Regional spinal cord blood flow in rats after severe cord trauma

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.

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.


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.


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.


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.


1991 ◽  
Vol 75 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Charles H. Tator ◽  
Michael G. Fehlings

✓ In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury. The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site. These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.


1976 ◽  
Vol 45 (6) ◽  
pp. 647-659 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator

✓ Spinal cord blood flow (SCBF) was measured in the primate thoracic spinal cord using the 14C-antipyrine autoradiographic technique that allowed clear differentiation between white and gray matter blood flow. Individual SCBF values were obtained for 0.1-sq mm areas of the thoracic cord cross section. White matter blood flow was homogeneous throughout with a mean value of 10.3 ± 0.2 ml/100 gm/min. Graymatter flow was more variable with lower values in the dorsal horns and higher values in the central gray and anterior horns. Mean gray-matter flow was 57.6 ± 2.3 ml/100 gm/min. Arterial pO2 was 123 ± 2 torr, pCO2 was 40.2 ± 0.5 torr and pH was 7.327 ± 0.010. Mean arterial blood pressure was 113 ± 3 mm Hg and core temperature was 36.4° ± 0.1° C.


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