Hypoxia prolonged

The main complications associated with nitrous oxide inhalation occur as a result of hypoxia. Prolonged administration may also be harmful. Nitrous oxide is rapidly absorbed on inhalation. 

Hannah S, Mecklenburgh K, Rahman I, Bellington GJ, Greening A, Haslett C, Chilvers ER Hypoxia prolongs neutrophil survival in vitro. FEBS Lett 1995 372 233-237. 

Deprived of their substrate in severe or prolonged hypoxia, some ATPase-driven systems, including ion pumps, may become impaired. Further, with the decrease in the availability of O2 as its terminal electron acceptor, the mitochondrial transport chain becomes increasingly unable to accept reducing equivalents from cellular metabolic processes. Hence the intracellular pH falls, subjecting the cell as a whole to a reductive stress and favouring those enzyme systems with acid pH optima. 

A new product being developed currently is a mattress to treat hypoxia (lack of oxygen) in newborn babies. It is known that reducing the body temperature of the new born has a positive effect therefore they are treated with cold towels, medicine, chilled rooms to keep the temperature. This treatment could be substituted by the treatment with a PCM mattress, thereby optimizing and prolonging the temperature regulating effect. 

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. 

Excitotoxicity leads to increased Ca2+ and Zn2+, which can activate cytotoxic intracellular pathways. The prolonged availability of extracellular glutamate during hypoxia-ischemia is transduced by neuronal membrane receptors into potentially lethal intracellular ionic derangements, in particular, intracellular Na+ and Ca2+ overload. Excitotoxic... 

Due to the reduced supply of fluid, secretion of nasal mucus decreases. In coryza, nasal patency is restored. However, after vasoconstriction subsides, reactive hyperemia causes renewed exudation of plasma fluid into the interstitial space, the nose is stuffy again, and the patient feels a need to reapply decongestant. In this way, a vicious cycle threatens. Besides rebound congestion, persistent use of a decongestant entails the risk of atrophic damage caused by prolonged hypoxia of the nasal mucosa. 

Until recent times, the only toxicological hazards attributable to nitrous oxide were those common to asphyxiants, with death or permanent brain injury occurring only under conditions of hypoxia. A number of untoward and toxic effects have now been associated with exposure. One of the earliest findings was that patients given 50% nitrous oxide and 50% oxygen for prolonged periods, to induce continuous sedation, developed bone marrow depression and granuloqn openia. The bone marrow usually returned to normal within a matter of days once the nitrous oxide was removed, but several deaths from aplastic anemia have been recorded. ... 

Skeletal myoblasts can survive prolonged periods of hypoxia [77]. Like fetal cardiomyocytes, skeletal myoblasts survive and may engraft (although this is controversial) when injected into the border zone of an AMI. 

Early after-depolarizations are purported to be the mechanism giving rise to torsades de pointes. Conditions or drugs known to prolong the action potential, especially by interventions that decrease the outward potassium currents, facilitate development of torsades de pointes tachyarrhythmias. Early after-depolarizations may develop in association with hypokalemia, hypoxia, acidosis, and a wide range of pharmacological agents that interfere with outward currents or enhance inward currents. Antiarrhythmic agents, in particular sotalol. 

Pregnancy duration prolonged Offspring, high birth weights, increased peri-/postnatal pup mortality due to hypoxia and insufficient maternal care if birth process is prolonged or painftil (dystocia)... 

Most drugs used in anaesthesia are metabolised in the liver by phase I reactions, mediated by cytochrome P-450 enzymes. These are susceptible to destruction by cirrhosis, so that the biotransformation of drugs, such as opioids (except morphine), benzodiazepines, barbiturates, and inhalational agents, may be markedly altered in severe liver disease. These enzymes are found in the centrilobular areas, which are more prone to hypoxia. In contrast, the enzymes responsible for phase II reactions, found predominantly in the peripheral areas, often function normally even in advanced disease. The disposition of benzodiazepines that are eliminated primarily by glucuronidation, e.g. lorazepam and oxazepam, are unaffected by chronic liver disease. For drugs with low hepatic extraction, advanced hepatocytic dysfunction decreases phase I and II biotransformation with a reduced clearance and prolongation of the elimination half-life. This is often partially offset by an increased free fraction due to decreased protein binding. 

Hanna JP, Ramundo ML. Rhabdomyolysis and hypoxia associated with prolonged propofol infusion in children. Neurology 1998 50(l) 301-3. 

A comparison between aminoalcohol and aminoacid derivatives F-I reveals that the latter have equal potency in locomotive activity and muscles tests. They have prolonged ethanol anesthesia and are active only in the tonic phase of corazole convulsion tests. Methiodide H is highly effective against hypoxia.511... 

Comparable studies in turtle hepatocytes found (Land and Hochachka, 1995) quite a complex situation. Under conditions of prolonged oxygen lack, the expression of four proteins in turtle hepatocytes was preferentially up-regulated, while the expression of five proteins was preferentially down-regulated. The hypoxia dependence of this system appeared similar to... 

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