TY - JOUR
T1 - Dexamethasone therapy of triethyltin induced cerebral edema
AU - Studer, Rebecca K.
AU - Siegel, Barry A.
AU - Morgan, Janet
AU - Potchen, E. James
N1 - Funding Information:
Female rats of Wistar origin weighing 180-200 g were used in the experiments and were maintained on standard rat chow and water ad lib. Since 1 Presented in part at the Workshop on the Effects of Steroids in Brain Edema, Mainz, West Germany, June 19, 1972. This work was supported by Research Grant ROl-HE-12237, and Training Grant TOl-GM01747 from the National Institutes of Health, and by U.S. Atomic Energy Commission Grant AT(ll-l)-1653 under which this document becomes AEC No. CO-1653-133. We acknowledge the technical assistance of James B. Jones. Reprint requests to: Dr. Barry A. Siegel, 510 S. Kingshighway Blvd., St. Louis, Missouri 63110.
PY - 1973/3
Y1 - 1973/3
N2 - After administration of 1.25 mg/kg triethyltin bromide daily to rats for 7 days, cerebral edema results characterized by increased brain water and sodium, normal brain potassium, decreased cerebral blood volume, and without evidence for increased microvascular permeability to albumin and pertechnetate. Concurrent administration of dexamethasone diminishes mortality and the severity of brain edema and also significantly decreases brain, liver, and blood levels of triethyltin. It seems likely that the beneficial effect of steroid therapy in this model is at least in part due to enhanced excretion or catabolism of triethyltin bromide.
AB - After administration of 1.25 mg/kg triethyltin bromide daily to rats for 7 days, cerebral edema results characterized by increased brain water and sodium, normal brain potassium, decreased cerebral blood volume, and without evidence for increased microvascular permeability to albumin and pertechnetate. Concurrent administration of dexamethasone diminishes mortality and the severity of brain edema and also significantly decreases brain, liver, and blood levels of triethyltin. It seems likely that the beneficial effect of steroid therapy in this model is at least in part due to enhanced excretion or catabolism of triethyltin bromide.
UR - http://www.scopus.com/inward/record.url?scp=0015597941&partnerID=8YFLogxK
U2 - 10.1016/0014-4886(73)90165-9
DO - 10.1016/0014-4886(73)90165-9
M3 - Article
C2 - 4696112
AN - SCOPUS:0015597941
SN - 0014-4886
VL - 38
SP - 429
EP - 437
JO - Experimental Neurology
JF - Experimental Neurology
IS - 3
ER -