Oxygen hypoxia

The nervous system is vulnerable to attack from several directions. Neurons do not divide, and, therefore, death of a neuron always causes a permanent loss of a cell. The brain has a high demand for oxy gen. Lack of oxygen (hypoxia) rapidly causes brain damage. This manifests itself both on neurons and oligodendroglial cells. Anoxic brain damage may result from acute carbon monoxide, cyanide, and hydrogen sulfide poisonings. Carbon monoxide may also be formed in situ in the metabolism of dichloromethylene. 

Neuronal function depends on a constant supply of oxygen. Hypoxia, a decrease in oxygen availability, depresses neuronal activity. Interruption of blood flow to the brain for only a few seconds leads to unconsciousness. A prolonged lack of blood flow, which is characteristic of stroke, leads to permanent brain damage in the affected area. 

Chemoreceptors. The peripheral chemoreceptors include the carotid bodies, located at the bifurcation of the common carotid arteries, and the aortic bodies, located in the aortic arch. These receptors are stimulated by a decrease in arterial oxygen (hypoxia), an increase in arterial carbon dioxide (hypercapnia),... 

Bronchiolar smooth muscle is sensitive to changes in carbon dioxide levels. Excess carbon dioxide causes bronchodilation and reduced carbon dioxide causes bronchoconstriction. Pulmonary vascular smooth muscle is sensitive to changes in oxygen levels excess oxygen causes vasodilation and insufficient oxygen (hypoxia) causes vasoconstriction. The changes in bronchiolar and vascular smooth muscle tone alter the amount of ventilation and perfusion in a lung unit to return the V/Q ratio to one. 

Anoxia is the term used to describe lack of oxygen. Hypoxia is low oxygen level. Anoxia in humans results in immediate unconsciousness, convulsions, and paralysis. Hypoxia may have less profound effects, depending on the level. Hypoxic effects become worse as the duration increases. 

Cyanide binds to Fe in heme-containing proteins. This inhibits the terminal cytochrome complex IV of the electron transport chain. The blocklock of complex IV by cyanide depletes ATP culminating in cell death. Oxygen is unable to reoxidize the reduced cytochrome a3. Thus, cellular respiration is inhibited, as well as ATP production, in essence depriving the cells, tissue, and, ultimately, the whole body of oxygen. Hypoxia evolves into metabolic acidosis and decreased oxygen saturation. The extent of lactic acidosis indicates the severity of the cyanide... 

Vitamin C Oxygen (hypoxia) Antioxidant Esteban et al. (2010) Yoshida et al. (2009)... 

Anoxia Anoxia is the absence of oxygen in inspired gases or in arterial blood and/or in the tissues. This is closely related to hypoxia, which is a severe oxygen deficiency in the tissues. One can think of anoxia as the most extreme case of hypoxia. 

Hypoxia A condition characterized by a deficiency of oxygen reaching the tissue. Hz See Hertz. 

Lack of oxygen in blood or tissues. Tissue hypoxia can be caused by injury, inflammation, or tumor growth, due to disruption of blood supply. Tissue hypoxia is normally associated with acidosis, as anaerobic metabolism leads to production of lactic acid. 

Ethylene is an anesthetic gas with a rapid onset of action and a rapid recovery from its anesthetic effects. It provides adequate analgesia but has poor muscle-relaxant properties. The advantages of ethylene include minimal bronchospasm, laryngospasm, and postanesthesia vomiting. A disadvantage of ethylene is hypoxia. This gas is supplied in red cylinders. Mixtures of ethylene and oxygen are flammable and explosive. 

A classification of the causes of hypoxia is presented in Table II. Only anoxic anoxia (due to decreased ambient oxygen or to respiratory disease) has arterial P02 values decreased (with accompanying decreased venous P02 values). However, hemic, ischemic, and histoxic hypoxia may be present (termed non-ventilatory hypoxia) with normal arterial P02 values. Thus the best evaluation of hypoxia is an analysis of both arterial and venous... 

Darley-Usmar, V., O Leary, V. and Stone, D. (1989). The glutathione status of perfused rat hearts subjected to hypoxia and teoxygenation the oxygen paradox. (Corrected and republished article originally printed in Free Rad. Res. Commun. 5, 283-289. 

It is known that the endothelial cells lining the capillary bed are markedly damaged during hyperoxic exposure. However, it is not at present known whether this damage is due to free-radical-induced injury of the endothelial cells or whether endothelial cells are simply responding to the diminished blood flow produced by the severe vasoconstriction. The theoretical basis for free-radical involvement is sound and it has been proposed that low oxygen tensions (hypoxia) followed by periods of reoxygenation are the most likely explanation for the disorder (Kelly, 1993). 

P. H. Saglio, M. C. Drew, and A. Pradet, Metabolic acclimation to anoxia induced by low (2-4kPa partial pressure) oxygen pre-treatment (hypoxia) in root tips of Zea mays, Plant Physiology S6 61 (1988). 

Hypoxia Arterial blood gases, Ventilation, oxygen... 

The principal function of the circulatory system is to supply oxygen and vital metabolic substrates to cells throughout the body, as well as removal of metabolic waste products. Circulatory shock is a life-threatening condition whereby this principal function is compromised. When circulatory shock is caused by a severe loss of blood volume or body water it is called hypovolemic shock, the focus of this chapter. Regardless of etiology, the most distinctive manifestations of hypovolemic shock are arterial hypotension and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic... 

The goal of oxygen therapy is to maintain Pao2 above 60 mm Hg (8 kPa) or Sao2 above 90% in order to prevent tissue hypoxia and preserve cellular oxygenation.1 Increasing the Pao2 much further confers little added benefit and may increase the risk of C02 retention, which may lead to respiratory acidosis. An arterial blood gas should be obtained after 1 to 2 hours to assess for hypercapnia. 

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