triethyltin and Brain-Edema

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

Brain edema was produced by injecting triethyltin (TET) into the right cerebral hemisphere via the internal carotid artery in rats. TET induced a dose-related increase in mortality rate and brain water content. Immediately after TET-injection (2 mg/head), saline, glycerol (125 mg/ml) or the N-methyl-D-aspartate receptor antagonist (R)-4-(3-Phosphono-2-propenyl)-2-piperazine carboxylic acid (D-CPP-ene; 0.083 and 0.25 mg/ml) was continually infused via the right internal jugular vein at 20 microliters/min for 6 h. The mortality rate and brain water content were significantly decreased after infusion of 0.25 mg/ml D-CPP-ene, but only somewhat reduced after glycerol infusion when compared with the saline group. The results suggest that continual intravenous posttreatment with D-CPP-ene is useful for treatment of brain edema.

Topics: Animals; Body Water; Brain; Brain Edema; Carotid Artery, Internal; Dose-Response Relationship, Drug; Excitatory Amino Acid Antagonists; Infusions, Intravenous; Injections, Intra-Arterial; Injections, Intravenous; Male; Piperazines; Rats; Rats, Inbred F344; Receptors, N-Methyl-D-Aspartate; Survival Analysis; 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 effect of hexachlorophene (HCP; 2,2'-methylenebis(3,4,6-trichlorophenol), cuprizone (CPZ; bicyclohexone oxaldihydrazone) and triethyl tin (TET; triethyl tin sulphate) in producing vacuoles in the brain of the Sprague-Dawley rat has been quantified by image analysis of the extent of the spongy change in the white matter. The state of the astrocytes was assessed by immunocytochemical staining for glial fibrillary acidic protein (GFAP). HCP and TET caused a dose-related spongiosis, but cuprizone had no significant effect on the brain. With chronic HCP treatment, the spongiosis was accompanied by astrocyte hypertrophy and proliferation, and the extent of the gliotic reaction was related to the dose of HCP. The results demonstrate that HCP can produce and maintain astrocyte proliferation in the rat brain. Such an agent was required for use in an investigation of a putative tumour promoter in the rat.

Topics: Animals; Body Weight; Brain; Brain Edema; Cuprizone; Dose-Response Relationship, Drug; Drinking; Eating; Hexachlorophene; Male; Organ Size; Rats; Rats, Inbred Strains; Triethyltin Compounds; Vacuoles

Assessment of perinatal brain oedema is complicated by normal changes in brain water that accompany the marked physiological, biochemical and morphological alterations occurring during this phase of development. Multiexponential analysis of transverse decay curves (TDCs), derived from 128 echo CPMG images, of white matter (WM) made oedematous by either exposure of animals to triethyltin (TET) or cryogenic cortical lesions revealed a second, slower decay component not apparent in controls. More significantly, an obvious difference was noted between the TET and cryogenic lesion fast decay components which might serve as a basis to differentiate non-invasively cytotoxic and vasogenic oedemas.

Topics: Aging; Animals; Animals, Newborn; Body Water; Brain; Brain Edema; Cerebral Cortex; Hypoxia; Magnetic Resonance Spectroscopy; Rabbits; Spinal Cord; Triethyltin Compounds

The vacuolar degeneration of central myelin was produced in Sprague-Dawley rats by oral administration of triethyl tin. The wet weight of brain stems which seems to reflect the degree of accumulation of water increased during the administration of the toxin, whereas the activity of 2', 3'-cyclic nucleotide 3'-phosphodiesterase altered less remarkably. When TET was withdrawn from the drinking water, the rats showed a dramatic clinical improvement along with reduction in wet weight of brain stems. Treatment with acetazolamide following TET inhibited the clinical improvement and reduction in wet weight of brain stems. The present results indicates that central myelin has plasticity in recovering from the vacuolar degeneration by removing the accumulated fluid and carbonic anhydrase is possibly involved in the dehydration of myelin in such a recovery phase.

Topics: 2',3'-Cyclic-Nucleotide Phosphodiesterases; Acetazolamide; Animals; Body Water; Brain Edema; Brain Stem; Carbonic Anhydrases; Female; Microscopy, Electron; Myelin Sheath; Organ Size; Rats; Rats, Inbred Strains; Trialkyltin Compounds; Triethyltin Compounds; Vacuoles

Hyperbaric oxygenation (HO) was used to treat the brain toxic edema excited by triethyltin++ chloride. Microscopic examination of the brains of two groups of animals (with and without HO) revealed the decay of pathologic signs of brain edema and reparative responses in the nervous tissue induced by HO.

Topics: Animals; Brain Edema; Hyperbaric Oxygenation; Rabbits; Trialkyltin Compounds; Triethyltin Compounds

To better understand the role of myelin-associated water in the differentiation of white and gray matter in magnetic resonance (MR) imaging, changes in MR relaxation processes were studied in rabbits during myelination and after induction of cytotoxic edema with triethyltin (TET). Normal rabbits were killed at various age intervals ranging from premature (28 days' gestation) to adult, and changes in MR relaxation times (T1 and T2) and in water and electrolyte content were determined for various areas of brain and muscle. Similar measurements were made in rabbits of comparable age exposed to TET. Light and electron microscopy and MR imaging were used to follow myelin development and morphological changes induced by TET. During the first 30 postnatal days, both T1 and T2 declined by 50% in normal rabbits, a fall that paralleled the loss in brain water and sodium that occurred during the same period. Exposure to TET prolonged T1 and T2 in white but not gray matter, reflecting the accumulation of sodium and water (edema fluid) in white matter areas. Multiexponential analysis revealed a second, longer component in T2 magnetization decay of TET-exposed white matter, presumably attributable to accumulation of non-ordered water within intramyelinic vacuoles, a supposition consistent with electron microscopic and MR imaging findings. In contrast to reports by others, changes in T1 (but not T2) closely correlated with alterations in brain water (r = 0.93, df = 39). The absence of tissue disruption in the animals in the present study may account for these differences, but further studies will be required both to resolve this question and to fully understand MR images of white matter edema in mature and immature brain.

Topics: Aging; Animals; Animals, Newborn; Body Water; Brain; Brain Edema; Gestational Age; Magnetic Resonance Imaging; Microscopy, Electron; Organ Size; Rabbits; Sodium; Trialkyltin Compounds; Triethyltin Compounds

For clarification of the beneficial effects of the extract of Ginkgo biloba (EGB) on triethyltin (TET) toxicity in rats, the phosphodiesterase (PDE) activities of the cerebral tissue were measured under in vitro and ex vivo conditions. Under in vitro conditions, low concentrations of EGB (0.25-4.0 mg/L) activated the enzyme, whereas after higher concentrations (5-250 mg/L), dose-dependent inhibition of the enzyme activity was observed. In the lower concentration range, the extract also partially restored the high-affinity PDE activity (measured with 0.25 microM cyclic AMP) of the particulate fraction of the brain inhibited by TET in vitro. In contrast, the inhibitory influence of TET on the low-affinity PDE activity (measured with 50 microM cyclic AMP) of the particulate fraction was enhanced by the extract. Although treatment with a single large dose of EGB lowered the particulate PDE activities of the brain of normal rats, no effects of the extract could be detected in animals after repeated daily administrations of EGB during a 4-day period. Curative treatment of the TET-intoxicated rats with EGB during a 7-day period accelerated the recovery of the edematous state of the white matter caused by the intoxication and also normalized the lowered PDE activity of the particulate fraction of the edematous brain tissue. Furthermore, when preventively administered, EGB counteracted both the edema formation and the fall in PDE activity observed with treatment by TET alone. These observations strongly suggest that some beneficial effects of EGB might be due to its modulating influences on cellular cyclic AMP levels via activation of membrane-bound PDE.

Topics: 3',5'-Cyclic-AMP Phosphodiesterases; Animals; Brain; Brain Edema; Male; Plant Extracts; Rats; Rats, Inbred Strains; Trialkyltin Compounds; Triethyltin Compounds

The effect of intracarotid hyperosmolar mannitol on the blood-brain barrier (BBB) in triethyl tin (TET)-induced rat brain edema was examined by using intravenous Evans blue (EB, MW 68,000) and Adriamycin (ADM, MW 580) as tracers. Three ml of 1.4 M mannitol solution were administered through the right carotid artery during 45 s for BBB opening. The barrier was opened for 60-120 minutes and then re-established. The reversibility was preserved in TET-treated rats and controls. In fact, the intravenous injection of EB stained both TET-treated and non-treated cerebral hemispheres with mannitol-induced transient BBB disruption, but not without BBB disruption. BBB was resistant to both high and low molecular weight substances in TET-induced edema. The importance of this hyperosmotic studies provides the evidence for normal BBB function in TET-induced brain edema.

Topics: Animals; Blood-Brain Barrier; Brain Edema; Carotid Arteries; Doxorubicin; Evans Blue; Hypertonic Solutions; Infusions, Intra-Arterial; Male; Mannitol; Molecular Weight; Rats; Rats, Inbred Strains; Triethyltin Compounds

Triethyl tin(TET)-induced cerebral oedema has been studied in cats by magnetic resonance imaging (MRI), and the findings correlated with the histology and fine structure of the cerebrum following perfusion-fixation. MRI is a sensitive technique for detecting cerebral oedema, and the distribution and severity of the changes correlate closely with the morphological abnormalities. The relaxation times, T1 and T2 increase progressively as the oedema develops, and the proportional increase in T2 is approximately twice that in T1. Analysis of the magnetisation decay curves reveals slowly-relaxing and rapidly-relaxing components which probably correspond to oedema fluid and intracellular water respectively. The image appearances taken in conjunction with relaxation data provide a basis for determining the nature of the oedema in vivo.

Topics: Animals; Brain Chemistry; Brain Edema; Cats; Female; Magnetic Resonance Spectroscopy; Triethyltin Compounds; Water

Cytotoxic brain edema has been produced in rats by subacute intoxication with triethyltin (TET). Some animals were allowed to recover spontaneously, others were post-treated with an extract of Ginkgo biloba (EGB) for 1 to 4 weeks, beginning 3 days after intoxication was stopped. The time course of the resolution of the edema was studied biochemically and morphologically by light microscopy, histochemistry and electron microscopy (EM). Morphometric evaluation showed that the spontaneous reabsorption of TET-induced edema was very slow: it was evident only 2 weeks after ending TET administration and it required more than 4 weeks to be completed. EGB therapy markedly decreased the vacuolation, as well as the abnormal levels of water and sodium contents, 1 week after beginning the treatment. Less influence of EGB was observed at the later stages. During spontaneous recovery, astroglial cells in the edematous white matter of TET-intoxicated animals showed short and swollen processes containing few organelles, low levels of NADH- and NADPH-tetrazolium reductase activities and glial fibrillary acidic protein (GFAP)-immunofluorescence for about 2 weeks. During EGB therapy the astrocytes regained their cellular processes, containing intense oxidative enzyme activities and GFAP-immunofluorescence as early as after 1 week of treatment. In the EM, astrocytes often appeared hypertrophic, surrounding myelin vacuoles and displaying phagocytosis of myelin debris. We conclude that EGB can accelerate the reabsorption of TET-induced cerebral edema and improve the astroglial reaction.

Topics: Animals; Astrocytes; Brain; Brain Chemistry; Brain Edema; Male; Plant Extracts; Rats; Rats, Inbred Strains; Triethyltin Compounds; Water

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

Topics: Adenosine Triphosphatases; Brain; Brain Edema; Poisoning; Rats; Research; Tin; Toxicology; Triethyltin Compounds

Topics: Brain Edema; Central Nervous System; Cerebellum; Edema; Electrons; Microscopy; Microscopy, Electron; Microscopy, Phase-Contrast; Myelin Sheath; Pathology; Pharmacology; Rats; Research; Spinal Cord; Tin; Toxicology; Triethyltin Compounds

Topics: Animals; Brain Chemistry; Brain Edema; Chemistry Techniques, Analytical; Dexamethasone; Injections, Intraperitoneal; Ions; Pharmacology; Potassium; Rabbits; Research; Sodium; Tin; Toxicology; Triethyltin Compounds; Water