
FOLLOWUS
1. Institute of Materia Medica
2. CAMS & PUMC
3. ,China
纸质出版日期:1997
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[1]邓文斌,冯亦璞.EFFECT OF DL-3-N-BUTYLPHTHALIDE ON BRAIN EDEMA IN RATS SUBJECTED TO FOCAL CEREBRAL ISCHEMIA[J].Chinese Medical Sciences Journal,1997(02):102-106.
EFFECT OF DL-3-N-BUTYLPHTHALIDE ON BRAIN EDEMA IN RATS SUBJECTED TO FOCAL CEREBRAL ISCHEMIA[J]. Chinese medical sciences journal, 1997, (2): 102-106.
[1]邓文斌,冯亦璞.EFFECT OF DL-3-N-BUTYLPHTHALIDE ON BRAIN EDEMA IN RATS SUBJECTED TO FOCAL CEREBRAL ISCHEMIA[J].Chinese Medical Sciences Journal,1997(02):102-106. DOI:
EFFECT OF DL-3-N-BUTYLPHTHALIDE ON BRAIN EDEMA IN RATS SUBJECTED TO FOCAL CEREBRAL ISCHEMIA[J]. Chinese medical sciences journal, 1997, (2): 102-106. DOI:
<正> The present study evaluated the effect of dl-3-n-butylphthalide(NBP)
a novel brain protective agent
on brain edema in rats following focal ischemia. Edema was induced by occluding the right middle cerebral artery (MCAO).producing permanent focal ischemia in the right cerebral hemisphere
which developed ip-silateral brain edema reproducibly. Edema was assessed 24 h after MCA occlusion by determining the brain water content from wet and dry weight measurements
and the sodium
potassium concentrations with ion-selective electrodes. In this model
NBP at the dose of 80
160 and 240 mg/kg po 15 min after MCAO prevented from brain edema in a dose-dependent manner. A significant reduction of sodium content and an increase in potassium level were observed in all drug-treated groups. It showed that NBP strongly attenuated brain water entry
sodium accumulation and potassium loss. Nimodipine treatment(5mg/kg sc) also reduced brain edema (P<0. 05). The results suggest that a strong anti-edema activity of NBP may pla
The present study evaluated the effect of dl-3-n-butylphthalide(NBP)
a novel brain protective agent
on brain edema in rats following focal ischemia. Edema was induced by occluding the right middle cerebral artery (MCAO).producing permanent focal ischemia in the right cerebral hemisphere
which developed ip-silateral brain edema reproducibly. Edema was assessed 24 h after MCA occlusion by determining the brain water content from wet and dry weight measurements
and the sodium
potassium concentrations with ion-selective electrodes. In this model
NBP at the dose of 80
160 and 240 mg/kg po 15 min after MCAO prevented from brain edema in a dose-dependent manner. A significant reduction of sodium content and an increase in potassium level were observed in all drug-treated groups. It showed that NBP strongly attenuated brain water entry
sodium accumulation and potassium loss. Nimodipine treatment(5mg/kg sc) also reduced brain edema (P<0. 05). The results suggest that a strong anti-edema activity of NBP may play an important role to contribute to the treatment of ischemic damage.
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