Biomedical subjects

S W Yum

Publications and source records attributed to S W Yum.

5 recordsLinked to original sources

PubMed1990

Comparison of the neuroprotective effects of the N-methyl-D-aspartate antagonist MK-801 and the opiate-receptor antagonist nalmefene in experimental spinal cord ischemia.

Both N-methyl-D-aspartate (NMDA)-receptor antagonists and opiate-receptor antagonists have been shown to limit tissue damage after ischemic central nervous system injury. We compared the neuroprotective effects of the noncompetitive NMDA-receptor antagonist MK-801 and the opiate-receptor antagonist nalmefene in a model of global spinal cord ischemia and reperfusion in unanesthetized rabbits. MK-801 (1 mg/kg) or nalmefene (0.1 mg/kg) was administered intravenously 5 minutes after reperfusion. MK-801 treatment and nalmefene treatment each significantly improved the neurologic and histologic outcome compared with saline controls. Differences in these outcome measures between MK-801 treatment and nalmefene treatment did not reach statistical significance. Our results are consistent with the hypothesis that multiple factors, including endogenous opioids and excitatory amino acids, contribute to the secondary tissue injury after central nervous system ischemia. These data also provide further evidence that therapeutic interventions with opiate-receptor antagonists or NMDA antagonists may be beneficial in limiting neurologic dysfunction after ischemic brain or spinal cord injury.

Animals↗

PubMed1990

Alteration in extracellular amino acids after traumatic spinal cord injury.

It has recently been demonstrated that N-methyl-D-aspartate antagonists limit tissue damage after spinal cord trauma, implicating excitatory amino acids in the secondary injury response. To determine whether spinal cord trauma alters the concentrations of extracellular amino acids, microdialysis was conducted in spinal cord during and after administration of impact trauma. Extracellular concentrations of excitatory, inhibitory, and nontransmitter amino acids were elevated after trauma, with the degree of increase related to severity of injury. Moderate trauma resulted in an immediate but transient increase (200-400%) in the extracellular levels of all amino acids measured. Severe trauma produced a more prolonged and significant increase (400-630%) in the concentrations of extracellular amino acids, including aspartate and glutamate. These results are consistent with the hypothesis that excitatory amino acids may contribute to delayed tissue injury after central nervous system trauma.

Amino Acids↗

PubMed1990

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

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.

Animals↗

PubMed1990

Effects of TRH-analog treatment on tissue cations, phospholipids and energy metabolism after spinal cord injury.

Effects of thyrotropin-releasing hormone analog CG3703 on biochemical changes following impact spinal cord trauma were investigated by 31P magnetic resonance spectroscopy, atomic absorption spectrophotometry, high-pressure liquid chromatography and radioimmunoassay using parallel injury models in rabbits and rats. Treatment with CG3703 at 45 min after trauma in rabbits significantly attenuated decreases in intracellular pH and reversed increases in phosphodiester to phosphomonoester ratio, as shown by 31P magnetic resonance spectroscopy. The improved phosphodiester/phosphomonoester ratio was correlated with improved ATP status after treatment, although there was no improvement in aerobic bioenergetic capacity as reflected by phosphocreatine to inorganic phosphate ratios. In rats, treatment with CG3703 significantly reduced changes in tissue cations (Na+, K+, Mg2+) and water content following trauma, but did not significantly alter the accumulation of free fatty acids or thromboxane B2. Thus, the beneficial effects of treatment with thyrotropin-releasing hormone or thyrotropin-releasing hormone analogs on outcome following traumatic spinal cord injury may be due, in part, to actions relating to ion homeostasis.

Animals↗

PubMed1989

Traumatic spinal cord injury in rabbits decreases intracellular free magnesium concentration as measured by 31P MRS.

The mechanisms by which traumatic injury to the central nervous system cause irreversible tissue damage remain speculative. Recent reports suggest that a decrease in tissue total and free Mg2+ concentration may be an important factor in the development of such injury after experimental brain trauma. Although total Mg changes have been reported following spinal cord trauma, no studies have examined spinal cord-free Mg2+. In the present study, we have used phosphorus magnetic resonance spectroscopy to determine intracellular free Mg2+ concentration and atomic absorption spectrophotometry to measure total tissue Mg concentration in rabbit spinal cord prior to and following impact trauma. We report that intracellular free Mg2+ concentration decreases from a pre-injury value of 0.80 +/- 0.12 mM (mean +/- S.E.M.) to 0.31 +/- 0.05 mM at 2 h post-trauma. Following injury there was an associated decrease in total tissue Mg and K concentration, but no alterations in tissue Na or water content.

Animals↗