Cerebroprotective effect of dexamethasone by increasing the tolerance to hypoxia and preventing brain oedema in newborn piglets with experimental pneumothorax

Impaired Early Neurologic Outcome in Newborn Piglets Reoxygenated with 100% Oxygen Compared with Room Air after Pneumothorax-Induced Asphyxia

“…The experimental protocol followed in this study was set up on the basis of our extensive laboratory practice during a period of 20 y, documenting evidence that pneumothoraxasphyxiated piglets are able to survive the asphyxiation load (for up to 4 h) without further mechanical respiratory support (7,36). Newborns should be ventilated as long as necessary to obtain reasonable blood gas values, avoiding lung and other organ injury as much as possible.…”

Dexamethasone Prevents Hypoxic-Ischemic Brain Damage in the Neonatal Rat

“…A 3-h recovery period with the dam was followed by 3 h in 8% oxygen wit11 92% nitrogen in a plastic chamber inside a neonatal incubator with an air temperature of 37°C. This well-established model of pelinatal cerebral hypoxiaischemia reliably produces ipsilateral infarction of the striatum, thalamus, hippocampus, and overlying cortex (1 [8][9][10][11][12][13][14][15][16][17][18][19][20]. The experimental protocol was approved by the Animal Care Committee of The Hospital for Sick Children.…”

“…Treatment with veIy high doses of glucocorticoids (3-6 n~g/kg dexamethasone or 15-30 mg/kg methylprednisolone) have both reduced pathologic damage induced by experimental spinal cord trauma (5,6) and improved neurologic outcome after human spinal cord injury (7). Reductions in cerebral edema caused by tumors, infarction, pneumothorax, or convulsions with glucocorticoid therapy have also been reported (8)(9)(10)(11)(12). However, until the present study, glucocorticoid therapy did not appear to be effective in reducing brain damage due to cerebral hypoxia-ischemia.…”

“…In our study, we investigated the effect of glucocorticoid administration on the extent of brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat (1 [8][9][10][11][12][13][14][15][16][17][18][19][20]. The results demonstrate that in the neonate, rather than exacerbating neuronal damage, glucocorticoid administration before an episode of hypoxia-ischemia actually protects the brain from injury.…”

Reply to Abdul-Khaliq et al.

“…Firstly although methylprednisolone was given in the same dose (30 mg/kg) as in our study I am not sure of either the route of administration, the number of doses or the timing of the doses. In our own study the timing of the doses was based on evidence that de novo protein synthesis is involved in the cerebroprotective effect of corticosteroids [2]. Secondly the duration of the circulatory arrest period was unfortunately not speci®ed.…”