Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates

1976 ◽  
Vol 45 (6) ◽  
pp. 660-676 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator

✓ Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period post-trauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.

1980 ◽  
Vol 53 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Diana Dow-Edwards ◽  
Vincent DeCrescito ◽  
John J. Tomasula ◽  
Eugene S. Flamm

✓ A study of the effects of spinal cord injury upon spinal cord blood flow was carried out in cats. A 400 gm-cm impact produced an overall reduction in spinal cord blood flow of 24% in the white matter and 30% in the gray matter, as determined by 14C-antipyrine autoradiography. At the level of the injury, white-matter flow was 8.1 ml/100 gm/min, a reduction of 49%, and in the gray matter, 12.5 ml/100 gm/min, a reduction of 76%. Treatment with aminophylline and isoproterenol improved the overall blood flow in the spinal cord. At the level of the injury, white-matter flow after this treatment was no longer significantly different from control values. The gray-matter flow remained decreased to 26.2 ml/100 gm/min, a reduction of only 47%. It is proposed that aminophylline and isoproterenol may increase cyclic adenosine monophosphate (AMP) and prevent platelet aggregation along the endothelial surfaces of the microcirculation, and may thereby help to maintain improved perfusion of the injured spinal cord.


1978 ◽  
Vol 49 (6) ◽  
pp. 844-853 ◽  
Author(s):  
Alex S. Rivlin ◽  
Charles H. Tator

✓ Spinal cord blood flow (SCBF) was measured in 12 albino rats following acute cord injury produced by the extradural clip compression technique. Severe injury was produced with the clip compressing the cord with a force of 180 gm for 5 minutes, an injury previously shown to produce a severe functional deficit. Regional SCBF was measured 15 minutes, 2 hours, and 24 hours after injury by the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. At 15 minutes and 2 hours, white and gray matter blood flow was severely diminished, and, at 24 hours, there was only minimal improvement. Focal decreases in blood flow were seen in white and gray matter for a considerable distance proximal and distal to the site of cord trauma. Thus, it has been confirmed in this model that severe cord compression injury produces severe posttraumatic ischemia in the cord which lasts for at least 24 hours.


1981 ◽  
Vol 54 (5) ◽  
pp. 620-626 ◽  
Author(s):  
J. Robert S. Hales ◽  
John D. Yeo ◽  
Stefanie Stabback ◽  
Alan A. Fawcett ◽  
Raymond Kearns

✓ Blood flow for the whole spinal cord (SCBF), central cord (largely gray matter), and peripheral cord (largely white matter) has been measured at all segmental levels using radioactive microspheres in conscious sheep. Whole SCBF was greatest in the lower cervical and lumbar enlargements and least in the upper cervical and thoracic regions. This was attributable partly to regional variations in gray-matter blood flow but principally to regional variations in the proportion of gray and white matter present. Whole SCBF for the total cord was 14.5 ± 0.8 ml/100 gm/min, central cord flow was 40.6 ± 3.5 ml/100 gm/min, and peripheral cord flow was 9.7 ± 1.9 ml/100 gm/min. Blood flow was not affected by sodium pentobarbital provided the level of anesthesia, arterial pressure, and blood gases was carefully regulated. Laminectomy usually resulted in a marked increase in central cord blood flow at the site of cord exposure, lasting about 90 minutes; this increase was not necessarily reflected in whole SCBF because of the absence of any change in blood flow in the relatively large proportion of peripheral cord. This effect of laminectomy could adversely influence results obtained from studies using invasive techniques to measure SCBF.


1989 ◽  
Vol 71 (3) ◽  
pp. 403-416 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator ◽  
R. Dean Linden

✓ 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.


Neurosurgery ◽  
1986 ◽  
Vol 18 (4) ◽  
pp. 428-432 ◽  
Author(s):  
Christopher M. Wallace ◽  
Charles H. Tator

Abstract 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.


Author(s):  
M. Christopher Wallace ◽  
Charles H. Tator

ABSTRACT:A decrease in spinal cord blood flow (SCBF) is a known sequela of spinal cord injury. The radioactive microsphere technique permits repeated measurement of spinal cord blood flow (SCBF) and cardiac output (CO) in the same experimental animal. The purpose of this study was to adapt the radioactive microsphere technique for use in the rat extradural clip compression injury model used in our laboratory.Thirteen adult Wistar rats were anaesthetized and ventilated. Mean systemic arterial pressure (MSAP) was recorded continuously. Control animals (n = 8) did not have a surgical procedure whereas the injured animals (n = 5) underwent a C7-T1 laminectomy followed by a one minute, 50 gram extradural clip compression injury at Tl. Radioactive microspheres were used for two blood flow and CO determinations in both groups.MSAPfell 59% in the injured animals (p<0.01), but this was not accompanied by significant changes in heart rate or CO. There was a 50% reduction in SCBF in the injured cord (p<0.02), and there were significant reductions in cerebral blood flow (p<0.05) and cerebellar blood flow (p<0.02) following spinal cord injury.


1980 ◽  
Vol 52 (3) ◽  
pp. 335-345 ◽  
Author(s):  
Dean C. Lohse ◽  
Howard J. Senter ◽  
John S. Kauer ◽  
Richard Wohns

✓ 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.


1976 ◽  
Vol 45 (6) ◽  
pp. 638-646 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator

✓ The effect of spinal cord trauma on the vasculature and blood flow of the spinal cord is reviewed. Both quantitative and nonquantitative studies are critically discussed and reasons sought for some of the major controversies that have arisen. Differences in methodology, species variation, and variation in the degree and type of cord injury may all be important factors in producing the conflicting results reported in the literature. In general, it can be said that trauma has a profound effect on the vasculature and blood flow in the cord and that severe compression injury of the cord causes marked ischemia in the gray and white matter.


Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 882-886 ◽  
Author(s):  
Avraham Rubinstein ◽  
Ehud Arbit

Abstract Regional spinal cord blood flow (SCBF) was measured in a group of rats under conditions of normothermia, normocarbia, normoxia, and normal blood pressure, using the hydrogen clearance technique. Regional SCBF in the cervical white matter was 26.8 ± 1 (SE) ml/100 g/min and in the cervical gray matter 53.6 ± 2.5; in the thoracic white matter it was 22.2 ± 2.4 ml/100 g/min and in the thoracic gray matter 41.2 ± 12/6 ml/100 g/min; and in the lumbar gray matter it was 52.3 ± 1.9 ml/100 g/min. The effect of changes in blood pressure on SCBF (autoregulation) was investigated in nine rats. We have observed that SCBF remains relatively constant in the blood pressure range of 45 to 165 mm Hg and assumes a passive flow below or above this range.


1980 ◽  
Vol 53 (6) ◽  
pp. 756-764 ◽  
Author(s):  
Eugen J. Dolan ◽  
Ensor E. Transfeldt ◽  
Charles H. Tator ◽  
Edward H. Simmons ◽  
Kenneth F. Hughes

✓ Distraction is considered to be a factor in many spinal cord injuries. With a specially designed distraction apparatus and the 14C-antipyrine autoradiographic technique, the effect of distraction on spinal cord blood flow (SCBF) in cats was studied. Distraction was performed at L2–3 at a rate of 0.25 cm/10 min, and the spinal evoked response (SER) was monitored by stimulating the sciatic nerve and recording at T-13. The SCBF was assessed in five control animals, four animals in whom the SER was markedly altered by distraction, and five animals after the SER had been abolished and an additional 0.5 cm distraction applied. Control cats had gray- and white-matter flows of 44.5 ± 1.4 (SEM) and 10.5 ± 0.4 ml/100 gm/min, respectively. Distraction to the point of marked SER alteration caused a 50% loss of SCBF at and caudal to the distraction site. An additional 0.5 cm distraction produced total abolition of SCBF at the distraction site and for a considerable distance rostral and caudal to it. Thus, it is shown that spinal distraction causes cord ischemia similar to that seen with other types of spinal cord injury. In addition, distraction severe enough to cause loss of the SER has already produced severe cord ischemia.


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