Hypoxia brain

At rest, the brain consumes 20% of the total oxygen that the whole body consumes. Global brain ischemia occurs when the arterial blood pressure cannot maintain a sufficient cerebral perfusion pressure. This happens with cardiac dysfunction, shock, and critical increase in intracranial pressure. Cerebral hypoxia is the deprivation of oxygen with a maintained cerebral blood flow. Pure hypoxia will occur in rare instances such as reduced atmospheric oxygen, which is an extremely rare cause of brain hypoxia, or as a result of drowning. Most cases occur in a combination of hypoxia and ischemia since pure hypoxia very often causes cardiac arrest and, thus, interruption of cerebral blood flow. The combination of both hypoxia and ischemia leads to more serious neuronal damage than hypoxia alone. 

Seizures occur more infrequently in horses than in dogs and cats. Seizures are seen in adult horses from brain trauma, bacterial meningitis, viral encephalitis and, rarely, hepatic encephalopathy or vascular accidents. Convulsions are seen in young neonatal foals with NMS as a result of brain hypoxia and in Arabian foals aged 3-9 months (idiopathic Arabian epilepsy). Anticonvulsant therapy is used to prevent the spread of the seizure focus, increase (raise) the seizure threshold and decrease the electrical excitement of abnormal... 

Heavy tobacco smoking is especially dangerous for the fetus. Maternal smoking of more than 20 cigarettes a day is associated with maternal anemia, fetal brain hypoxia, and fetal polyglobulia (an abnormal increase in circulating red blood cells).35... 

Neubauer, J.A., Melton, J.E., and Edehnan, N.H. 1990. Modulation of respiration during brain hypoxia. 7. Appl. Physiol. 68 441. 

Fetal guinea pig and newborn piglet model stndies have demonstrated that brain tissue hypoxia results in brain cell membrane damage as evidenced by increased membrane lipid peroxidation and decreased Na+, K+-ATPase activity. Brain hypoxia was found to increase the NMDA receptor agonist-dependent Ca + in synaptosomes of hypoxic as compared to normoxic fetuses (Mishra and Delivoria-Papadopoulos, 1999). 

Grossman, R.G. and Williams, V.F. Electrical Activity and Ultrastructure of Cortical Neurones and Synapses in Ischaemia. In "Brain Hypoxia", p. 61o Eds. Brierly, J.B. and Meldrum, B.S. 

That the hyperpolarization might be an artefact can t be excluded on grounds of the ion-exchange electrode data available at present but on the other hand, hyperpolarization as an initial response to hypoxia has been observed with other methods, e.g. Gross-man, R.G. and Williams, In Brain Hypoxia, Eds. Brierly, J.B. and Meldrum, B.S, S.1.M.P./William Heineman. S.1. M.P./Medical Books Ltd., London, 1971. However the hyperpolarization is not present if anaesthetised animals are paralysed with Flaxedil. 

Wasicko MJ, Melton JE, Neubauer JA, Krawciw N, Edelman NH. Cervical sympathetic and phrenic nerve responses to progressive brain hypoxia. J Appl Physiol 1990 68 53-58. 

Conceptually, the most straightforward way to demonstrate the ventilatory effects of brain hypoxia is to expose peripherally chemodenervated animals to a hypoxic environment. The results of sueh studies, however, are not uniform with the major eonfounding variable being arousal state. In awake, unanaesthetized, chemodenervated animals both exeitation and depression have been reported (as reviewed in Ref 2). The response most often observed consists of tachypnea with variable effects on tidal volume and httle or no ehange in alveolar ventilation. In one study, the tachypnea was related to an inerease in systemic metabolic rate and reversed by adrenergic blockade (3). 

The souree of the hyperpolarization almost definitely includes either a global or regionally speeific alteration in the balance of inhibitory and excitatory neurotransmitters/neuromodulators. In the progressive brain hypoxia model, good... 

It is our view that the most convineing examples of direct, i.e., chemoreceptor-like, hypoxic excitation of motor output mediated by discrete sites in the CNS are excitation of sympathetic discharge and gasping brought about by severe brain hypoxia. 

From this brief review, it is apparent that brain hypoxia most hkely modulates respiratory output in an anatomically and metabohcaUy diverse manner. In addition, a variety of circumstances, including state of arousal, stage of development, and even heredity, impact upon these responses. 

Depressant effects (other than those from neuronal failure due to energy depletion) may well reflect a residue of mechanisms that have evolved to deal with the peculiar challenge of the perinatal period. Nonspecific effects of brain hypoxia have been described, but more recent work points to direct excitation of medullary neurons by hypoxia as seen in both the sympathoexcitatory neurons of the RVLM and the putative pacemaker neurons of the pre-BdtC. In our view, the role of the excitation of the pre-BdtC in the genesis of gasping has been established and the possibility that hypoxia may modulate eupneic breathing has been raised. 

Melton JE, Yu QP, Neubauer JA, Edehnan NH. Modulation of respiratory responses to carotid sinus nerve stimulation by brain hypoxia. J Appl Physiol 1992 73 2166-2171. 

---