The role of free radicals in cerebral hypoxia and ischemia

Hypoxic-ischemic insult decreases glutamate uptake by hippocampal slices from neonatal rats: prevention by guanosine.

Perinatal hypoxia is still one of the greatest threats to the newborn child, even in developed countries. However, there is a lack of works which summarize up-to-date information about that huge topic. Our review covers a broader spectrum of recent results from studies on mechanisms leading to hypoxia-induced injury. It also resumes possible primary causes and observed behavioral outcomes of perinatal hypoxia. In this review, we recognize two types of hypoxia, according to the localization of its primary cause: environmental and placental. Later we analyze possible pathways of prenatal hypoxia-induced injury including gene expression changes, glutaminergic excitatory damage (and a role of NMDA receptors in it), oxidative stress with ROS and RNS production, inflammation and apoptosis. Moreover, we focus on the impact of these pathophysiological changes on the structure and development of the brain, especially on its regions: corpus striatum and hippocampus. These brain changes of the offspring lead to impairments in their postnatal growth and sensorimotor development, and in their motor functions, activity, emotionality and learning ability in adulthood. Later we compare various animal models used to investigate the impact of prenatal and postnatal injury (hypoxic, ischemic or combinatory) on living organisms, and show their advantages and limitations.

/pdf/impact-of-perinatal-hypoxia-on-the-developing-brain-u9ecv27fyk.pdf

Impact of perinatal hypoxia on the developing brain.

The developing brain is susceptible to hypoxic damage because of its high oxygen and energy requirements. Hypoxia-induced inflammatory response has been recognized as one of the main culprits in the development of hypoxic brain injury. In this regard, a hallmark feature is microglial activation which results in overproduction of inflammatory cytokines, free radicals and nitric oxide. Concomitantly, activated microglia exhibit enhanced expression of ion channels such as Kv1.2, Kv1.1 and Nav which further promote the release of inflammatory cytokines, chemokines and reactive oxygen species. Through the above-mentioned inflammatory mediators, activated microglia induce neuronal loss, axonal damage and oligodendroglial death along with myelination disturbances. Our recent studies have extended that tumor necrosis factor-alpha, interleukin-1beta, monocyte chemoattractant protein-1 and macrophage colony stimulating factor produced by activated microglia are linked to the pathogenesis of periventricular white matter damage in the hypoxic brain. It is envisaged that a better understanding of the interactions between microglia and neurons, axons and oligodendrocytes is key to the development of effective preventive and therapeutic strategies for mitigation of hypoxic brain injury.

Role of microglia in the process of inflammation in the hypoxic developing brain.

The effects of mildronate [3-(2,2,2-trimethylhydrazinium) propionate], an inhibitor of L-carnitine biosynthesis and an anti-ischaemic drug, were examined in various in-vivo conditions to investigate the neuropharmacological profile after acute administration. Mildronate (200 mg/kg, acute intraperito

Mildronate exerts acute anticonvulsant and antihypnotic effects.

Pregnant rats were exposed to intermittent hypobaric hypoxia (at a simulated altitude of 7000 m or 5000 m) and the excitability of cortical neurons of their pups was tested. Stimulation of the sensorimotor cortex of rats prenatally exposed to hypoxia shortened the duration of cortical afterdischarges in 12-day-old rats, but did not change the excitability in 25-day-old animals. Shortening of the first afterdischarge in 35-day-old rats but the prolongation of the first afterdischarge in adult rats (as compared to the duration of cortical afterdischarges in rats not exposed to prenatal hypoxia) were registered. The possible mechanisms of different excitability of cortical neurons in rats prenatally exposed to hypobaric hypoxia are discussed.

/pdf/excitability-changes-of-cortical-neurons-during-the-318nugldcs.pdf

Excitability changes of cortical neurons during the postnatal period in rats exposed to prenatal hypobaric hypoxia.

The favourable development of foetus is connected with the sufficient oxygen requirement. The brain of the foetus is extraordinarily sensitive to the disorders of oxygen supply. Ischemic brain injury connected with perinatal asfyxia is a frequent cause of hypoxic encephalopathy. An increased tolerance of the brain could be achieved by using peptide grows factors, inhibition of nitric oxide or modifying the glutamate receptors activity. Cerebral hypoxia evolves mainly in the case interruption of the feto-placental circulation or cardiorespiratory failure in the neonate. For making the diagnosis of neonatal encephalopathy is important to determine clinical neurological and systemic deragements in the first few days of life. Assessment of prognosis is generally based on a combination of clinical features and abnormalities of examination methods (electroencephalography, computer tomography).

Perinatal complication: hypoxic-ischemic encephalopathy.

Summary The possible protective action of L-carnitine on neuronal excitability was studied in 21-day-old male Wistar rats with implanted electrodes. Administration of L-carnitine did not change the elicitation and duration of the epileptic seizures (cortical afterdischarges, ADs) in rats under normobaric oxygen atmosphere conditions. However, in animals exposed to 30 min hypobaric hypoxia the duration of the ADs was shortened after the second, fourth and sixth stimulation (in comparison with the first evoked ADs) while carnitine-treated rats retained their neuronal excitability and the duration of ADs was shortened only after the third stimulation.

/pdf/carnitine-pretreatment-can-partially-change-the-excitability-2kr5h7oox0.pdf

Carnitine pretreatment can partially change the excitability of the immature nervous tissue.

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Excitability changes of cortical neurons during the postnatal period in rats exposed to prenatal hypobaric hypoxia.

Perinatal complication: hypoxic-ischemic encephalopathy.

Carnitine pretreatment can partially change the excitability of the immature nervous tissue.