triethyltin and Disease-Models--Animal

Current experimental models of brain edema are described and evaluated for their contribution to the knowledge of basic processes involved in its production as well their contribution to the understanding of different clinical forms. The participation of each main pathogenic mechanism in a given experimental model is analyzed and proves to vary with each particular model and site studied. The importance of various experimental models in the evaluation of different therapeutic procedures directed to control the genesis and evolution of brain edema is stressed.

Topics: Animals; Brain Edema; Brain Injuries; Brain Ischemia; Brain Neoplasms; Cats; Disease Models, Animal; Freezing; Hypertension; Hypotonic Solutions; Ouabain; Radiation Injuries, Experimental; Rats; Triethyltin Compounds

We investigated the multicompartmental nature of T2 decay in a specific white matter edema model.. Triethyltin (TET) intoxication was produced in six male New Zealand White rabbits. Images were obtained over the 23-day study duration using a 64-echo Carr-Purcell-Meiboom-Gill (CPMG) sequence (repetition time = 3000 msec, echo time = 20 msec). T2 decay curves were extracted from 0.7 x 0.7 x 3.0 mm3 voxels in the corpus callosum and contiguous white matter tracts, cortex, thalamic nuclei, hypothalamic nuclei, and the masseter muscles. The curves were fit with biexponential functions.. Increased signal intensity in the corpus callosum was evident 2-3 days after the first TET injection. At this time, a substantial slowly relaxing component appeared in the decay curves of the corpus callosum and, to a lesser extent, in the thalamus and hypothalamus. Changes in the rabbits' body weight, general physical condition, and neurologic state paralleled the growth and regression of the second, slowly relaxing component.. The appearance and regression of a slowly decaying second component in the T2 decay curve is consistent with the formation and shrink-age of intracellular vesicles in the intramyelin sheaths of central white matter.

Topics: Animals; Body Water; Brain; Brain Edema; Cerebral Cortex; Corpus Callosum; Disease Models, Animal; Follow-Up Studies; Hypothalamus; Intracellular Membranes; Magnetic Resonance Imaging; Male; Rabbits; Sensitivity and Specificity; Thalamus; Triethyltin Compounds

The question of what happens to cholesterol in the adult central nervous system during its slow turnover has been addressed using rats with brain and spinal cord labeled with [4-14C]cholesterol upon intracerebral injection of labeled cholesterol into rats at 10-12 days of age. At six months after injection, 14C was found only in the brain and spinal cord and was slowly released via the rat's urine. When labeled rats were given demyelinating agents (triethyl tin chloride, hexachlorophene, sodium cyanide) and when experimental allergic encephalomyelitis was induced, a measurable increase in urinary 14C label above control levels was found. It was concluded that there is a direct relationship between the experimental demyelination induced and the increased release of cholesterol metabolites into urine. The study suggests that a clinical method could be developed to determine the rate of central nervous system demyelination by measuring the amount of urinary cholesterol metabolites.

Topics: Animals; Carbon Radioisotopes; Central Nervous System Diseases; Cholesterol; Demyelinating Diseases; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Hexachlorophene; Rats; Rats, Inbred Lew; Rats, Sprague-Dawley; Sodium Cyanide; Starvation; Triethyltin Compounds

Topics: Animals; Brain Edema; Disease Models, Animal; Male; Rats; Rats, Inbred Strains; Trialkyltin Compounds; Triethyltin Compounds