Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair

PURPOSE: Motor-evoked potentials (MEPs) were monitored during thoracoabdominal aortic aneurysm (TAAA) repair to assess spinal cord ischemia and evaluate the subsequent protective strategies to prevent neurologic deficit. METHODS: Between January 1996 and December 1997, 52 consecutive patients with type I (n = 24) and type II (n = 28) TAAA underwent surgery (mean patient age, 60 years; range, 21-78 years). The surgical protocol included left heart bypass, cerebrospinal fluid drainage, and monitoring transcranial myogenic MEPs. When spinal cord ischemia was detected, distal aortic pressure and mean arterial pressure were increased. By means of sequential crossclamping, MEPs were used to identify critical intercostal or lumbar arteries. RESULTS: Reproducible MEPs could be recorded in all patients, and spinal cord ischemia was detected within 2 minutes. During distal aortic perfusion, 14 patients (27%) showed rapid decrease in the amplitude of MEPs to less than 25% of baseline, indicating spinal cord ischemia, which could be corrected by increasing distal aortic pressure. The mean distal aortic pressure to maintain adequate cord perfusion was 66 mm Hg; however, it varied among individuals between 48 and 110 mm Hg. In 24 patients (46%), MEPs disappeared after segmental clamping and returned after reattachment of intercostal arteries. In 9 patients (17%), MEPs disappeared completely, but no intercostal arteries were found. After aortic endarterectomy, 6 or 8 mm Dacron grafts were anastomosed to intercostal arteries, and MEPs returned after reperfusion. Using this aggressive surgical approach based on MEPs, no early or late paraplegia occurred in this series. CONCLUSION: Monitoring of MEPs is an effective technique to assess spinal cord ischemia. Operative strategies based on MEPs prevented neurologic deficits in patients treated for type I and II TAAA.     

Effects of spinal cord ischemia on evoked potential recovery and postischemic regional spinal cord blood flow

The effects of spinal cord ischemia on spinal cord blood flow (SCBF) and somatosensory (SSEP) and motor (MEP) evoked potentials were investigated in a rabbit model of reversible spinal cord ischemia. Spinal cord ischemia was produced by balloon occlusion of the infrarenal aorta for 30, 60, and 90 min. SCBF, SSEPs, and MEPs were measured before, during, and 1 h after aortic occlusion. Aortic occlusion produced absolute ischemia of the caudal cord followed by hyperemia upon reperfusion. SSEP's and MEP's were obliterated during ischemia but demonstrated gradual albeit incomplete recovery following reperfusion with amplitude recovery inversely proportional to the duration of ischemia. Later peaks were more severely affected by a given period of ischemia than were early waves. In general, SSEP's were more resistant to ischemia than were MEP's although the differences were not significant.     

Aprotinin reduces injury of the spinal cord in transient ischemia

OBJECTIVE: The protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit spinal cord ischemia model. DESIGN: Randomized, controlled, prospective study. SETTING: University research laboratory. SUBJECTS: New Zealand white rabbits (36) of both sexes. METHODS: In 24 animals, ischemia was induced with midline laparotomy and clamping the aorta just distal to left renal artery and proximal to aortic bifurcation for 20 min. Aprotinin was given 30000 KIU as a short intravenous injection after anesthesia, and was followed by 10000 KIU/h by continuous infusion in group 1 (n = 12). Similar volume of saline solution was used in control group of animals (group 2, n = 12). Group 3 of animals (sham group, n = 12) were anesthetized and subjected to laparotomy without aortic occlusion. Physiological parameters and somatosensory evoked-potentials (SEP) were monitored in animals before ischemia, during ischemia and in the first 60 min of reperfusion. Their neurological outcome was clinically evaluated up to 48 h postischemia. Their motor function was scored, and the intergroup differences were compared. The animals were sacrificed after two days of postischemia. Their spinal cord, abdominal aorta, and its branches were processed for histopathological examination. RESULTS: In group 3, SEP amplitudes did not change during the procedures, and all animals recovered without neurologic deficits. At the end of ischemic period, the average amplitude was reduced to 53+/-7% of the baseline in all ischemic animals. This was followed by a gradual return to 89+/-8 and 81+/-13% of the initial amplitude after 60 min of reperfusion in group 1 and group 2 correspondingly (P > 0.05). The average motor function score was significantly higher in group 1 than group 2 at 24 and 48 h after the ischemic insult (P < 0.05). Histological observations were clearly correlated with the neurological findings. CONCLUSION: The results suggest that aprotinin reduces spinal cord injury and preserves neurologic function in transient spinal cord ischemia in rabbits.     

Transient spinal ischemia in rat: characterization of spinal cord blood flow, extracellular amino acid release, and concurrent histopathological damage

Extracellular concentrations of amino acids in halothane-anesthetized rats were measured using a microdialysis fiber inserted transversely through the dorsal spinal cord at the level of the lumbar enlargement in conjunction with HPLC and ultraviolet detection. After a 2-h washout and a 1-h control period, 20 min of reversible spinal cord ischemia was achieved by the inflation of a Fogarty F2 catheter passed through the femoral artery to the descending thoracic aorta. After 2 h of postischemic reperfusion, animals were transcardially perfused with saline followed by 10% formalin or 4% paraformaldehyde. The glutamate concentration in the dialysate was significantly elevated after 10 min of occlusion and returned to near-baseline during the first 30 min of reperfusion. Taurine was elevated significantly 0.5 h postocclusion and continued to increase throughout the 2 h of reperfusion. Glycine concentrations showed a tendency to be slightly above baseline during the reperfusion period. Glutamine concentrations modestly increased following 2 h of reperfusion. No significant changes in aspartate, asparagine, and serine were detected. In control animals no significant changes in any amino acids were detected. To assess the role of complete spinal ischemia on spinal glutamate release, studies were carried out using cardiac arrest. Twenty minutes after induction of cardiac arrest, the glutamate concentration was increased about 350-400%. In a separate group of animals, spinal cord blood flow (SCBF) and its response to decreased CO2 were measured using a laser probe implanted into the epidural space at the level of the L2 vertebral segment. SCBF decreased to 5-6% of the control during aortic occlusion. After reversible ischemia, marked hyperemia was seen for the first 15 min, followed by hypoperfusion at 60 min. Under control-preischemic conditions a decrease in arterial CO2 content caused a decrease in SCBF of about 25%. This autoregulatory response was almost completely absent when assessed 60 min after a 20-min interval of aortic occlusion. Histopathological analysis of spinal cord tissue from these animals demonstrated heavy neuronal argyrophilia affecting small and medium-sized neurons located predominantly in laminae III-V. These changes corresponded to signs of irreversible damage at the ultrastructural level. Occasionally, small areas of focal necrosis, located in the dorsolateral part of the dorsal horn and anterolateral part of the ventral horn, were found. The results are consistent with a role for glutamate in ischemically induced spinal cord damage and suggest that taurine elevation detected during the early reperfusion period may serve as an important indicator of irreversible spinal cord neuronal damage.     

Monitoring of evoked potentials during spinal cord ischaemia: experimental evaluation in a rabbit model

OBJECTIVES: Somatosensory evoked potentials (SEPs), spinal evoked potentials (Spinal-EPs), and motor-evoked potentials (MEPs) were monitored in a rabbit model of spinal cord ischaemia to evaluate their accuracy and relationship to clinical status. METHODS: A modified rabbit spinal cord ischaemia model of infrarenal aortic occlusion for 21 min was employed (30 rabbits). After baseline SEPs, Spinal-EPs, and MEPs were obtained, evoked potentials were recorded continuously during and after clamping of the aorta (30 min). Neurological outcome at 24 h was correlated with evoked potentials, and histopathological findings. RESULTS: Fifteen animals became paraplegic. MEPs were always abolished after clamping of the aorta while Spinal-EPs and SEPs remained. The sensory evoked potentials (SEPs and Spinal-EPs) were the least sensitive to spinal cord ischaemia, and their presence had no correlation with the final clinical status (50% of false negatives). This was consistent with histopathological examination that showed damage almost entirely confined to the anterior horn, while the dorsal columns were generally well preserved. High spine MEPs evoked by twitch stimulation was the best predictor of clinical outcome (0% of false negatives, 0% of false positives). CONCLUSIONS: SEPs and Spinal-EPs cannot be used as safe monitors of ischaemia of the spinal cord. High spine MEPs evoked by twitch stimulation was the most useful for real-time evaluation of spinal cord ischaemia, and the best predictor of neurologic outcome during reperfusion.     

Inhibition of neutrophil adhesion does not prevent ischemic spinal cord injury

Paraplegia may occur after transient aortic occlusion as a consequence of primary ischemia to the spinal cord or injury during the reperfusion period. In animal models of ischemia/reperfusion there is evidence that reperfusion injury may be modulated partially by neutrophils. The efficacy of the neutrophil adherence blocking murine monoclonal antibody (MAb 60.3) was assessed in spinal cord ischemia/reperfusion in rabbits. Spinal cord ischemia was accomplished by balloon catheter occlusion of the infrarenal aorta. Neurologic assessment was graded as normal, partial neurologic deficit, or complete paralysis. Electrophysiologic monitoring with somatosensory evoked potentials was used to determine the optimal length of time of occlusion. Animals were treated randomly with 2 mg/kg of intravenous Mab 60.3 (n = 8) or saline solution (n = 9) with the investigator unaware of treatment. Mean occlusion times were no different between groups (control, 32.7 +/- 3.6 minutes versus MAb, 32.4 +/- 6.0 minutes). Five (55%) saline-treated and four (50%) MAb 60.3-treated animals became paraplegic. Animals with initial paraparesis all progressed to flaccid paraplegia within 24 hours. We conclude that spinal cord injury after transient aortic occlusion is independent of the CD11/CD18 glycoprotein complex of the neutrophil. Injury in this setting may occur during ischemia and thus may not be dependent on neutrophils or reperfusion.     

Effect of xylitol and trehalose on dry resistance of yeasts

Nitric Oxide (NO) has been implicated as a mediator of neuronal injury in vascular stroke. On the other hand, NO is suggested to play a neuroprotective role by increasing blood flow during cerebral ischemia. In order to evaluate the role of NO in the spinal cord ischemia, effects of nitric oxide synthase (NOS) inhibition on the recovery of reflex potentials after a transient spinal cord ischemia were examined in urethane-chloralose anesthetized spinal cats. Spinal cord ischemia was produced by occlusion of the thoracic aorta and the both internal mammary arteries for 10 min. Regional blood flow (RBF) in the spinal cord was continuously measured with a laser-Doppler flow meter. The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials elicited by electrical stimulation of the tibial nerve, were recorded from the L7 or S1 ventral root. The recovery process of spinal reflex potentials was reproducible when the oclusion was repeated twice at an interval of 120 min. Pretreatment with N(G)-monomethyl-L-arginine (L-NMMA, 10 mg/kg), a NOS inhibitor significantly accelerated the recovery of PSR potentials after spinal cord ischemia. The accelerating effect of L-NMMA on the recovery of PSR potentials was abolished by co-administration of L-arginine (1 mg/kg/min) but not by that of D-arginine (1 mg/kg/min). L-NMMA failed to improve RBF in the spinal cord during ischemia and reperfusion. Nitroprusside (10 microg/kg/min), a NO donor, retarded the recovery of PSR potentials after spinal cord ischemia. These results suggest that NO production has a significant influence on the functional recovery after transient spinal cord ischemia.     

Renal ACE immunohistochemical localization in NIDDM patients with nephropathy

PURPOSE: A new protective method against the spinal cord ischemia that occurs during aortic clamping was investigated in dogs. Oxygenated blood containing prostaglandin E1 (PGE1) was administered at the clamped aortic segment, and the effect was evaluated by measurement of the sensory evoked spinal potential (SESP). METHODS: In 30 dogs, a thoracotomy was made with dissection of the thoracic aorta. After intravenous heparin (100 units/kg) was administered, the proximal and distal descending thoracic aortas were cross-clamped for 60 minutes. Group A (n=10) received oxygenated blood at the rate of 1.0 ml/kg/min. Groups B (n=10) and C (n=10) received oxygenated blood at the same rate, with PGE1 at the dosage of 25 and 50 ng/kg/min, respectively. The infusion was continuously administered throughout the entire period of ischemia. SESP was measured with epidural electrodes before clamping, 10 and 60 minutes after clamping, and 10 and 60 minutes after declamping. Neurologic outcome was assessed at 24 hours after the operation and graded according to the method of Tarlov. RESULTS: There was no significant hemodynamic change in any group. At 60 minutes after damping and at 10 and 60 minutes after declamping, the amplitude of SESP was lower than that at preclamping in groups A and B (p < 0.05). At 60 minutes after damping and at 10 and 60 minutes after declamping, the SESP was more markedly decreased in group A compared with groups B and C. Regarding postoperative neurologic outcome, the dogs with SESP amplitude of more than 50% of the preclamping control value at 60 minutes after clamping showed neither paralysis nor paraplegia. Seven of nine dogs with less than 50% SESP amplitude showed neurogenic deficit. In a comparison of groups A, B, and C, the Tarlov score for group A dogs was significantly lower than that for group C dogs (p < 0.05). CONCLUSION: In this model, PGE1 administration at the rate of 50 ng/kg/min showed sufficient spinal cord protection against ischemia without a decrease in the blood pressure. Further studies are needed to determine the dose that will provide the maximal protective effect and to determine the maximum duration of ischemia against which PGE1 shows protective effects.     

Memantine for prevention of spinal cord injury in a rabbit model

BACKGROUND: This study was conducted to investigate the effect of memantine, a noncompetitive N-methyl-d-aspartate receptor antagonist, on the neurologic outcome of spinal cord ischemia after aortic occlusion. MATERIALS AND METHODS: New Zealand White rabbits were anesthetized and spinal cord ischemia was induced for 40 minutes by infrarenal aortic occlusion. Animals were randomly allocated to 3 groups. Group 1 (n = 8, control) received no pharmacologic intervention, group 2 (n = 8) received intra-aortic memantine infusion (20 mg/kg) after aortic crossclamping, and group 3 (n = 8) was treated with systemic memantine infusion (20 mg/kg) 45 minutes before aortic occlusion. Neurologic status was scored by the Tarlov system (in which 4 is normal and 0 is paraplegia) at 12, 24, 36, and 48 hours after the operation. Lumbar spinal root stimulation potentials and motor evoked potentials from lower limb muscles were monitored before, during, and after the operation. After the animals were killed, the spinal cords were studied histopathologically. RESULTS: All potentials disappeared shortly after aortic crossclamping. They returned earlier in both memantine-treated groups than in the placebo group. Histologic examination of spinal cords revealed a few abnormal motor neurons in memantine-treated rabbits but found extensive injury in the control group. At 12 hours the median Tarlov scores were 0 in the control group (group 1), 2 in the intra-aortic memantine group (group 2, P =.001 versus control), and 3 in the systemic group (group 3, P =.0002 versus control). At 24 hours median Tarlov scores were 0, 2.5 (P =.0002), and 4 (P =. 0002), respectively. Finally, at both 36 and 48 hours median Tarlov scores were 0, 3 (P =.0006), and 4 (P =.0002), respectively. CONCLUSION: Memantine significantly reduced neurologic injury related to spinal cord ischemia and reperfusion after aortic occlusion.     

Changes in human evoked spinal potentials (ESP) by epidural lidocaine

Controversies exist on the sites of action of epidural anesthesia. Leading opinion says that it works on spinal nerve root. We examined ESP and tactile sensations in 4 patients during epidural anesthesia with lidocaine to determine the effects of the anesthesia on spinal cord. Prolongation of latency and decrease in amplitude of ESP appeared 10 min after injection of 1.5% lidocaine 4 ml, each parameter reaching maximum value of 115% and 60% of the control value 30 min afterwards, respectively. Then they started to recover slowly, reaching normal values 150 min later. Changes in ESP and tactile sensation were closely related. Decreases in amplitude to 90%, 80%, 60% of the control values were observed for hypesthesia, analgesia, and anesthesia, respectively. We conclude that the spinal cord also is an important site of action of epidural anesthesia.     

Systemic hypothermia after spinal cord compression injury in the rat: does recorded temperature in accessible organs reflect the intramedullary temperature in the spinal cord?

This article addresses one basic issue regarding the use of systemic hypothermia in the acute management of spinal cord injury, namely, how to interpret temperature recordings in accessible organs such as the rectum or esophagus with reference to the spinal cord temperature. Thirty-six rats, divided into six groups, were randomized to laminectomy or to severe spinal cord compression trauma, and were further randomized to either a cooling/rewarming procedure or continuous normothermia (esophageal temperature 38 degrees C) for 90 min. The first procedure comprised normothermia during the surgical procedure, followed by lowering of the esophageal temperature from 38 degrees C to 30 degrees C (the hypothermic level), a 20-min steady-state period at 30 degrees C, rewarming to 38 degrees C, and finally a 20-min steady-state period at 38 degrees C. The esophageal, rectal, and epidural temperatures were recorded in all animals. The intramedullary temperature was also recorded invasively in four of the six groups. We conclude that the esophageal temperature is safe and easy to record and, in our setting, reflects the epidural temperature. The differences registrated may reflect a true deviation of the intramedullary temperature due to initial environmental exposure and secondary injury processes. Our results indicate that the esophageal temperature exceeds the intramedullary temperature during the initial recording and final steady state following rewarming, but not during the most crucial part of the experiment, the hypothermic period. The core temperature measured in the esophagus can therefore be used to evaluate the intramedullary temperature during alterations of the systemic temperature and during hypothermic periods.     

Electrophysiologic study of trace changes in the excitability of the rat spinal cord

In white rats, retention of the amplitude asymmetry of the monosynaptic reflex responses (MSRR) in the ventral roots of the spinal lumbosacral segments due to removal of half of the cerebellum, was studied. The MSRR asymmetry remained after the consequent spinal cord section at the thoracic level if it had existed over 20 min (fixation period) before this section. When tested with electric stimuli applied to the nerves of muscles-antagonists, the stable MSRR asymmetry could be unidirectional or reciprocal. Prolonged unilateral stimulation of the muscle nerve central end in the spinal rat with stimuli of different frequency and intensity evoked no MSRR amplitude asymmetry during subsequent bilateral testing of the same nerves. But in decerebrated rats the MSRR asymmetry has frequently appeared after such stimulation. Asymmetry of the reticular descending influence is supposed to play a major role in the trace stable changes of excitability of the spinal cord neuronal substrate as well as different capacities of different neurons (or their elements) for fixation and retention of such changes.     

Expression and structure of senescence marker protein-30 (SMP30) and its physiological function

STUDY DESIGN: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. OBJECTIVES: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective effects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. SETTING: Departments of Neurosurgery and Biochemistry, Cerrahpa?a Medical School, Istanbul, Turkey. METHODS: Twenty-five female Wistar Albino rats were used. There were five rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining five rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a flow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacrificed and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). RESULTS: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group I (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/gww in group 3 (epidural cooling), the differences being statistically significant. CONCLUSION: The results indicated that epidural cooling of traumatized spinal cord is effective in preventing secondary damage due to the peroxidation of lipid membranes.     

Differential expression of heat shock proteins in normal and failing human hearts

OBJECTIVE: To predict spinal cord ischemia after endovascular stent graft repair of descending thoracic aortic aneurysms, temporary interruption of the intercostal arteries (including the aneurysm) was performed by placement of a novel retrievable stent graft (Retriever) in the aorta under evoked spinal cord potential monitoring. METHODS: From February 1995 to October 1997, endovascular stent graft repair of descending thoracic aortic aneurysms was performed in 49 patients after informed consent was obtained. In 16 patients with aneurysms located in the middle and distal segment of the descending aorta, the Retriever was placed temporarily before stent graft deployment. The Retriever consisted of two units of self-expanding zigzag stents connected in tandem with stainless steel struts. Each strut was collected in a bundle fixed to a pushing rod, and the stent framework was lined with an expanded polytetrafluoroethylene sheet. The Retriever was delivered beyond the aneurysm through a sheath and was retracted into the sheath 20 minutes later. A stent graft for permanent use was deployed in patients whose predeployment test results with the Retriever were favorable. Evoked spinal cord potential was monitored throughout placement of the Retriever and stent grafting until the next day. RESULTS: The Retriever was placed in 17 aneurysms in 16 patients. There were no changes in amplitude or latency of evoked spinal cord potential records obtained before or during Retriever placement. After withdrawal of the Retriever, all aneurysms were excluded from circulation immediately after permanent stent grafting. There were no changes in evoked spinal cord potential, nor were neurologic deficits seen after stent graft deployment in any patient. CONCLUSIONS: These results suggest that predeployment testing with the Retriever under evoked spinal cord potential monitoring is promising as a predictor of spinal cord ischemia in candidates for stent graft repair of thoracic aortic aneurysms.     

Effects of caudal traction of the spinal cord on evoked spinal cord potentials in the cat

This study attempts clarify the mechanism of neurological deficits in tethered cord syndrome using evoked spinal cord potentials (ESCPs). ESCPs in response to both sciatic nerve (SN-ESCP) and spinal cord stimulation (SC-DESCP) were recorded from the dorsal epidural space. With a fixed degree of caudal traction on the spinal cord in ten cats for 2-4 hours, ESCPs were increased in amplitude in the N1 and N2 deflections of the SC-DESCPs to 158% and 154% at L5 and decreased to 91% and 76% after transient augmentation at L3. On the other hand, the amplitude in the N1 deflection of the SN-ESCPs at L3 and L5 was decreased to 40% and 68%. These findings suggest that not only the force but also the duration of traction influence the degree of the spinal cord dysfunction. When the spinal cords of 17 cats received compression with traction and without traction, the SN-ESCPs of the former became positive earlier than that of the latter. The extent of the recovery in amplitude of both SC-DESCPs and SN-ESCPs propagated over compression site was far limited in the former than in the latter. These results would indicate that the spinal cord subjected to traction is vulnerable to compression.     

Intraoperative monitoring of the motor pathway using transtracheal stimulation of the cervical spine in dogs

Although SEP monitoring of the spinal cord has been a well established method recently, not an ultimate, perfectly developed technique for monitoring of the motor system is known so far, particularly, because of the disturbing effect of narcotic drugs and relaxants on the motor evoked potentials. In this study the upper part of the spinal cord was stimulated in 14 anesthetized and relaxed dogs with a cathode attached to the intratracheal tube and an anode fixed to the cervical spinous processes. Single and serial stimuli were applied. Recordings were obtained from the exposed right femoral nerve and quadriceps muscle. Averaging was necessary when using serial stimulations. Responses were consequent and reproducible during regular anesthesia. The origin of the different responses in the spinal cord is discussed. The method seems to be appropriate for intraoperative monitoring of the thoracolumbar spine.     

Effects of hypoxia on the ventral root motor-evoked potential in the in vitro spinal cord preparation

STUDY DESIGN: This study investigated the effects of hypoxia and glucose on motor functions of spinal cord, monitoring ventral root motor-evoked potential in the in vitro cervical cord preparations. OBJECTIVE: To study ischemia-induced changes in ventral root motor-evoked potential of spinal cord. SUMMARY OF BACKGROUND DATA: Previous studies demonstrated ischemic changes caused by local circulatory impairment might be a major pathophysiologic basis of neuron damage in cord compression. METHODS: Ventral root motor-evoked potential elicited by stimulation of ventrolateral funiculus was recorded from the ventral root in the isolated spinal cord preparations obtained from a newborn rat. The preparations were exposed to artificial cerebrospinal fluid equilibrated with severe or mild hypoxia for 90 minutes. Inhibitory and excitatory neurotransmitter antagonists were added to artificial cerebrospinal fluid to investigate synaptic transmission. The artificial cerebrospinal fluids containing various concentrations of glucose were used to study the glucose's effects. RESULTS: Ventral root motor-evoked potential consisted of the early and late components, which were excitatory transsynaptic potentials. The amplitudes were increased in the early phase of severe hypoxia and declined in the prolonged exposure. In mild hypoxia, there was a sustained increase of the amplitudes. The application of inhibitory neurotransmitter antagonists abolished the augmentation of the amplitudes in the early phase of severe hypoxia. Hypoxia without glucose accelerated hypoxic change. CONCLUSION: Inhibitory synaptic transmission was depressed preferentially in the early phase of severe hypoxia or in mild hypoxia. Excitatory and inhibitory transmissions were suppressed in prolonged severe hypoxia. Glucose deficiency aggravated hypoxic inhibition of synaptic transmissions.     

Influence of interleukin-1 beta on bradykinin-induced responses in guinea pig peritoneal macrophages

The aim of the present study was to compare the effects of intrathecal tetracaine (a sodium channel blocker) with those of moderate hypothermia on glutamate concentrations of intrathecal dialysate, hindlimb motor functions, and histopathology in spinal cord ischemia. New Zealand White rabbits implanted with an intrathecal dialysis probe were assigned to one of the three groups (seven in each): control (temperature 38 degrees C), tetracaine (tetracaine 0.5%, 0.6 mL, given intrathecally 30 min before ischemia, 38 degrees C), or moderate hypothermia (32 degrees C). Spinal cord ischemia (20 min) was produced by occlusion of the abdominal aorta during isoflurane (1%) anesthesia. Glutamate concentrations significantly increased during ischemia in all groups, but the levels in the moderate hypothermia group were significantly lower than those in the control and tetracaine groups. Neurologic status (24 and 48 h after reperfusion) and histopathology (48 h) in the moderate hypothermia group were significantly better than in the other two groups. There were no significant differences between the tetracaine and control groups in either glutamate concentrations, neurologic status, or histopathology. We conclude that intrathecal tetracaine does not provide any protection against ischemic spinal cord injury, whereas moderate hypothermia does. IMPLICATIONS: Sodium channel blockers, including local anesthetics, have been shown to reduce glutamate release in brain ischemia and have a neuroprotective effect. However, in the present study, intrathecal tetracaine did not attenuate either glutamate release or the neurologic or histopathologic outcome in spinal cord ischemia, whereas moderate hypothermia did.     

Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury. Involvement of nitric oxide

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1 h. However, a significant increase in SCEP latency was seen at the end of 5 h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.     

Effects of coil orientation and magnetic field shield on transcranial magnetic stimulation in cats

To obtain suitable stimulus conditions for transcranial magnetic stimulation, the evoked compound muscle action potential (ECMAP), evoked spinal cord potential (ESCP), and magnetic and electric fields were analyzed in cats with and without the use of a magnetic field shield. Cats were stimulated using a figure 8 magnetic coil placed on the cranium above the motor cortex. The maximum ECMAP amplitude was recorded when the electric current in the coil was in the mediolateral direction, regardless of whether a magnetic shield with a 5 x 5 cm window was used. ECMAP and ESCP thresholds were reduced when magnetic shielding was in place. Due to the edge effect, the strengths of the magnetic and electric fields were highest in the brainstem area, which is an inhomogeneous volume conductor of the cat's cranium. A large induced electric field directed caudally elicited ECMAP and ESCP responses effectively when a magnetic shield with a 5 x 5 cm window was in place.