The effect of norepinephrine on the spinal cord circulation and its possible implications in the pathogenesis of acute spinal trauma

1977 ◽  
Vol 47 (4) ◽  
pp. 567-576 ◽  
Author(s):  
Robert A. Crawford ◽  
Ian R. Griffiths ◽  
James McCulloch
Keyword(s):  
Spinal Cord ◽  
Bolus Injection ◽  
Spinal Injury ◽  
Spinal Cord Blood Flow ◽  
Arterial Infusion ◽  
Content Type ◽  
Barrier Disruption ◽  
Before And After ◽  
Hydrogen Clearance ◽  
Fine Print

✓ The effect of intra-arterially administered norepinephrine (NE) upon spinal cord blood flow (SCBF), before and after disruption of the blood-cord barrier was studied in dogs. Barrier disruption was accomplished with an intra-arterial bolus injection of 2.5 M urea. Multiple ligations of branches of the posterior aorta and cannula placements ensured that the urea was directed to the lumbar and sacral segments of the cord. The SCBF was measured by the hydrogen clearance method. Intra-arterial urea by itself had no significant effect on SCBF. The intra-arterial infusion of NE (12 µg/min and 30 µg/min) was without overall effect on SCBF. However, if the blood-cord barrier had been previously disrupted with hypertonic urea, both concentrations of NE resulted in large reductions in SCBF. No such reductions in SCBF were seen with blood-cord barrier disruption and NE if the animals had been pre-treated with the α-blocker, phenoxybenzamine (1.5 mg/kg). Some aspects of the possible involvement of NE in the pathophysiology of acute spinal injury are discussed.

Local spinal cord blood flow in experimental traumatic myelopathy

1975 ◽  
Vol 42 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Thomas F. Doyle ◽  
Albert N. Martins
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Normal Range ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Lateral Funiculus ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury ◽  
Before And After ◽  
Hydrogen Clearance

✓ Focal blood flow was measured in the lateral funiculus and center of the spinal cord in the rhesus monkey both before and after a 600 gm-cm injury at T-10. Measurements made by the hydrogen clearance technique showed that blood flow in the lateral funiculus more than doubled within 4 hours after injury, returned to normal by 8 hours, and remained in the normal range for 24 hours. At no time was a hypoperfusion in the lateral funiculus present. Blood flow in the center of the spinal cord, at the level of the lesion, began to fall within 1 hour following injury and continued to fall for 4 hours. These data challenge the notion that spreading ischemia of the white matter is an important factor in the pathophysiology of experimental spinal cord injury.

Effects of laminectomy on spinal cord blood flow

1978 ◽  
Vol 48 (2) ◽  
pp. 232-238 ◽  
Author(s):  
Douglas K. Anderson ◽  
Gregory R. Nicolosi ◽  
Eugene D. Means ◽  
L. Edward Hartley
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Reference Sample ◽  
Significant Decline ◽  
Entire Length ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Sample Method ◽  
Fine Print

✓ 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.

Protein kinase inhibition by fasudil hydrochloride promotes neurological recovery after spinal cord injury in rats

2000 ◽  
Vol 93 (1) ◽  
pp. 94-101 ◽  
Author(s):  
Masahito Hara ◽  
Masakazu Takayasu ◽  
Kazuhiko Watanabe ◽  
Atsushi Noda ◽  
Teruhide Takagi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Protein Kinase ◽  
Treated Group ◽  
Neurological Recovery ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Protein Kinase Inhibition ◽  
Cord Injury ◽  
Fine Print

Object. In Japan fasudil hydrochloride (HA1077), a protein kinase inhibitor, is widely administered to prevent vasospasm in patients after subarachnoid hemorrhage. The effects of fasudil on experimental spinal cord injury (SCI) were investigated and compared with those obtained using methylprednisolone. Methods. Spinal cord contusion was induced in rats by applying an aneurysm clip extradurally to the spinal cord at T-3 for 1 minute. After injury three groups of rats were treated with intravenously administered saline (control), intraperitoneally administered fasudil (10 mg/kg), or intravenously administered methylprednisolone (four 30 mg/kg injections). Neurological recovery was evaluated periodically over 1 month by using a modified combined behavioral scale and histopathological examination. Leukocyte infiltration near the injury site was evaluated by measuring myeloperoxidase (MPO) activity at 24 hours. Spinal cord blood flow was measured at intervals up to 3 hours after injury by using laser Doppler flowmetry. In rats in the fasudil-treated group significant improvement in modified combined behavioral score was demonstrated at each time point, whereas in the methylprednisolone-treated rats no beneficial effects were shown. In the fasudil-treated group, reduction of traumatic spinal cord damage was evident histologically in the caudal portion of the injured areas, and tissue MPO activity in tissue samples was reduced. Spinal cord blood flow was not significantly different between fasudiltreated and control group rats. Conclusions. Fasudil hydrochloride showed promise of effectiveness in promoting neurological recovery after traumatic SCI. Possible mechanisms of this effect include protein kinase inhibition and decreased infiltration by neutrophils.

Spinal cord concussion

1990 ◽  
Vol 72 (6) ◽  
pp. 894-900 ◽  
Author(s):  
Thomas J. Zwimpfer ◽  
Mark Bernstein
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Spinal Injury ◽  
Cord Compression ◽  
Neurological Deficits ◽  
Content Type ◽  
Young Males ◽  
Cord Injury ◽  
Sensory Disturbances ◽  
Fine Print

✓ The hallmark of concussion injuries of the nervous system is the rapid and complete resolution of neurological deficits. Cerebral concussion has been well studied, both clinically and experimentally. In comparison, spinal cord concussion (SCC) is poorly understood. The clinical and radiological features of 19 SCC injuries in the general population are presented. Spinal cord injuries were classified as concussions if they met three criteria: 1) spinal trauma immediately preceded the onset of neurological deficits; 2) neurological deficits were consistent with spinal cord involvement at the level of injury; and 3) complete neurological recovery occurred within 72 hours after injury. Most cases involved young males, injured during athletics or due to falls. Concussion occurred at the two most unstable spinal regions, 16 involving the cervical spinal and three the thoracolumbar junction. Fifteen cases presented with combined sensorimotor deficits, while four exhibited only sensory disturbances. Many patients showed signs of recovery with the first few hours after injury and most had completely recovered within 24 hours. Only one case involved an unstable spinal injury. There was no evidence of ligamentous instability, spinal stenosis, or canal encroachment in the remaining 18 cases. Two patients, both children, suffered recurrent SCC injuries. No delayed deterioration or permanent cord injuries occurred. Spinal abnormalities that would predispose the spinal cord to a compressive injury were present in only one of the 19 cases. This suggests that, as opposed to direct cord compression, SCC may be the result of an indirect cord injury. Possible mechanisms are discussed.

The effect of nimodipine and dextran on axonal function and blood flow following experimental spinal cord injury

1989 ◽  
Vol 71 (3) ◽  
pp. 403-416 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator ◽  
R. Dean Linden
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Compression Injury ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Dextran 40 ◽  
Treatment Groups ◽  
Cord Injury ◽  
Fine Print

✓ There is evidence that posttraumatic ischemia is important in the pathogenesis of acute spinal cord injury (SCI). In the present study spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, and motor and somatosensory evoked potentials (MEP and SSEP) were recorded to evaluate whether the administration of nimodipine and dextran 40, alone or in combination, could increase posttraumatic SCBF and improve axonal function in the cord after acute SCI. Thirty rats received a 53-gm clip compression injury on the cord at T-1 and were then randomly and blindly allocated to one of six treatment groups (five rats in each). Each group was given an intravenous infusion of one of the following over 1 hour, commencing 1 hour after SCI: placebo and saline; placebo and dextran 40; nimodipine 0.02 mg/kg and saline; nimodipine 0.02 mg/kg and dextran 40; nimodipine 0.05 mg/kg and saline; and nimodipine 0.05 mg/kg and dextran 40. The preinjury physiological parameters, including the SCBF at T-1 (mean ± standard error of the mean: 56.84 ± 4.51 ml/100 gm/min), were not significantly different (p > 0.05) among the treatment groups. Following SCI, there was a significant decrease in the SCBF at T-1 (24.55 ± 2.99 ml/100 gm/min; p < 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p < 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p < 0.0001), and the SSEP (p < 0.002). Only the combination of nimodipine 0.02 mg/kg and dextran 40 increased the SCBF at T-1 (43.69 ± 6.09 ml/100 gm/min; p < 0.003) and improved the MEP-C (p < 0.0001), MEP-N (p < 0.04), and SSEP (p < 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p < 0.0001) and somatosensory tracts (p < 0.0001) of the cord. This study provides quantitative evidence that an increase in posttraumatic SCBF can significantly improve the function of injured spinal cord axons, and strongly implicates posttraumatic ischemia in the pathogenesis of acute SCI.

Studies in experimental spinal cord trauma

1974 ◽  
Vol 40 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Lynn S. Hedeman ◽  
M. Kent Shellenberger ◽  
J. H. Gordon
Keyword(s):  
Spinal Cord ◽  
Pilot Study ◽  
Spinal Cord Trauma ◽  
Significant Elevation ◽  
Small Pilot Study ◽  
Content Type ◽  
Essentially Normal ◽  
Before And After ◽  
Fine Print

✓ The authors report a study of levels of norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) in the traumatized spinal cords of dogs, and with alpha-mehtyltyrosine before and after injury. There was a significant elevation of DA 15 to 45 minutes after injury. NE was significantly reduced. Twenty-four hours of pretreatment with alpha-methyltyrosine depleted cord catecholamines and prevented trauma-induced DA elevation. Alpha-methyltyrosine given 15 minutes after the trauma did not prevent this trauma-related DA elevation. In a small pilot study in cats, DA was elevated and NE remained essentially normal.

A percutaneous technique for producing intraspinal mass lesions in experimental animals

1973 ◽  
Vol 38 (4) ◽  
pp. 438-447 ◽  
Author(s):  
John L. Doppman ◽  
Roy Ramsey ◽  
Raymond J. Thies
Keyword(s):  
Spinal Cord ◽  
Percutaneous Technique ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Experimental Animals ◽  
Balloon Catheters ◽  
Perfusion Studies ◽  
Fluoroscopic Control ◽  
Mass Lesions ◽  
Fine Print

✓ The authors describe a percutaneous technique for producing extra- and intramedullary mass lesions in the dog and monkey. Small balloon catheters introduced through needles into the spinal canal can be positioned under fluoroscopic control to simulate epidural masses or masses within the cord. Selective spinal cord arteriography and silicone perfusion studies demonstrate the effect of such masses on spinal cord blood flow.

Effects of a single large dose of methylprednisolone sodium succinate on experimental posttraumatic spinal cord ischemia

1984 ◽  
Vol 61 (1) ◽  
pp. 124-130 ◽  
Author(s):  
Edward D. Hall ◽  
Daniel L. Wolf ◽  
J. Mark Braughler
Keyword(s):  
Spinal Cord ◽  
Sodium Succinate ◽  
Spinal Cord Ischemia ◽  
Repeated Measurements ◽  
Intravenous Dose ◽  
Lumbar Spinal Cord ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Methylprednisolone Sodium Succinate ◽  
Fine Print

✓ The ability of a single large intravenous dose of methylprednisolone sodium succinate (MPSS: 15, 30, or 60 mg/kg) to modify the evolution of lumbar spinal cord ischemia in cats undergoing a contusion injury of 500 gm-cm is examined. Repeated measurements of spinal cord blood flow (SCBF) in the dorsolateral funiculus were made via the hydrogen clearance technique before and for 4 to 5 hours after injury. The mean preinjury SCBF for all animals was 12.29 ± 0.77 ml/100 gm/min. Following injury, SCBF began to decrease progressively in vehicle-treated animals to a level of 7.71 ml/100 gm/min, a fall of 37.3%. In contrast, cats that received a 30-mg/kg intravenous dose of MPSS at 30 minutes after injury maintained SCBF within normal limits (p < 0.05 at 3 and 4 hours after contusion). A 15-mg/kg MPSS dose was less effective at preventing posttraumatic white matter ischemia, and a 60-mg/kg dose was essentially ineffective. It was determined that the 30-mg/kg MPSS dose was optimal for supporting SCBF when the drug was given at 30 minutes after spinal trauma, and a second series of experiments was carried out to examine the ability of this dose, when given at longer latencies, to improve decreased flow. Methylprednisolone given at 1½ hours after injury in four cats produced a slight (12.7%) but transient improvement in SCBF, and when administered at 4½ hours in another three animals was totally ineffective. These results show that MPSS in a 30-mg/kg dose can prevent posttraumatic spinal cord ischemia. However, it would appear that the ability of the steroid to reverse the ischemia once it has developed is limited, and probably lost, within a few hours of onset. This further suggests that the ischemic process is irreversible and underscores the need for early treatment with a large MPSS dose in order to prevent full development of ischemia and to promote neurological recovery.

Tracheostomy placement in patients with complete cervical spinal cord injuries: American Spinal Injury Association Grade A

2004 ◽  
Vol 100 (1) ◽  
pp. 20-23 ◽  
Author(s):  
James S. Harrop ◽  
Ashwini D. Sharan ◽  
Edward H. Scheid ◽  
Alexander R. Vaccaro ◽  
Gregory J. Przybylski
Keyword(s):  
Risk Factors ◽  
Spinal Cord ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Acute Injury ◽  
Smoking History ◽  
American Spinal Injury Association ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

Object. The authors sought to identify variables that predispose patients with acute American Spinal Injury Association (ASIA) Grade A cervical spinal cord injury (SCI) to require tracheostomies for ventilator support or airway protection. Methods. A retrospective analysis was performed of 178 consecutive patients with a cervical ASIA Grade A SCI who were admitted through the Delaware Valley SCI Center at Thomas Jefferson Hospital during a 6-year period. Exclusion criteria included injury occurring more than 48 hours prior to admission, death within 14 days of admission or nontraumatic SCI. Twenty-two patients were excluded based on these criteria. Parameters evaluated in the remaining population (156 patients) included demographics, cervical vertebral ASIA level, tracheostomy placement, pneumonia, premorbid pulmonary disease, smoking history, evidence of direct thoracic/lung trauma, operative intervention, associated appendicular trauma, and preexisting medical comorbidities. The ASIA classification of the 156 patients included in this analysis were C-2 (eight), C-3 (11), C-4 (64), C-5 (36), C-6 (20), C-7 (13), and C-8 (four). Tracheostomies were performed in 107 of these 156 patients. Statistical analysis revealed a significant relationship between tracheostomy and patient age (p = 0.0048), preexisting medical conditions (p = 0.0417), premorbid lung disease (p = 0.0177), higher cervical ASIA level (p < 0.0001), and the presence of pneumonia (p < 0.0001). No patient with a C-8 ASIA A injury required tracheostomy, whereas all C-2 and C-3 ASIA A—injured patients underwent tracheostomies. Patients older than 45 years of age with ASIA A levels between C-4 and C-7 more commonly required tracheostomy (p < 0.005) than patients younger than 45 years of age. Conclusions. Several risk factors were identified that corresponded to the frequent tracheostomy placement in the acute injury phase after complete cervical SCI. Early tracheostomy may be considered in patients with multiple risk factors to reduce duration of stay in the intensive care unit and facilitate ventilatory weaning.

Spinal Cord Blood Flow in Experimental Transient Traumatic Paraplegia

1980 ◽  
Vol 52 (3) ◽  
pp. 335-345 ◽  
Author(s):  
Dean C. Lohse ◽  
Howard J. Senter ◽  
John S. Kauer ◽  
Richard Wohns
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Spinal Cord Blood Flow ◽  
Flow Measurements ◽  
Content Type ◽  
The Mean ◽  
Blood Flow Measurements ◽  
Fine Print

✓ Blood flow in the lateral funiculus of the thoracic spinal cord was measured in 24 anesthetized cats using the hydrogen clearance method. In a control series of eight nontraumatized animals, blood flow measurements were taken from the T-5 and T-6 segments for 6 consecutive hours. The mean spinal cord blood flow (SCBF) in the control group was 12.8 ± 3.51 (SD) ml/min/100 gm on the basis of 107 measurements over 6 hours. In the experimental groups, 16 animals were similarly prepared. The spinal cords of these animals were then traumatized by dropping a 20-gm weight 5 cm (100 gm-cm trauma) or 13 cm (260 gm-cm trauma) onto the T-5 segment. Previous experiments have shown that these trauma levels lead to a transient paraplegia of less than 10 and 30 days' duration, respectively. Two hundred blood flow measurements from T-5 and T-6 were taken over the 6 hours following trauma. In the seven animals of the 100 gm-cm group, mean SCBF after trauma from the T-5 segment was 12.6 ± 3.45 (SD) ml/min/100 gm on the basis of 50 measurements taken over 6 hours; not significantly different from the controls (p > 0.70). In the 260 gm-cm group, mean SCBF from T-5 for 6 hours after trauma was 17.3 ± 6.60 (SD) ml/min/100 gm; significantly higher than controls (p < 0.001). Mean SCBF 3 to 6 hours after trauma was significantly elevated over controls (p < 0.05). The mean hyperemia in the 260 gm-cm group was found to be due to marked hyperemia in only four animals of the series, while five animals maintained blood flows in the normal range. This experiment provides quantitative evidence that white matter ischemia does not occur in spinal cord injuries that can be expected to produce only transient paraplegia. The data support the concept that white matter ischemia in the acute phase of severe spinal cord trauma may be related to secondary injury and subsequent permanent paraplegia.

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