Various indices of brain metabolism and activity in a model of chronic neurological dysfunction: triethyl tin intoxication in the rat.
A number of pathological agents of interest in the therapy of cerebrovascular disease can retard the development of the neurologic deficit induced by triethyl tin. Locomotor activity was decreased at a time when no evidence of neurologic deficit could be detected. Conduction velocity in the peripheral as well as assessed from measurement of cerebral blood flow, local cerebral glucose utilization, brain water and electrolyte content as well as neuropathology were measured before and frank deficit could be clinically detected.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D014220:Trialkyltin Compounds / Q000633:toxicity*; D014267:Triethyltin Compounds / Q000633:toxicity*; D014867:Water / Q000378:metabolism
D014220:Trialkyltin Compounds; D014267:Triethyltin Compounds; D014867:Water; C031575:triethyltin; D012964:Sodium; D005947:Glucose; D011188:Potassium