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Sökning: L773:0001 6268 > Uppsala universitet > Hillered Lars

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1.
  • Clausen, Fredrik, et al. (författare)
  • Cerebral glucose metabolism after traumatic brain injury in the rat studied by C-13-glucose and microdialysis
  • 2011
  • Ingår i: Acta Neurochirurgica. - : Springer Science and Business Media LLC. - 0001-6268 .- 0942-0940. ; 153:3, s. 653-658
  • Tidskriftsartikel (refereegranskat)abstract
    • Following traumatic brain injury (TBI), a disturbed cerebral glucose metabolism contributes to secondary brain damage. To study local cerebral glucose metabolism after TBI, we delivered C-13-labeled glucose into brain tissue by microdialysis (MD). MD probes were inserted bilaterally into the parietal cortex of rat brain, one probe in the shear stress zone of the injury and the other at the corresponding contralateral coordinates. A moderately severe controlled cortical contusion was used to model TBI. Dialysate concentrations of glucose, pyruvate, lactate, and glycerol were measured, and following derivatization, C-13 enrichments of the compounds were determined by gas chromatography-mass spectrometry. We found that C-13-labeled glucose was rapidly converted into C-13-lactate and C-13-glycerol. In the hours following TBI, concentrations and C-13 enrichments of lactate and glycerol increased. The findings confirm the occurrence of anaerobic local glucose metabolism early after TBI. Only a small fraction of the glycerol was newly synthesized, suggesting that the hypothesis that most of the released glycerol after TBI comes from degradation of membrane phospholipids still holds. We conclude that the combination of microdialysis and stable isotope technique is a useful tool for investigating local glucose metabolism following brain injury.
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2.
  • Samuelsson, Carolina, et al. (författare)
  • Microdialysis patterns in subarachnoid hemorrhage patients with focus on ischemic events and brain interstitial glutamine levels
  • 2009
  • Ingår i: Acta Neurochirurgica. - : Springer-Verlag. - 0001-6268 .- 0942-0940. ; 151:5, s. 437-446
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: This observational microdialysis (MD) study of 33 subarachnoid hemorrhage patients explores brain interstitial levels of glutamine, glutamate, lactate and pyruvate, and their relationship to clinical status and clinical course at the neurointensive care unit. METHODS: The focus was on ischemic events, defined by clinical criteria or by radiology, and the significance of brain interstitial glutamine levels and lactate/pyruvate (L/P) ratio. RESULTS: Eleven out of 12 periods with an ischemic MD pattern, defined as lactate/pyruvate (L/P) ratios exceeding 40, were either related to delayed ischemic neurological deficits (DIND) or CT-verified infarcts, confirming that L/P above 40 is a specific ischemic and pathological MD measure. Poor admittance WFNS grade (WFNS 4-5) patients had lower glutamine at the onset of monitoring than what good admittance WFNS grade (WFNS 1-3) patients had (P < 0.05). Interstitial glutamine increased over time in most patients. A "glutamine surge" was defined as a period where the interstitial glutamine concentration increased at least 150 microM over 12 h. Fifteen patients had a DIND and associated MD patterns were glutamine surges (n = 12) and/or L/P>40 (n = 6). Seven patients received vasospasm treatment; in five of these the only DIND-associated MD pattern was a glutamine surge. Seventy percent of the glutamine surges occurred during ongoing propofol sedation, and there was no association between extubations and glutamine surges. There was no difference in mean glutamine levels during the monitoring period between patients with favorable 6-month outcome and patients with poor 6-month outcome. CONCLUSION: We suggest that an increasing interstitial glutamine trend is a dynamic sign of augmented astrocytic metabolism with accelerated glutamate uptake and glutamine synthesis. This pattern is presumably present in metabolically challenged, but yet not overt ischemic tissue.
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3.
  • Tsitsopoulos, Parmenion P., et al. (författare)
  • Association of the bleeding time test with aspects of traumatic brain injury in patients with alcohol use disorder
  • 2020
  • Ingår i: Acta Neurochirurgica. - : SPRINGER WIEN. - 0001-6268 .- 0942-0940. ; 162:7, s. 1597-1606
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-aim Traumatic brain injury (TBI) and alcohol use disorder (AUD) can occur concomitantly and be associated with coagulopathy that influences TBI outcome. The use of bleeding time tests in TBI management is controversial. We hypothesized that in TBI patients with AUD, a prolonged bleeding time is associated with more severe injury and poor outcome. Material and methods Moderate and severe TBI patients with evidence of AUD were examined with bleeding time according to IVY bleeding time on admission during neurointensive care. Baseline clinical and radiological characteristics were recorded. A standardized IVY bleeding time test was determined by staff trained in the procedure. Bleeding time test results were divided into normal (<= 600 s), prolonged (> 600 s), and markedly prolonged (>= 900 s). Normal platelet count (PLT) was defined as > 150,000/mu L. This cohort was compared with another group of TBI patients without evidence of AUD. Results Fifty-two patients with TBI and AUD were identified, and 121 TBI patients without any history of AUD were used as controls. PLT was low in 44.2% and bleeding time was prolonged in 69.2% of patients. Bleeding time values negatively correlated with PLT (p < 0.05). TBI patients with markedly prolonged values (>= 900 s) had significantly increased hematoma size, and more frequently required intracranial pressure measurement and mechanical ventilation compared with those with bleeding times < 900 s (p < 0.05). Most patients (88%) with low platelet count had prolonged bleeding time. No difference in 6-month outcome between the bleeding time groups was observed (p > 0.05). Subjects with TBI and no evidence for AUD had lower bleeding time values and higher platelet count compared with those with TBI and history of AUD (p < 0.05). Conclusions Although differences in the bleeding time values between TBI cohorts exist and prolonged values may be seen even in patients with normal platelet count, the bleeding test is a marker of primary hemostasis and platelet function with low specificity. However, it may provide an additional assessment in the interpretation of the overall status of TBI patients with AUD. Therefore, the bleeding time test should only be used in combination with the patient's bleeding history and careful assessment of other hematologic parameters.
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4.
  • Zetterling, Maria, et al. (författare)
  • Temporal patterns of interstitial pyruvate and amino acids after subarachnoid haemorrhage are related to the level of consciousness : a clinical microdialysis study
  • 2009
  • Ingår i: Acta Neurochirurgica. - : Springer Science and Business Media LLC. - 0001-6268 .- 0942-0940. ; 151:7, s. 771-780
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Temporal patterns of brain interstitial amino acids after subarachnoid haemorrhage (SAH) were studied in relation to energy metabolite levels and to the severity of the initial global ischaemia as reflected by the level of consciousness at admission. METHOD: Intracerebral microdialysis was used to measure brain interstitial amino acids and the energy metabolites glucose, lactate, and pyruvate during five days in 19 patients. Patients who were conscious (n = 11) were compared to those who were unconscious on admission (n = 8). FINDINGS: Eight non-transmitter amino acids (alanine, asparagine, glutamine, isoleucine, leucine, phenylalanine, serine and tyrosine), as well as glycine and pyruvate showed a pattern of increasing concentrations starting at 60-70 h after the onset of SAH. The conscious patients showed more pronounced elevations of non-transmitter amino acids, glycine, taurine and pyruvate compared to the unconscious patient group. Pyruvate levels were initially critically low for all patients, then normalised in the conscious patients but remained low in the unconscious group. CONCLUSIONS: There was an increase of the cerebral interstitial levels of non-transmitter amino acids and glycine which correlated temporally to pyruvate levels, more pronounced in patients conscious on admission. Pyruvate levels in these patients normalised, but remained reduced in the unconscious patients. The increase of the non-transmitter amino acids and glycine could reflect an increased amino acid turnover in an attempt at repairing the injured brain, which could have been hampered by the lower pyruvate levels. Interstitial pyruvate may be a useful marker of the energy metabolic situation in the acutely injured brain.
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