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Arch Dis Child 2012;97(Suppl 2):A1-A539 A87 Abstracts anisms. In a neonatal stroke rat model, we recently show that collateral recruitment contributes to infarct size variability.Non-specific and selective NO synthase (NOS) inhibition were evaluated on cerebral blood-flow changes and outcome in a P7 rat model of arterial occlusion (left middle cerebral artery electrocoagulation with 50 min occlusion of both common carotid arteries). Blood-flow changes were measured by using ultrasound imaging with sequential Doppler recordings in both internal carotid arteries and basilar trunk. Cortical perfusion was measured by using laser Doppler flowmetry. We showed that global NOS inhibition significantly reduced collateral support and cortical perfusion (collateral failure), and worsened the ischemic injury in both gender. Conversely, endothelial NOS inhibition increased blood-flows and aggravated volume lesion in males, whereas in females blood-flows did not change and infarct lesion was significantly reduced. These changes were associated with decreased phosphorylation of neuronal NOS at Ser 847 in males and increased phosphorylation in females at 24 hours, respectively. Neuronal NOS inhibition also increased blood-flows in males but not in females, and did not significantly change infarct volumes compared to their respective PBS-treated controls.In conclusion, both nNOS and eNOS appear to play a key role in modulating arterial blood flow during ischemia mainly in male pups with subsequent modifications in infarct lesion. ANTENATAL TAURINE SUPPLEMENTATION REDUCES CEREBRAL CELL APOPTOSIS IN FETAL RATS WITH INTRAUTERINE GROWTH RESTRICTION

Background: Perinatal asphyxia remains an important cause of brain injury in full term infants. Induced hypothermia has shown substantial benefit to asphyxiated newborns. Seizures are a common feature of hypoxic-ischaemic encephalopathy (HIE) and have been shown to exacerbate brain injury in HIE. Anticonvulsive treatment is a matter of debate. Studies have shown a high frequency of off-label drug therapy in neonates, particular for levetiracetam (LEV).

Background and aims:We have recently shown that Dextromethorphan is neuroprotective against excitotoxic and hyperoxic-induced brain injury. Beside its antagonistic effect on the NMDA [N-methyl-D-aspartate] receptor, DM also acts on sigma (σ) receptors. Sigma agonists have been shown to be neuroprotective in several adult animal models of brain injury. Neuroprotection by sigma agonists is accomplished by a variety of mechanisms like inhibition of presynaptic glutamate release and attenuation of postsynaptic glutamate-evoked Ca2+ influx. The selective σ1 receptor agonist Pre-084 [2-(4-Morpholinethyl) 1-phenylcyclohexanecarboxylate hydrochloride] has been shown to be neuroprotective in in-vitro and in-vivo studies of adult brain injury. The aim of this study was to evaluate the effect of Pre-084 in NMDAR-mediated excitotoxic brain injury in newborn mice.