17β-estradiol protects 7-day old rats from acute brain injury and reduces the number of apoptotic cells.

Objective: To test a possible neuroprotective activity of 17β-estradiol in the neonatal rat brain exposed to hypoxic-ischemia (controlled hypoxia after unilateral carotid artery ligation).

Methods: Seven-day-old Wistar rats underwent ligation of the left common carotid artery followed by 80 minutes hypoxia in 8% oxygen inducing an ipsilateral brain damage. Seven days later (d14), brains were analyzed quantitatively using a macroscopic and microscopic score for structural damage, hemisphere volumes were calculated, and immunohistochemistry for cleaved-caspase-3 (marker for apoptotic cells) was performed.

Spastic paresis after perinatal brain damage in rats is reduced by human cord blood mononuclear cells.

Brain damage around birth may cause lifelong neurodevelopmental deficits. We examined the therapeutic potential of human umbilical cord blood-derived mononuclear cells containing multipotent stem cells to facilitate motor recovery after cerebral hypoxic-ischemic damage in neonatal rats. Left carotid artery ligation followed by 8% O(2) inhalation for 80 min was performed on postnatal d 7, succeeded by intraperitoneal transplantation of human umbilical cord blood-derived mononuclear cells on postnatal d 8 in a sham-controlled design.

Creatine protects the immature brain from hypoxic-ischemic injury.

Objective: We tested the neuroprotective effects of creatine against hypoxic-ischemic injury in the immature brain.

Methods: Hippocampal slices were prepared from fetal guinea pigs at 0.9 gestation and incubated in artificial cerebrospinal fluid (aCSF) equilibrated with carbogen.

Perinatal brain damage--from pathophysiology to prevention.

Children undergoing perinatal brain injury often suffer from the dramatic consequences of this misfortune for the rest of their lives. Despite the severe clinical and socio-economic significance, no effective clinical strategies have yet been developed to counteract this condition. This review describes the pathophysiological mechanisms that are implicated in perinatal brain injury.

Intracisternal application of endotoxin enhances the susceptibility to subsequent hypoxic-ischemic brain damage in neonatal rats.

Perinatal brain damage is associated not only with hypoxic-ischemic insults but also with intrauterine inflammation. A combination of antenatal inflammation and asphyxia increases the risk of cerebral palsy >70 times. The aim of the present study was to determine the effect of intracisternal (i.

Neuroprotective effects of magnesium on metabolic disturbances in fetal hippocampal slices after oxygen-glucose deprivation: mediation by nitric oxide system.

Objective: We investigated the effects of magnesium on metabolic disturbances in hippocampal slices prepared from fetal guinea pigs after oxygen-glucose deprivation (OGD).

Methods: Metabolic disturbances were assessed by measuring changes in energy metabolism and protein synthesis. In addition we determined cyclic guanosine monophosphate (cGMP) concentrations in the slices after OGD, as a measure of nitric oxide (NO) production, to clarify whether a possible neuroprotective effect of magnesium is mediated in part through the NO system.