Abstract
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.
Highlights
Intraventricular hemorrhage (IVH) results from the rupture of the germinal matrix hemorrhage through the ependymal into the lateral ventricle and is a common and serious disorder in premature infants [1, 2]
Premature infants with severe IVH have a high risk of brain damage and progression to posthemorrhagic hydrocephalus (PHH), which can result in increased mortality and neurologic morbidities such as seizure, cerebral palsy, and developmental retardation in survivors [3,4,5]
The pathogenesis of brain damage and the progression to PHH from severe IVH has not been completely delineated, it is known that the contact of blood and blood products in the subarachnoid space leads to an inflammatory response that can cause obliterative arachnoiditis
Summary
Intraventricular hemorrhage (IVH) results from the rupture of the germinal matrix hemorrhage through the ependymal into the lateral ventricle and is a common and serious disorder in premature infants [1, 2]. The pathogenesis of brain damage and the progression to PHH from severe IVH has not been completely delineated, it is known that the contact of blood and blood products in the subarachnoid space leads to an inflammatory response that can cause obliterative arachnoiditis. This condition can cause dysfunction in arachnoid granulations, which can reduce cerebrospinal fluid (CSF) resorption and increase intracranial pressure, resulting in a venous infarction with reduced cerebral perfusion [6,7,8]. New and effective therapeutic modalities with strong anti-inflammatory capabilities to treat brain injury and the progression to PHH after severe IVH would be of great value
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
