It has been known that various derangements in ionic homeostasis develop following neural
trauma. In particular,
potassium efflux out of and
calcium influx into the cells are thought to play important roles in causing cell damage. Concomitantly we have previously reported that increased extracellular
potassium per se provoked by
head injury induces convulsive seizure such that the sustained high extracellular
potassium leads to animal death. The purpose of the present study was further to examine the beneficial effect of drugs which could inhibit such detrimental ion movements in experimental
head injury. Awake male mice of dd-strain were restrained and subjected to
head injury using a
bakelite weight of 30 gm dropped from a height of 17.6 cm above the skull. This injury resulted in immediate
loss of consciousness in 100%, convulsive seizure in about 70% and death in about 30% of animals. The severity of consciousness disturbance was evaluated by a pair of indices in time interval; time required for the recovery of righting reflex (RR) and for the recovery of spontaneous movement (SM).
Ethacrynic acid, a loop
diuretics, blocks carrier-mediated
chloride transport into astroglia associated with
sodium and water in the presence of high extracellular
potassium. Animals were treated with either 0.5-1.0 mg/kg or 2.0-4.0 mg/kg of
ethacrynic acid administered via tail vein 10 min before injury. In the other group of animals, a
calcium entry blocker,
flunarizine was injected intraperitoneally in doses 5, 10 and 20 mg/kg one hour pre-insult.(ABSTRACT TRUNCATED AT 250 WORDS)