Neurochemical Research

, Volume 32, Issue 11, pp 1843–1848 | Cite as

The Study of Na+, K+-ATPase Activity of Rat Brain during Crush Syndrome

Original Paper
First Online:
Received:
Accepted:

Abstract

Crush syndrome (CS) results from severe traumatic damage to the organism that is characterized by stress, acute homeostatic failure of the tissues, and myoglobinuria with severe intoxication. This leads to an acute impairment of kidneys and heart. The peripheral and central nervous systems are also the subject of significant changes in CS. Na+, K+-ATPase is a critical enzyme in neuron that is essential for the regulation of neuronal membrane potential, cell volume as well as transmembrane fluxes of Ca++ and Excitatory Amino Acids. In the present study, Na+, K+-ATPase activity of rat brain regions [Olfactory lobes (OL), Cerebral cortex (CC), Cerebellum (CL), and Medulla oblongata (MO)] during CS was investigated. Experimental model of CS in albino rats was induced by 2-h of compression followed by 2, 24, and 48-h of decompression of femoral muscle tissue. In this study, we have observed elevation in Na+, K+-ATPase activity above normal/control levels in all parts of brain (OL: 34.4%; CC: 1.0%; CL: 3.3% and MO: 45%) during 2-h compression in comparison to controls.

Keywords

Na+ K+-ATPase in crush syndrome ATPases in brain 
This is a preview of subscription content, log in to check access.

Notes

Acknowledgments

The authors acknowledge the receipts of financial assistance from Department of Science and Technology, New Delhi under FIST program and financial support given by University Grants Commission under Innovative Research program.

References

  1. 1.
    Ly Permiakov NK, Zimina LN (1982) In: Acute kidney failure (russian). Moscow 129–135Google Scholar
  2. 2.
    Zimina LN (1985) Pathological anatomy of mio-renal syndrome in conditions of modern treatment. Arch Pathol 1:44–50Google Scholar
  3. 3.
    Better OS (1999) Rescue and salvage of casualties suffering from the crush syndrome after mass disasters. Mil Med 164:366–369PubMedGoogle Scholar
  4. 4.
    Kuzis K, Coffin JD, Eckenstein FP (1999) Time course and age dependence of motor neuron death following facial nerve crush injury: role of fibroblast growth factor. Exp Neurol 157:77–87PubMedCrossRefGoogle Scholar
  5. 5.
    Dong Z, Cheng X, Gu Y (1998) Effect of crushing of sciatic nerve on neuron of lumbar spinal cord. Chung Kuo Hsiu Fu Chung Chien Wai Ko Tsa Chih 12:113–116PubMedGoogle Scholar
  6. 6.
    Wyse ATS, Bavaresco CS, Bandinelli C et al (2001) Nitric oxide synthase inhibition by L-NAME prevents the decrease of Na+,K+-ATPase activity in midbrain of rats subjected to arginine administration. Neurochem Res 26:515–520PubMedCrossRefGoogle Scholar
  7. 7.
    Grisar T (1984) Glial and neuronal Na+-K+ pump in epilepsy. Ann Neurol 16:128–134CrossRefGoogle Scholar
  8. 8.
    Lees GJ (1991) Inhibition of sodium-potassium-ATPase: a potentially ubiquitous mechanism contributing to central nervous system neuropathology. Brain Res Rev 16:283–300PubMedCrossRefGoogle Scholar
  9. 9.
    Albers RW, Siegel GJ (1999) Membrane transport. In: Siegel GJ, Agranoff BW, Albers RW, Fisher SK, Uhler MD (eds) Basic neurochemistry. Lippincott-Raven, Philadelphia, pp 95–118Google Scholar
  10. 10.
    Jones DH, Matus AI (1974) Isolation of synaptic plasma membrane from brain by combination flotation-sedimentation density gradient centrifugation. Biochim Biophys Acta 356:276–287PubMedCrossRefGoogle Scholar
  11. 11.
    Tsakiris S, Deliconstantinos G (1984) Influence of phosphatidylserine on (Na+, K+)-stimulated ATPase and acetylcholinesterase activities of dog brain synaptosomal plasma membranes. Biochem J 22:301–307Google Scholar
  12. 12.
    Gomorri G (1962) Determination of inorganic phosphate in serum and plasma. In: Varley H (ed) Practical clinical biochemistry, 3rd edn. Inter-science Publishers, New York, pp 448–450Google Scholar
  13. 13.
    Lowry OH, Rosebrough NJ, Farr AL, Randall RJ (1951) Protein measurement with the Folin phenol reagent. J Biol Chem 193:265–275PubMedGoogle Scholar
  14. 14.
    Knaryan VH, Arakelyan LN, Marouchyan GL, Kevorkian GA (2002) High affinity glutamate uptake in rat brain slices in experimental crush syndrome. Med Sci Monit 8:75–79Google Scholar
  15. 15.
    Kevorkian GA, Kanayan AS, Khachatryan HF et al (2001) Protein synthesis in white rats brain and myocardium ultrastructure components at experimental crush syndrome. Med Sci Armenia 4:1–6Google Scholar
  16. 16.
    Hendrickx HH, Safar P, Baer BP, Basford RE (1984) Brain lactate and alanine-glutamate ratios during and after asphyxia in rats. Neurochem Res 12:129–140Google Scholar
  17. 17.
    Hayrapetyan HL, Khachatryan HF, Mardanyan SS et al (2000) Activity of enzymes of adenyline compounds metabolism during crush and decompression of muscle tissue. Part II. Adenosine deaminase activity at experimental crush syndrome. Med Sci Monit 6:1068–1076PubMedGoogle Scholar
  18. 18.
    Stahl WL (1986) The Na, K-ATPase of nervous tissue. Neurochem Int 8:449–476CrossRefPubMedGoogle Scholar
  19. 19.
    Better OS, Stein JH (1990) Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 322:825–829PubMedCrossRefGoogle Scholar
  20. 20.
    Venugopal J, Ramakrishna S (2005) Inhibition of ATPases enzyme activities on brain disturbing normal estrous cycle. Neurochem Res 3:315–323CrossRefGoogle Scholar
  21. 21.
    Tsakiris T, Angelogianni P, Tesseromatis C, Tsakiris S, Tsopanakis C (2006) Alterations antioxidant status, protein concentration, Acetylcholinesterase, Na+, K+-ATPase, and Mg2+-ATPase Activities in Rat Brain after Forced Swimming. Int J Sports Med 27:19–24PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  1. 1.Department of ZoologyGoa UniversityPanajiIndia

Personalised recommendations