities in both tumorous and healthy MCAs in all but one patient (p < 0.002), as exhibited on TCD ultrasonography; and 3) a mean increase of greater than 60% in blood flow volume in tumorous and healthy CCAs in all patients (p < 0.013), as revealed on color Doppler ultrasonography studies. CONCLUSIONS: Preliminary data show that SCS can modify locoregional blood flow in high-grade malignant tumors in the brain, thus indicating that SCS could be used to improve blood flow, oxygenation, and drug delivery to such tumors and could be a useful adjuvant in chemoradiotherapy.     

Relationship of spinal cord blood flow to vascular anatomy during thoracic aortic cross-clamping and shunting

No satisfactory explanation exists as to why paraplegia occurs despite distal aortic perfusion during thoracic aortic operations. We studied the hemodynamics, paraplegia rate, and spinal cord blood flow with radioactive microspheres in 17 male adult baboons, with particular reference to the arteria radicularis magna. The groups consisted of control animals, subjected to cross-clamping for 60 minutes, and animals with aorto-aortic shunts operational for 60 minutes. There were no significant left ventricular hemodynamic advantages with shunting. Shunting significantly increased lumbar spinal cord blood flow (p = 0.0009), which correlated with the distal aortic mean pressure (r = 0.59, p = 0.008). However, lower thoracic spinal cord blood flow did not increase during shunting (p = 0.2) and did not correlate with the distal aortic pressure (r = 0.11, p = 0.64). This is due to the vascular anatomy of the anterior spinal artery, which was, as in man, smaller above (0.278 mm) than below (0.744 mm) the entry of the arteria radicularis magna. Resistance to flow, as calculated by Poiseuille's equation, was 51.7 times greater up the anterior spinal artery as compared with down this artery. The vascular anatomy explains the absence of paraplegia in one baboon in the cross-clamp group and paraplegia in one baboon in the shunt group. Thus, distal aortic perfusion protects the spinal cord below the arteria radicularis magna but not above it.     

Effect of epidural clonidine on spinal cord blood flow and regional and central hemodynamics in pigs

Epidural clonidine is reported to produce analgesia in humans. To investigate the effect of epidural injection of this alpha 2-adrenoceptor agonist on spinal cord blood flow as well as on regional and central blood flow and hemodynamics, 11 anesthetized pigs were studied. Each pig received clonidine in increments of 3, 10 and 30 micrograms/kg, each dose given in a volume of 5 ml via a lumbar epidural catheter. The tip of the catheter was located in the lumbar epidural space. The microsphere method was used to measure regional circulation. The measurements were made 45 min after each dose. Each pig served as its own control. The lowest dose of epidural clonidine (3 micrograms/kg) did not affect regional blood flow to the spinal cord or to any other organ. The intermediate and high doses were associated with local vasoconstriction in the lumbar and thoracic parts of the spinal cord that produced a statistically significant reduction in flow of 25-35% (P less than 0.05). Blood flow to the brain, cerebellum and the cervical parts of the spinal cord was not significantly changed, nor was renal blood flow. In the adrenal and in skeletal muscles a marked reduction of the blood flow occurred after the high dose, 61% and 78%, respectively. These findings indicate that epidural clonidine 3 micrograms/kg, a dose of clinical interest, is not likely to produce dangerous vasoconstriction in the spinal cord.     

Anatomical changes in human motor cortex and motor pathways following complete thoracic spinal cord injury

A debilitating consequence of complete spinal cord injury (SCI)is the loss of motor control. Although the goal of most SCItreatments is to re-establish neural connections, a potentialcomplication in restoring motor function is that SCI may resultin anatomical and functional changes in brain areas controllingmotor output. Some animal investigations show cell death inthe primary motor cortex following SCI, but similar anatomicalchanges in humans are not yet established. The aim of this investigationwas to use voxel-based morphometry (VBM) and diffusion tensorimaging (DTI) to determine if SCI in humans results in anatomicalchanges within motor cortices and descending motor pathways.Using VBM, we found significantly lower gray matter volume incomplete SCI subjects compared with controls in the primarymotor cortex, the medial prefrontal, and adjacent anterior cingulatecortices. DTI analysis revealed structural abnormalities inthe same areas with reduced gray matter volume and in the superiorcerebellar cortex. In addition, tractography revealed structuralabnormalities in the corticospinal and corticopontine tractsof the SCI subjects. In conclusion, human subjects with completeSCI show structural changes in cortical motor regions and descendingmotor tracts, and these brain anatomical changes may limit motorrecovery following SCI.     

Prevention of spinal cord ischemia after thoracic aortic occlusion

Paraplegia has been a devastating and unpredictable complication following surgical procedures necessitating temporary occlusion of the thoracic aorta. This study was undertaken to investigate the effect of the pressure gradient between the aortic pressure distal to the occlusion and cerebrospinal fluid pressure (CSFP), defined as "Relative spinal cord perfusion pressure" (RSPP) on the development of ischemia to the spinal cord by using somatosensory evoked potentials (SEP). In 30 mongrel dogs, the thoracic aorta just distal to the left subclavian artery was occluded for either 30 or 120 minutes until SEP disappeared. RSPP was maintained at 20, 30 or 40 mmHg in each dog by adjusting the degree of occlusion of th aorta and/or changing CSFP by withdrawal of cerebrospinal fluid or injection of normal saline into the subarachnoid space. SEP were recorded as a cortical response to the electrical stimulation of bilateral peroneal nerves. SEP did not disappear for 30 or 120 minutes when RSPP was 40 mmHg. It would be concluded that 40 mmHg or higher of RSPP is necessary in order to prevent the spinal cord ischemia due to the temporary occlusion of the thoracic aorta.     

R-phenylisopropyl-adenosine increases spinal cord blood flow after intrathecal injection in the rat.

The A1-adenosine receptor agonist, R-phenylisopropyl-adenosine (R-PIA), demonstrated antinociceptive properties in animal studies after intrathecal administration. In the evaluation of a drug for possible spinal injection in humans, the effects of intrathecal R-PIA on spinal cord blood flow (SCBF) were investigated using the laser-Doppler flow-metry technique in anesthetized rats. In low doses (0.1-1 nmol), no change in SCBF was recorded, whereas larger doses (10-100 nmol) caused a significant increase in SCBF. No change in systemic arterial blood pressure could be seen, except for a decrease after administration of the largest dose of R-PIA (100 nmol). It is concluded that R-PIA in doses of 10 nmol and larger induces an increase in SCBF after intrathecal injection in anesthetized rats and that an increase in blood flow is seen before any effect on the systemic circulation is detected. It can also be deduced that the antinociceptive effects of R-PIA after intrathecal injection are not a consequence of spinal ischemia and that disturbances in local blood flow cannot be expected to constitute a neurotoxic factor.     

Response of spinal cord blood flow and motor and sensory evoked potentials to aortic ligation

To produce spinal cord ischemia in the lamb, ligation of the thoracic aorta was performed for 15, 30, and 45 minutes in three animals each. Spinal cord blood flow and motor and sensory evoked potentials were measured before, during, and after aortic ligation. Ischemia with a blood flow of zero during ligation was encountered in the thoracic and lumbar cords, followed by hyperemia upon release of the ligature. Both somatosensory and motor evoked potentials were obliterated during aortic ligation and gradually recovered following resumption of flow. Motor and sensory evoked potentials behaved similarly to high aortic ligation.     

急性脊髓损伤中脊髓血流量与神经功能损害的关系

目的 :观察脊髓损伤 (SCI)后伤段脊髓血流量的动态变化 ,探讨其与脊髓神经功能损害的关系。方法 :Allen′s法致伤大鼠脊髓 ,于伤前和伤后 1、4、8、2 4、72、1 6 8h和 1个月 ,采用氢清除法测量脊髓血流量 ,参照Konrad的方法记录脊髓运动诱发电位 (MEP) ,应用斜板试验评价大鼠的运动功能。结果 :SCI后伤段脊髓血流量明显下降 (P <0 0 5或 0 0 1 ) ,与脊髓MEP的变化和运动功能的损害呈显著相关关系。结论 :脊髓损伤后缺血在脊髓神经功能损害中有重要意义 ,可能是SCI后继发性损伤形成的主要因素之一。     

Control of blood flow in the cat spinal cord

Spinal cord blood flow (SCBF) and the effect of end-tidal CO2 concentration (ETCO2) on SCBF (CO2 reactivity) were studied in the lumbar spinal cord of cats by means of the hydrogen-clearance technique Hydrogen gas was administered by inhalation, and its level in spinal cord tissue was estimated amperometrically with small (75 micrometers) platinum electrodes. The average SCBF's at normocapnia (ETCO2 = 4%) of the ventral horn gray matter and of the white matter at several locations were 43.2 and 16.2 ml . 100 gm-1 . min-1, respectively. For gray and white matter, the values of CO2 reactivity, estimated by the coefficient of the regression of SCBF (ml . 100 gm-1 . min-1) on ETCO2 (ml . 100 ml-1) were 11.6 and 2.1, respectively. No differences in SCBF or CO2 reactivity were observed between intact animals kept under N2O-O2 ventilation and decerebrated animals with no anesthesia. After an acute spinal section, ventral horn SCBF and CO2 reactivity (measured eight segments below the cordotomy) were not altered, in spite of the profound neural depression present (that is, spinal shock). Orthodromic (dorsal root) stimulation of the ventral horn neurons induced an average increase in blood flow of 128% above control values. Antidromic (ventral root) motoneuron activation failed to produce any significant changes in ventral horn blood flow.     

Effects of laminectomy on spinal cord blood flow

The effect of a one-segment (L-2) laminectomy on spinal cord blood flow (SCBF) was determined by the reference sample method using isotope-labeled microspheres. The SCBF was measured before laminectomy (control) and at 15 minutes postlaminectomy with the dura exposed (Series 1), 1 hour postlaminectomy with the laminectomy site closed (Series 2), 24 hours postlaminectomy with the laminectomy site closed (Series 3), and 24 hours postlaminectomy with the dura exposed (Series 4). With the laminectomy site open, SCBF was significantly depressed (22% to 45%) along the entire length of the spinal cord at 15 minutes postlaminectomy. At 1 hour postlaminectomy (with the laminectomy site closed), SCBF approached control values, although areas with significantly lowered flow were still observed in all portions of the spinal cord. By 24 hours postlaminectomy, SCBF had returned to prelaminectomy levels. However, if within 1 hour preceding the 24-hour SCBF measurement, the laminectomy site was reopened, SCBF tended to fall at and caudad to the laminectomy site. These data indicate that laminectomy can cause a significant decline in SCBF. At the present time, the mechanism(s) for this laminectomy-induced depression of SCBF are unknown, although a temperature-induced vasoconstriction is suspected.