Possibility of influence of hemofiltration in mechanisms of glutamate excitotoxicity in ischemic stroke

Возможность влияния гемофильтрации в механизмах глутаматной эксайтотоксичности при ишемическом инсульте
Almagul Zhussupova 1, Agzam Zhumadilov 2, Sholpan Nurmanova 1, Alexander Zlotnik 2, Askhat Bekmukhanbetov 2, Marat Abduov 2, Igor Kim 2
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1 JSC “Astana Medical University”, Astana, Kazakhstan
2 National Scientific Center Oncology and Transplantology, Astana, Kazakhstan
J CLIN MED KAZ, Volume 4, Issue 34, pp. 20-24.
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ABSTRACT

Currently, much attention has been paid to the value of the presence of biomarkers in blood and cerebrospinal fluid in acute ischemic stroke. The results of experimental studies have shown that an increase in biomarkers particularly glutamate demonstrated high sensitivity and specificity with a positive prognostic value. High levels of glutamate could be regarded as a marker for high risk of development of cerebral tissue infarction. However, the fact that the reduced level of glutamate in the blood of patients with an ischemic stroke might lead to positive results need to be confirmed in further clinical studies.

CITATION

Zhussupova A, Zhumadilov A, Nurmanova S, Zlotnik A, Bekmukhanbetov A, Abduov M, et al. Possibility of influence of hemofiltration in mechanisms of glutamate excitotoxicity in ischemic stroke. Journal of Clinical Medicine of Kazakhstan. 2014;4(34):20-4.

REFERENCES

  • Astrup J., Siesjo B., Symon L. Thresholds in cerebral ischemia – the ischemic penumbra, Stroke, 1981, No.12(6), pp.723-725.
  • Abstracts 22-nd International Conference on Stroke and Cerebral Circulation Stroke,1977, No.1, pp.71-76.
  • Acute Stroke Management: Part II Stroke clinical updates, 1993, No.3, pp. 21-24.
  • Toole J. Cerebrovascular Disease. – N.Y.5-th Ed; 1995.
  • Toole J. Management of Acute Ischemic Stroke. Winston-Salem; 1995.
  • Adams H., Brott T.,Growell R. Guidelines for the management of patients with acute ischemie stroke. Stroke,1994, No.9, pp.1913.
  • Gusev EI. Ishemicheskaja bolezn’ mozga: Aktovaja rech’ (Ischemic brain disease: it acts), Medicina, Moskva,1992, 35 p.
  • Vereshhagin N.V., Morgunov V.A., Gulevskaja T.S. Patologija golovnogo mozga pri ateroskleroze i arterial’noj gipertonii (Brain pathology in atherosclerosis and hypertension), M.: Medicina, 1997, 283 p.
  • Heiss W.D. Experimental evidence of ischemic thresholds and functional recovery. Stroke,1992, No.23, pp.1668-1672.
  • Siesjo B.K. Pathophysiology and treatment of focal cerebral ischemia stroke. Part II: Pathophysiology. J.Neurosurg, 1992, No.77(2), pp.169-184.
  • Siesjo B.K. Pathophysiology and treatment of focal cerebral ischemia stroke. Part II: Mechanisms of damage and treatment. J.Neurosurg, 1992, No.77(3), pp.337-354.
  • Baron J. von Kumer R., del Zoppo G. Treatment of acute ischaemic stroke: challenging the concept of a rigid and universal time window, Stroke,1995, No.12, pp.2219-2221.
  • Blanpied T.A., Clarke R.J., Johnson J.W. Amantadine inhibits NMDA receptors by accelerating channel elosure during channel block. J. Neurosci,2005, No.25, pp. 3312-3322.
  • Rodriguez-Yanez M., Sobrino T., Arias S. et al. Early biomarkers of clinical-diffusion mismatch in acute ischtmic stroke, Stroke, 2011, No.42(11), pp.2813-2818.
  • Zauner A., Bullock R., Kuta A.J., et al. Glutamate release and cerebral blood flow after severe human head injury. Acta Neurochir, 1996,No.67, pp.40-44.
  • Hawkins R.A. The blood-brain barrier and glutamate. Am. J. Clin. Nutr, 2009,No.90, pp.867-874.
  • Richards D.A., Tolias C.M., Sgouros S., Bowery N.G. Extracellular glutamine to glutamate ratio may predict outcome in the injured brain: A clinical microdialysis study in children. Pharmacol. Res.,2003, 48, pp.101-9.
  • Hawkins R.A., Mokashi A., Dejoseph M.R. et al. Glutamate permeability at the blood-brain barrier in insulinopenic and insulinresistant rats. Metabolism, 2010, 59, pp.258–266.
  • Rossi D.J., Oshima T., Attwell D. Glutamate release in severe brain ischaemia is mainly by reversed uptake, Nature, 2000, 403, pp.316-321.
  • Jensen A.M., Chiu S.Y. Differential intracellular calcium responses to glutamate in type 1 and type 2 cultured brain astrocytes. J. Neurosc,1991,11, pp.1674–1684.
  • Kato B.M., Lachica E.A., Rubel E.W. Glutamate modulates intracellular Ca2+ stores in brain stem auditory neurons, J. Neurophysiol,1996,76, pp.646-650. 
  • Castillo J., Davalos A., Naveiro J., Noya M. Neuroexcitatory amino acids and their relation to infarct size and neurological deficit in ischemic stroke, Stroke,1996, 27, pp.1060–1065.
  • Zauner A., Bullock R., Kuta A.J. et ai. Glutamate release and cerebral blood flow after severe human head injury, Acta Neurochir, 1996, 67, pp.40-44.
  • Castillo J., Davalos A., Alvarez-Sabin J. et al. Molecular signatures of brain injury after intracerebral hemorrhage. Neurology, 2002, 58, pp.624–629.
  • Johnston M.V., Trescher W.H., Ishida A., Nakajima W. Neurobiology of hypoxic-ischemic injury in the developing brain, Pediatr. Res.,2001,49, pp.735-741.
  • O’Kane R.L., Martinez-Lopez I., DeJoseph M.R. et al. Na+-dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) of the blood-brain barrier. A mechanism for glutamate removal. J. Biol. Chem,1999,274, pp.31891-31895.
  • Helms H.C., Madelung R., Waagepetersen H.S. et al. In vitro evidence for the brain glutamate efflux hypothesis: Brain endothelial cells cocultured with astrocytes display a polarized brain-to-blood transport of glutamate. Glia, 2012, 60, pp.882-893.
  • Bickel U., Yoshikawa T., Pardridge W.M. Delivery of peptides and proteins through the blood-brain barrier, Adv. Drug Deliv. Rev, 2001,46, pp.247-279.
  • Schlageter K.E., Molnar P., Lapin G.D., Groothuis D.R. Microvessel organization and structure in experimental brain tumors: Microvessel populations with distinctive structural and functional properties, Microvasc. Res, 1999, 58, pp. 312-328.
  • Krivonos O.V., Amosova N.A., Smolenceva I.G. Primenenie antagonista glutamatnyh NMDA- receptorov PK-Merc v ostrom periode insul’ta (The use of an antagonist of glutamate receptors NMDA- PK-Merz in the acute phase of stroke), Zhurnal nevrologii i psihiatrii, 2009, No.109(4), pp.72.
  • Kulesh S.D., Doroshenko E.M. Osobennosti metabolizma nejroaktivnyh aminokislot v ostrom periode ishemicheskogo insul’ta (Features metabolism of neuroactive amino acids in acute ischemic stroke), Zhurnal nevrologii i psihiatrii, 2000, No.5, pp.64-65.
  • Buchan A.M., Lesiuk H., Barnes K.A., Li H. et al. AMPA antagonists: Do they hold more promise for clinical stroke trials than NMDA antagonists? Stroke,1993, No.24, pp.148-152.
  • Ikonomidou C., Turski L. Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury? Lancet Neurol,2002, No.1, pp.383-386.
  • Hardingham G.E., Bading H. The Yin and Yang of NMDA receptor signalling. Trends, Neurosci, 2003, No.26, pp.81-89.
  • Gottlieb M, Wang Y, Teichberg Vl. Blood-mediated scavenging of cerebrospinal fluid glutamate, J. Neurochem, 2003, No.87, pp.119-126.
  • Teichberg Vl, Cohen-Kashi-Malina K, Cooper I, et al. Homeostasis of glutamate in brain fluids: An accelerated brain-to-blood efflux of excess glutamate is produced by blood glutamate scavenging and offers protection from neuropathologies, Neurosciens, 2009, No.158, pp.301-308.
  • Campos F., Sobrino T. Ramos-Cabrer P. et al. High blood glutamate oxaloacetate transaminase levels are associated with good functional outcome in acute ischemic stroke, J. Cereb Blood Flow Metab, 2011, No.31, pp.1378-1386.