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DOI 10.1179/016164107x166254

Медицинская библиотека · Neurological research · 2007

The pre-treatment effect on brain injury during restoration of normal perfusion pressure with hemodilution in a new rat model of chronic cerebral hypoperfusion.

Hai Jian, Lin Qi, Deng Dong-Feng, Pan Qing-Gang, Ding Mei-Xiu

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVES

To investigate the effect of hemodilution with high-concentration human serum albumin (HSA) on brain injury in a rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations.

METHODS

The animal model was established by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein and the ipsilateral common carotid artery, followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. The agent (20% HSA) or control solution (0.9% sodium chloride) was administered intravenously at a dosage of 1% body weight 24 hours before ligation of the fistula. Blood-brain barrier (BBB) disruption was judged by extravasation of Evans blue (EB) dye. EB, water content and the changes of myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in rat brains 24 hours after ligation of the fistula were determined.

RESULTS

EB and water content in rat brains of the pre-treated group were significantly decreased compared with the control group accompanied by reduction of MPO activity and enhancement of SOD activity.

DISCUSSION: Hemodilution with high-concentration HSA has a certain pre-treatment effect on brain injury after ligation of the fistula in rat model of chronic cerebral hypoperfusion, which may be resulted from improved microcirculation, decrease in inflammatory cell infiltration and inactivation of oxygen free radicals.

Для цитирования: Hai Jian, Lin Qi, Deng Dong-Feng, Pan Qing-Gang, Ding Mei-Xiu. The pre-treatment effect on brain injury during restoration of normal perfusion pressure with hemodilution in a new rat model of chronic cerebral hypoperfusion.. Neurological research. 2007. DOI: 10.1179/016164107x166254.

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