Phospholipids of normal and experimentally injured spinal cord of the miniature pig

Segler-Stahl, Kordula; Demediuk, Paul; Castillo, Ricardo; Watts, Colin; Moscatelli, Ezio A.

doi:10.1007/bf00964658

Cited by 18 publications

(11 citation statements)

References 18 publications

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“…In rabbits and cats, impact injury results in early ( 5 6 0 min) posttrauma increases in thromboxane levels in spinal cord and CSF, respectively (Hsu et al, 1985a). After spinal cord impact trauma to the miniature pig, total tissue levels of phospholipids and cholesterol were significantly decreased at the impact site when determined 3 hr postinjury (Segler-Stahl et al, 1985). Faden et al (1987) have also recently reported delayed changes in membrane lipids of rat spinal cord following impact injury, with an increased FFA content and a decreased phospholipid content at 24 hr.…”

Section: Introductionmentioning

confidence: 91%

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: Introductionmentioning

confidence: 91%

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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“…Alterations in tissue calcium levels were not examined by us, but changes in this cation have been reported to be significantly correlated with injury severity (Young and Koreh, 1986). The decline in total phospholipid content was the result of nonspecific degradation of most of the quantified phospholipid species, which is consistent with previoulsy reported phospholipid changes following SCI in the miniature pig (Segler-Stahl et al, 1985). Phospholipid changes were highly correlated with injury severity.…”

Section: Discussionsupporting

confidence: 73%

“…Membrane lipid hydrolysis has been demonstrated to follow SCI in a variety of animal models, including impact trauma in miniature pigs (Segler-Stahl et al, 1985), compression injury in cats (Demediuk et al, 1985a), impact trauma in dogs (Demediuk et al, 1985b), and impact trauma in rats . Impact injury in rats causes decreases in total tissue levels of magnesium (Lemke et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Lipid alterations correlate with tissue magnesium decrease following impact trauma in rabbit spinal cord

Lemke

Yum

Faden

1990

Molecular and Chemical Neuropathology

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Secondary neurochemical events contribute to progressive tissue damage and subsequent neurological deficit after traumatic spinal-cord injury (SCI). Among proposed injury factors are alterations of phospholipids and certain cations. To clarify the relationship of membrane lipid changes (phospholipids, cholesterol, and arachidonic acid) to changes in tissue content of water and selected ions (sodium, potassium, and magnesium) after SCI, these variables were examined in spinal-cord segments from anesthetized ventilated rabbits subjected to laminectomy or to moderate (40 g-cm) or severe (150 g-cm) impact trauma at the lumbar (L2) segment. Trauma caused significant increases in tissue sodium, water, and arachidonic acid content, and significant decreases in phospholipids, cholesterol, potassium, and magnesium content. Alterations in magnesium were significantly related to injury severity. In contrast, changes in spinal-cord water content occurred to a similar degree in the two injury groups, as did tissue sodium and potassium content. Decreases in phospholipids were strongly correlated with decreases in tissue magnesium content, whereas changes in sodium and potassium were less well-correlated. Because magnesium ions play a critical role with regard to cellular bioenergetic state, calcium flux, amino acid receptor function, and eicosanoid production, reductions in tissue magnesium after injury may be important in the progression of secondary tissue damage.

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“…These studies have suggested a twostep mechanism of neuronal impairment consisting of primary injury due to an external mechanical force and secondary injury due to additional damage initiated by the primary injury (Allen, 1914;Anderson et al, 1980;Fairholm and Turmbull, 1971;Griffiths, 1975;Tator and Fehling, 1991). The degree of secondary damage is influenced by a number of injury-promoting factors, including edema, ischemia, increased levels of neurotransmitters (Demediuk, et al, 1989), increased intracellular Ca level (Stokes et al, 1983;Young, 1985), and the presence of free radicals or nitric oxide (NO; Hamada et al, 1996a,b;Hsu et al, 1985;Selger-Stahl et al, 1985). In particular, NO is thought to play an important role in the secondary auto-destruction of neural tissue following spinal cord injuries.…”

Section: Introduction I N Patients With Spinal Cord Injury Mechanicalmentioning

confidence: 99%

Changes in Nitric Oxide and Expression of Nitric Oxide Synthase in Spinal Cord after Acute Traumatic Injury in Rats

Nakahara

Yone

Setoguchi

et al. 2002

Journal of Neurotrauma

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The aim of this study was to observe the time course of NO production and NOS expression in the spinal cord following acute traumatic injury. Rat spinal cord was injured by extradural static weight-compression, which resulted in an incomplete transverse spinal cord lesion with paralysis of the lower extremities. Using this model, measurement of NO by microdialysis and Griess reaction and histological and immunohistochemical examinations using polyclonal antibodies to nNOS and iNOS were performed from immediately to 14 days after injury. In injured cord, the amount of NO markedly increased immediately after injury and gradually decreased between 1 and 12 h after injury. A second wave of increase in NO level was observed at 24 h and 3 days after injury. Histologically, hematomas and necrotic changes were observed after injury and demyelination of nerve fibers increased with time in the compressed segment. Immunohistochemically, the number of cells with expression of nNOS was increased immediately to 12 h after injury. Expression of iNOS was observed from 12 h to 3 days after injury. These findings suggested that the initial maximal increase of NO production might be caused mainly by nNOS and that the second wave of increase in NO might be due mainly to iNOS.

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Phospholipids of normal and experimentally injured spinal cord of the miniature pig

Cited by 18 publications

References 18 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

Lipid alterations correlate with tissue magnesium decrease following impact trauma in rabbit spinal cord

Changes in Nitric Oxide and Expression of Nitric Oxide Synthase in Spinal Cord after Acute Traumatic Injury in Rats

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