2007Zhejiang Medical JournalRequires access

The mechanism of cognitive defect induced by chronic intermittent hypoxia in immature rats

Yong-Hai Zhou

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Abstract

Objective To investigate the mechanism of cognitive defect induced by intermittent hypoxia in immature rats.Methods Forty male Sprague-Dawley rats(3~4 week,80~100g) were randomly divided into four groups: 2-week intermittent hypoxia group(2IH),4-week intermittent hypoxia group(4IH),2-week control group(2C) and 4-week control group(4C);and 10 in each group.Intermittent hypoxia model was induced by an intermittent hypoxia cabin and the cabin was flushed with 99.99% nitrogen alternating with 99.50% oxygen.The time of one intermittent hypoxia cycle was 90s.At the end of experiments,the serum levels of 8-Iso-PGF2αwas determined by ELISA.Results The serum levels of 8-ISO-PGF2αin 2C,4C,2IH and 4IH groups were(1877.22±695.10) pg/ml,(1708.09±778.31)pg/ml,(17173.80±3082.34)pg/ml and(27098.44±7030.94)pg/ml,respectively.Compared with those in 2C,4C group,2IH and 4IH group had significantly higher levels of 8-ISO-PGF2α(P0.01,respectively).The ultrastructure of hippocampal neurons in intermittent hypoxia groups showed early apoptosis: the broken nuclear membrane,karyopyknosis and swollen mitochondria vacuoles.Conclusion Chronic intermittent hypoxia leads to oxidative stress,which may be associated with hippocampus damage and recognition degradation in weanling rats.

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Objective To investigate the mechanism of cognitive defect induced by intermittent hypoxia in immature rats.Methods Forty male Sprague-Dawley rats(3~4 week,80~100g) were randomly divided into four groups: 2-week intermittent hypoxia group(2IH),4-week intermittent hypoxia group(4IH),2-week control group(2C) and 4-week control group(4C);and 10 in each group.Intermittent hypoxia model was induced by an intermittent hypoxia cabin and the cabin was flushed with 99.99% nitrogen alternating with 99.50% oxygen.The time of one intermittent hypoxia cycle was 90s.At the end of experiments,the serum levels of 8-Iso-PGF2αwas determined by ELISA.Results The serum levels of 8-ISO-PGF2αin 2C,4C,2IH and 4IH groups were(1877.22±695.10) pg/ml,(1708.09±778.31)pg/ml,(17173.80±3082.34)pg/ml and(27098.44±7030.94)pg/ml,respectively.Compared with those in 2C,4C group,2IH and 4IH group had significantly higher levels of 8-ISO-PGF2α(P0.01,respectively).The ultrastructure of hippocampal neurons in intermittent hypoxia groups showed early apoptosis: the broken nuclear membrane,karyopyknosis and swollen mitochondria vacuoles.Conclusion Chronic intermittent hypoxia leads to oxidative stress,which may be associated with hippocampus damage and recognition degradation in weanling rats.

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Available abstract

Objective To investigate the mechanism of cognitive defect induced by intermittent hypoxia in immature rats.Methods Forty male Sprague-Dawley rats(3~4 week,80~100g) were randomly divided into four groups: 2-week intermittent hypoxia group(2IH),4-week intermittent hypoxia group(4IH),2-week control group(2C) and 4-week control group(4C);and 10 in each group.Intermittent hypoxia model was induced by an intermittent hypoxia cabin and the cabin was flushed with 99.99% nitrogen alternating with 99.50% oxygen.The time of one intermittent hypoxia cycle was 90s.At the end of experiments,the serum levels of 8-Iso-PGF2αwas determined by ELISA.Results The serum levels of 8-ISO-PGF2αin 2C,4C,2IH and 4IH groups were(1877.22±695.10) pg/ml,(1708.09±778.31)pg/ml,(17173.80±3082.34)pg/ml and(27098.44±7030.94)pg/ml,respectively.Compared with those in 2C,4C group,2IH and 4IH group had significantly higher levels of 8-ISO-PGF2α(P0.01,respectively).The ultrastructure of hippocampal neurons in intermittent hypoxia groups showed early apoptosis: the broken nuclear membrane,karyopyknosis and swollen mitochondria vacuoles.Conclusion Chronic intermittent hypoxia leads to oxidative stress,which may be associated with hippocampus damage and recognition degradation in weanling rats.

Key concepts: Intermittent hypoxia, Weanling, Hypoxia (environmental), Medicine, Hippocampal formation, Oxidative stress, Apoptosis, Internal medicine

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