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Dexamethasone does not prevent hydrocephalus after severe intraventricular hemorrhage in newborn rats.

08:00 EDT 25th October 2018 | BioPortfolio

Summary of "Dexamethasone does not prevent hydrocephalus after severe intraventricular hemorrhage in newborn rats."

The aim of this study was done to determine whether dexamethasone treatment prevents posthemorrhagic hydrocephalus (PHH) development and attenuates brain damage after severe IVH in newborn rats. Severe IVH was induced by injecting; 100 μL of blood into each lateral ventricle of postnatal day 4 (P4) Sprague-Dawley rats. Dexamethasone was injected intraperitoneally into rat pups at a dose of 0.5 mg/kg, 0.3 mg/kg, and 0.1 mg/kg on P5, P6, and P7, respectively. Serial brain magnetic resonance imaging and behavioral function tests, such as the negative geotaxis test and the rotarod test, were performed. On P32, brain tissues were obtained for histological and biochemical analyses. Dexamethasone treatment significantly improved the severe IVH-induced increase in the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive cells, glial fibrillary acidic protein-positive astrocytes and ED-1 positive microglia, and the decrease in myelin basic protein. IVH reduced a survival of 71%, that showed a tendency to improve to 86% with dexamethasone treatment, although the result was not statistically significant. However, dexamethasone failed to prevent the progression to PHH and did not significantly improve impaired behavioral tests. Similarly, dexamethasone did not decrease the level of inflammatory cytokines such as interleukin (IL) -1α and ß, IL-6, and tumor necrosis factor-α after severe IVH. Despite its some neuroprotective effects, dexamethasone failed to improve the progress of PHH and impaired behavioral tests after severe IVH.

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This article was published in the following journal.

Name: PloS one
ISSN: 1932-6203
Pages: e0206306

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Bleeding within the CEREBRAL VENTRICLES. It is associated with intraventricular trauma, aneurysm, vascular malformations, hypertension and in VERY LOW BIRTH WEIGHT infants.

A form of compensated hydrocephalus characterized clinically by a slowly progressive gait disorder (see GAIT DISORDERS, NEUROLOGIC), progressive intellectual decline, and URINARY INCONTINENCE. Spinal fluid pressure tends to be in the high normal range. This condition may result from processes which interfere with the absorption of CSF including SUBARACHNOID HEMORRHAGE, chronic MENINGITIS, and other conditions. (From Adams et al., Principles of Neurology, 6th ed, pp631-3)

The sudden loss of blood supply to the PITUITARY GLAND, leading to tissue NECROSIS and loss of function (PANHYPOPITUITARISM). The most common cause is hemorrhage or INFARCTION of a PITUITARY ADENOMA. It can also result from acute hemorrhage into SELLA TURCICA due to HEAD TRAUMA; INTRACRANIAL HYPERTENSION; or other acute effects of central nervous system hemorrhage. Clinical signs include severe HEADACHE; HYPOTENSION; bilateral visual disturbances; UNCONSCIOUSNESS; and COMA.

Antifibrinolytic hemostatic used in severe hemorrhage.

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