Disease relevance of Hypoxia, Brain

• Reports of myoclonus developing after anoxic brain injury, and its response to treatment with the serotonin precursor 5-hydroxytryptophan (5-HTP), drew special attention [1].
• Twelve patients with perinatal anoxic encephalopathy, 1 with encephalitis, and 1 with Down's syndrome had startle epilepsy [2].
• BACKGROUND AND PURPOSE: Cerebral arteriolar dilation to N-methyl-D-aspartate (NMDA) is a neuronally mediated multistep process that is sensitive to cerebral hypoxia and ischemia (H/I) [3].
• These results suggest that untimely activation of NMDAR and nitric oxide release during anoxia produce delayed inhibition of LTP induction and may be involved in the memory defects that occur subsequent to cerebral hypoxia [4].
• Increased serum levels of the S-100 protein are associated with hypoxic brain damage after cardiac arrest [5].

Psychiatry related information on Hypoxia, Brain

• The effects of rapid intracarotid injection of 20 to 100 mg of sodium amobarbital were studied in three patients with bilateral myoclonic status epilepticus due to Jakob-Creutzfeldt disease, sequelae to anoxic encephalopathy, and hepatic coma, respectively [6].
• CONCLUSIONS: Levodopa and benserazide can be of benefit in the few months following brain anoxia, especially on some of the motor disorders and apathy, but the benefit is inconstant and modest on memory disorders [7].

High impact information on Hypoxia, Brain

• The release of glutamate during brain anoxia or ischaemia triggers the death of neurons, causing mental or physical handicap [8].
• This stoichiometry predicts a minimum [Glu]o of 0.6 microM normally (tonically activating presynaptic autoreceptors and post-synaptic NMDA receptors), and 370 microM during brain anoxia (high enough to kill neurons) [9].
• This will facilitate a rise in the extracellular glutamate concentration to neurotoxic levels and contribute to the neuronal death occurring in brain anoxia and ischaemia [10].
• ODC activity and polyamine concentrations appear to be useful enzymatic markers for fetal brain hypoxia [11].
• Prion protein accumulation and neuroprotection in hypoxic brain damage [12].

Chemical compound and disease context of Hypoxia, Brain

• Arachidonic acid is released by phospholipase A2 when activation of N-methyl-D-aspartate (NMDA) receptors by neurotransmitter glutamate raises the calcium concentration in neurons, for example during the initiation of long-term potentiation and during brain anoxia [13].
• Fetal brain hypoxia was documented biochemically by a decrease in brain tissue levels of ATP and phosphocreatine [14].
• We speculate that endogenous release of angiotensin II, perhaps in the choroid plexus epithelium, decreases production of CSF after hypoxic brain injury [15].
• A 44-year-old man was brought unconscious to the emergency room; he was believed to have suffered anoxic brain damage probably due to carbon monoxide poisoning [16].
• Low-affinity A2B adenosine receptors (A2B ARs), which are expressed in astrocytes, are mainly activated during brain hypoxia and ischaemia, when large amounts of adenosine are released [17].

Biological context of Hypoxia, Brain

• Among 29 (61.7%) children with symptomatic etiology, 14 cases had prenatal etiology [tuberous sclerosis (TS), seven; vascular insult, three; cerebral malformations, three; Down syndrome, one child], 14 perinatal and one postnatal cause: anoxic brain damage after cardiac surgery [18].
• The present study tests the hypothesis that phenytoin, an antiepileptic agent known to block Na+ and Ca2+ channels, will prevent hypoxic brain injury in the fetus by preventing lipid peroxidation and preserving Na+,K(+)-ATPase activity [19].
• However, neither pretreatment with pharmacological doses of MK-801 or phencyclidine, nor severe, transient brain hypoxia, were able to clearly alter [18]FMM brain regional kinetics, indicating limited usefulness of this radioligand for in vivo PET investigations of the NMDA receptor [20].
• The N-methyl-D-aspartate (NMDA) subclass of glutamate receptors was examined in newborn infants dying between 25 weeks' gestation and term, either from acute cerebral hypoxia, or from other noncerebral conditions incompatible with life [21].
• This review provides an overview of the pathophysiology of neonatal hypoxic brain injury after DHCA, focusing on cellular mechanisms of necrosis, apoptosis, and glutamate excitotoxicity [22].

Anatomical context of Hypoxia, Brain

• The contrasting pharmacology and ionic dependence of the glutamate uptake carriers in the vesicle membrane and in the plasma membrane explain how glutamate (but probably not aspartate) can function as a neurotransmitter, and why the extracellular glutamate concentration rises to neurotoxic levels in brain anoxia [23].
• These results suggest that formation of new capillaries is an important mechanism to restore the O2 deficit in chronic brain hypoxia and that local rates of energy utilization may influence angiogenesis in different areas of the brain [24].
• The role of lactic acidosis of progressive brain hypoxia (PBH) as both a central chemoreceptor stimulant and a general respiratory depressant was assessed by preventing lactate formation both locally and globally with dichloroacetate (DCA) [25].
• In the search for potential biochemical markers of value for prognosis after acute hypoxic brain damage, amino acids and glucose were assessed in the cerebrospinal fluid (CSF) and glucose in blood [26].
• These results suggest that idebenone may stimulate the production of nitric oxide, probably through its direct action on nitric oxide synthase, thus producing its protective action on neurological disorders due to cerebral hypoxia or ischemia as a consequence of dilating the cerebral blood vessels [27].

Gene context of Hypoxia, Brain

• These data demonstrate the activation of the proangiogenic VEGF signaling cascade in patients with CM, probably reflecting compensatory mechanisms of general and focal brain hypoxia observed in these patients [28].
• These observations suggest that the elevation of serum S100B may mainly be caused by leakage following massive brain damage due to injury and cerebral hypoxia/ischemia, and in part by systemic hypoxic/traumatic tissue damage, depending on the survival time [29].
• Previous studies have demonstrated that brain hypoxia and ischaemia lead to the production of proinflammatory cytokines, including tumour necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and IL-6 [30].
• In previous studies, we have shown that cerebral hypoxia results in increased activation of MAPK-1 and MAPK-3 [31].
• Protection of striatal neurons by joint blockade of D1 and D2 receptor subtypes in an in vitro model of cerebral hypoxia [32].

Analytical, diagnostic and therapeutic context of Hypoxia, Brain

• We report the clinical and diffusion-weighted MRI (DWI) features of three patients with different types of anoxic brain injury: attempted hanging (hypoxic hypoxia), carbon monoxide poisoning (histotoxic hypoxia), and hanging with cardiac arrest (hypoxic-ischemic encephalopathy, HIE) [33].
• The significance of this important EEG decrease as well as the possible protective effect of etomidate against cerebral anoxia are discussed [34].
• This means that during the course of extracorporeal circulation brain hypoxia plays a pathological role assuming the typical picture of cellular oxidative damage and the acetyl-carnitine antagonizes these deleterious effects of hypoxia by a protective mechanism on the energy processes and then on the cellular enzymic activities [35].
• Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis) [36].

References