Lipocortin-1 fails to ameliorate cold-injury brain edema in the rat.
Based on evidence that corticosteroids exert their anti-inflammatory action via de novo synthesis of phospholipase A2 inhibitory proteins called lipocortins, we examined effects of high dose dexamethasone and recombinant human lipocortin-1 (annexin-I) on cold-injury brain edema in the rat. Since it takes several hours for lipocortins to be induced, dexamethasone (10 mg/kg) was injected intraperitoneally 3 hours before cold injury. Recombinant lipocortin-1 was administered intraventricularly at three different doses (0.01 mg/kg, 0.05 mg/kg, or 0.1 mg/kg: total volume 20 microliters), or via the internal carotid artery at a dose of 10(-7) M (2 ml). To induce cold injury, a liquid-nitrogen-cooled probe was placed on the exposed dura of male Wistar rats (330-370 kg) for 1 minute. Specific gravimetry and/or a wet-dry weighing method were used for measurement of brain edema at 24 or 48 hours after lesion production. In the present study, dexamethasone and recombinant lipocortin-1 failed to attenuate edema formation. The anti-inflammatory effects of dexamethasone or exogenous lipocortin-1 seemed unlikely to affect cold-injury brain edema.
Mima
T
T
Department of Neurosurgery, Kochi Medical School, Japan.
Shigeno
T
T
D000818:Animals; D017305:Annexin A1 / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000187:drug effects; D001921:Brain / Q000473:pathology; D001929:Brain Edema / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology*; D003907:Dexamethasone / Q000494:pharmacology; D006801:Humans; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology
D017305:Annexin A1; D011994:Recombinant Proteins; D003907:Dexamethasone