CHANGES IN INTENSITY OF HYPOXIC BRAIN DAMAGE IN RATS INDUCED BY HYPOXIC POSTCONDITIONING



Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

The present study has been aimed to estimate a neuroprotective effect of postconditioning (PostC) by using mild hypobaric hypoxia (360 mm Hg, 2 h) in a model of severe hypoxic brain injury (180 mm Hg, 3 h) in rats. PostC was performed by three trials of mild hypoxia with 24 h intervals, according to two different protocols - PostC was started 3 h (early PostC) or 24 h (delayed PostC) following severe hypoxia. Using histological methods and computer image analysis, loss of neurons in hippocampus and neocortex was analyzed 7 days after severe hypoxia. Severe hypoxia caused loss of 24% of neurons in layer V of the neocortex, 26% of neurons in СА1 region of hippocampus and 22% of neurons in СА4 region. Early PostC prevented loss of neurons in CA1 region of hippocampus and significantly reduced loss of neurons in neocortex (to 13%) and in CA4 region (to 10%). Delayed PostC fully prevented neuronal damage in CA4 region of hippocampus and neocortex and was to a large extent but not completely protective in CA1 region (12% of neurons were lost). The results show that PostC performed by hypobaric hypoxia has a pronounced neuroprotective effect, reducing the loss of neurons in vulnerable structures of brain (hippocampus and neocortex). The efficacy of neuroprotection depends upon the time of presentation of the first PostC session.

References

  1. Рыбникова Е.А., Хожай Л.И., Тюлькова Е.И. и др. Влияние гипобарической гипоксии на экспрессию белков ранних генов и структурные изменения нейронов мозга: корректирующий эффект прекондиционирования. Морфология, 2004, т. 125, вып. 2, c. 10-15.
  2. Самойлов М.О., Рыбникова Е.А., Тюлькова Е.И. и др. Влияние гипобарической гипоксии на поведенческие реакции и экспрессию ранних генов в мозге крыс: корректирующий эффект прекондиционирующего воздействия. Докл. PАН, 2001, т 81, № 1, c. 1-3.
  3. Chapuisat G., Dronne M.A., Grenier E. et al. In silico study of the influence of intensity and duration of blood flow reduction on cell death through necrosis or apoptosis during acute ischemic stroke. Acta Biotheor., 2010, v. 58, № 2-3, p. 171-190.
  4. Leconte C., Tixier E., Freret T. et al. Delayed hypoxic postconditioning protects against cerebral ischemia in the mouse. Stroke, 2009, v. 40, № 10, p. 3349-3355.
  5. Paxinos G. and Watson C. The Rat Brain in Stereotaxic Coordinates. 2nd. ed. San Diego, Acad. Press, 1986.
  6. Rybnikova E.A., Gluschenko T., Tulkova E. et al. Preconditioning induces prolonged expression of transcription factors pCREB and NF-kappaB in the neocortex of rats before and following severe hypobaric hypoxia. J. Neurochem., 2008, v. 106, № 3, p. 1450-1458.
  7. Rybnikova E.A., Sitnik N., Gluschenko T. et al. The preconditioning modified neuronal expression of apoptosis-related proteins of Bcl-2 superfamily following severe hypobaric hypoxia in rats. Brain Res., 2006, v. 1089, № 1, p. 195-202.
  8. Rybnikova E.A., Vataeva L., Tyulkova E. et al. Preconditioning prevents impairment of passive avoidance learning and suppression of brain NGFI-A expression induced by severe hypoxia. Beh. Brain. Re., 2005, v. 160, № 1, p. 107-114.
  9. Zhao H. I schemic postconditioning as a novel avenue to protect against brain injuvy after stroke. J. Cerebr. Blood Flow Metab., 2009, v. 29, № 5, p. 873-885.
  10. Zhao Z.Q., Corvera J.S., Halkos M.E. et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am. J. Physiol. Heart Circ. Physiol., 2003, v. 285, № 2, p. 579-588.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2012 Eco-Vector


СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: № 0110212 от 08.02.1993.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies