title: Temporal changes in edema, Na+, K+, and Ca++ in focal cortical stroke: GM1 ganglioside reduces ischemic injury.
abstract: Cortical focal ischemia in the rat was induced by middle cerebral artery occlusion (MCAo) together with permanent occlusion of the ipsilateral common carotid artery (CCAo) and a temporary (1 hr) occlusion of the contralateral CCA. By using a defined cortical tissue sampling procedure at 3, 6, 24, 72, 96, and 120 hr after the MCAo + CCAo, patterns of edema and ion (Na+, K+, and Ca++) changes in a primary and three peri-ischemic cortical areas are described. Ionic imbalances and edema formation have distinct patterns, are time dependent, and are different when comparing primary and peri-ischemic areas. Calcium increases to "neurotoxic" levels appear temporally independent of edema formation, reaching magnitudes 20 times greater than basal levels in the primary infarct area. Na+ increases correlate with increases in water, while K+ losses do not appear to be directly related to edema formation of Na+ and Ca++ increases. K+ losses are only significant in the primary infarct area. Rats treated with GM1 ganglioside (10 mg/kg, i.m.) daily showed significant reductions in edema, Na+ and Ca++ increases. These ganglioside effects were evident as early as 24 hr after the ischemic injury. Ca++ increases, which was maximal at 72 hr after the ischemic injury, was reduced by greater than 50% in GM1-treated animals. The mechanism by which GM1 is an effective neuroprotective agent may be evidenced by its effects on Ca++ influx/efflux processes in injury.
authors.affiliation: Division of Neuroscience, New York State Psychiatric Institute, Columbia University, New York 10032.
authors.forename: S E
authors.initials: SE
authors.lastname: Karpiak
authors.forename: C G
authors.initials: CG
authors.lastname: Wakade
authors.forename: A
authors.initials: A
authors.lastname: Tagliavia
authors.forename: S P
authors.initials: SP
authors.lastname: Mahadik
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D001929:Brain Edema / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism*; D002544:Cerebral Infarction / Q000188:drug therapy / Q000503:physiopathology; D007839:Functional Laterality; D005677:G(M1) Ganglioside / Q000627:therapeutic use*; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism*; D013997:Time Factors
chemical_list: D005677:G(M1) Ganglioside; D012964:Sodium; D011188:Potassium; D002118:Calcium