Regional canine spinal cord energy state after experimental trauma

Walker, Joanne G.; Yates, Ronald R.; Yashon, David

doi:10.1111/j.1471-4159.1979.tb11752.x

Cited by 18 publications

(6 citation statements)

References 29 publications

(8 reference statements)

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“…Phospholipase C activity has also been found to increase after experimental concussive head injury (Wei et al, 1982). Following spinal cord trauma, energy stores are rapidly depleted, with ATP levels falling to less than 20% of normal values (Walker et al, 1977;Anderson et al, 1980;Vink et al, 1987). This would be expected greatly to diminish the rates of FFA reacylation and de novo phospholipid synthesis, which require ATP and other high-energy intermediates (Dawson, 1973;Sun et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Changes in free fatty acids, phospholipids, and cholesterol following impact injury to the rat spinal cord

Demediuk

Daly

1989

J of Neuroscience Research

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Free fatty acids (FFA), phospholipid, and cholesterol levels were measured in spinal cord samples from rats subjected to low (25 g-cm), moderate (50 g-cm), or severe (100 g-cm) impact trauma to the T10 spinal segment. All degrees of injury caused early (15 min) declines in total phospholipids after trauma; phospholipid levels remained significantly below controls in rats subjected to moderate and severe injuries for up to 3 days, whereas phospholipids had returned to baseline values by 4 hr in the low injury group. Rapid and persistent decreases in cholesterol levels were observed for all injury groups. Severe trauma was associated with biphasic increases in FFA levels: levels were elevated at 5 and 15 min post-trauma and had declined by 30 min; a second elevation was observed at 1 hr, progressively increasing to reach a maximum at 24 hr, before declining over the next 6 days. Low and moderate injuries caused similar early total FFA increases; later increases were significantly smaller than in the severely injured group. Among the free fatty acids, significant increases were observed in palmitate, stearate, oleate, linoleate, linolenate, arachidonate, and docosahexaenoate. These findings indicate that traumatic spinal cord injury results in early, transient, postinjury membrane phospholipid hydrolysis, the magnitude of which is relatively independent of the severity of injury. More delayed and sustained lipid hydrolysis also occurs after trauma, the magnitude of which is related to the severity of injury.

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Section: Discussionmentioning

confidence: 99%

Changes in free fatty acids, phospholipids, and cholesterol following impact injury to the rat spinal cord

Demediuk

Daly

1989

J of Neuroscience Research

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“…It has been demonstrated recently that high extracellular K f stimulates the release of AA from CNS tissue in vivo and in vitro (Milby et al, 1981). Spinal cord injury also produces a decrease in energy supply (Walker et al, 1979) and N a + , K+-ATPase activity (Clendenon et al, 1978) that will limit AH2 reuptake systems (Sharma et al, 1963;Daniels et al, 1982).…”

Section: 0-mentioning

confidence: 99%

Loss of Ascorbic Acid from Injured Feline Spinal Cord

Pietronigro

Hovsepian

Demopoulos

et al. 1983

Journal of Neurochemistry

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Feline spinal cord contains 0.97 mM ascorbic acid, as measured by the dinitrophenylhydrazine method. Greater than 90% is maintained in the reduced form. When functioning normally, the CNS conserves its ascorbic acid with a turnover rate of 2% per h. Following contusion injury severe enough to produce paraplegia, ascorbic acid is rapidly lost from injured spinal tissue. Thus, ascorbic acid is decreased 30% by 1 h and 50% by 3 h following injury. Oxidized ascorbic acid is increased at 1, but not 3, h following impact. As a consequence of its many functions in CNS, loss of ascorbic acid may contribute to derangements in spinal cord function following injury.

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“…However, these were not accompanied by an increase in Pi or Lac, as would be expected if this was an acutely ischémie situation. Again, hydrocephalus appears to show some similarity to spinal cord trauma where there are decreases in ATP and PCr, associated with modest increases in Lac and modest reductions in blood flow (Walker et al, 1979;Anderson et al, 1982), in contrast to acute forebrain ischemia where decreases in ATP and PCr are associated with a large increase in Lac (Aureli et al, 1994). The compounds NAA, Inos, Cr, Asp, Glu, Gin, and Tau have been described as organic osmolytes (Verbalis and Gullans, 1991).…”

Section: Sequential Changes In Hydrocephalusmentioning

confidence: 91%

Progressive Changes in Cortical Metabolites at Three Stages of Infantile Hydrocephalus Studied byIn VitroNMR Spectroscopy

Jones

Harris²,

Rocca³

et al. 1997

Journal of Neurotrauma

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Infantile hydrocephalus is most often caused by an obstruction in the cerebrospinal fluid flow pathway and results in ventricular dilatation and chronic trauma to the surrounding brain. Surgical treatment alleviates the condition but does not cure or prevent neurological deficits. The H-Tx rat has severe hydrocephalus due to a spontaneous aqueduct obstruction in late gestation. In order to determine how hydrocephalus affects brain metabolism in tissue adjacent to the expanded ventricles, cortical extracts have been made from groups of hydrocephalic and control littermates with early, intermediate, and advanced hydrocephalus at 4, 11, and 21 days after birth. Extracts were analyzed with 1H and 31P NMR spectroscopy and metabolite peaks were quantified using an external standard. Metabolite concentrations were calculated relative to tissue wet weight and subsequently expressed relative to tissue dry weight, using values for water content obtained from additional groups of rats. In early hydrocephalus there was a significant decrease in the phosphomonoester phosphorylcholine, and there were small, nonsignificant changes in other compounds. By 11 days, in addition to phosphomonoesters, there were significant decreases in ATP, phosphocreatine, and in inorganic phosphate, but with no change in lactate. By 21 days there were also substantial decreases in cholines, inositol, creatine, glutamate, glutamine, aspartate, N-acetylaspartate, alanine, and taurine. It is concluded that the sequence of pathological events starts with changes in membrane lipids. This is followed by reductions in energy metabolite which leads to cell swelling with loss of intracellular osmolytes and neurotransmitters. These changes are discussed in relation to hydrocephalus pathophysiology and to prevention and reversibility with shunt treatment.

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Regional canine spinal cord energy state after experimental trauma

Cited by 18 publications

References 29 publications

Changes in free fatty acids, phospholipids, and cholesterol following impact injury to the rat spinal cord

Changes in free fatty acids, phospholipids, and cholesterol following impact injury to the rat spinal cord

Loss of Ascorbic Acid from Injured Feline Spinal Cord

Progressive Changes in Cortical Metabolites at Three Stages of Infantile Hydrocephalus Studied byIn VitroNMR Spectroscopy

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