Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotine-induced noradrenaline was investigated in perfused guinea pig hearts subjected to metabolic blockade that was caused either by anoxia or by cyanide intoxication. Noradrenaline, neuropeptide Y, and dihydroxyphenylethyleneglycol (DOPEG) were determined in the coronary venous overflow Neuropeptide Y is a sympathetic cotransmitter of noradrenaline, and concomitant release of both transmitters indicates an exocytotic, calcium-dependent release mechanism, whereas neuropeptide Y overflow does not occur during nonexocytotic noradrenaline release. Nonexocytotic, calcium-independent noradrenaline release, however, is associated with an increase of DOPEG overflow, which is the main intraneuronal metabolite of noradrenaline formed by monoamine oxidase if oxygen is present. Anoxia per se caused a nonexocytotic release of noradrenaline starting after 10 min of anoxia and reaching peak levels at 30 min. During anoxia, nicotine (3 and 10 mumol/l) accelerated and enhanced noradrenaline overflow, i.e., the period between the onset of anoxia and the begin of noradrenaline release was shortened and peak levels were increased. Nicotine-induced noradrenaline release was accompanied by neuropeptide Y overflow. The action of nicotine was further evaluated during energy depletion caused by cyanide. As anoxia did, cyanide administration alone resulted in noradrenaline release. In accordance with a nonexocytotic mechanism and due to the presence of oxygen, this release of noradrenaline was accompanied by an increase of DOPEG. When added 10 min after the onset of energy depletion, nicotine (10 mumol/l) caused a brief but marked enhancement of exocytotic noradrenaline release, since this release was calcium-dependent and was accompanied by a significant rise of neuropeptide Y overflow. In absence of extracellular calcium to avoid exocytosis, concomitant administration of nicotine (3-100 mumol/l) and cyanide caused a concentration-dependent acceleration of both the overflow of noradrenaline and DOPEG, whereas overflow of neuropeptide Y was not increased, thus indicating a nonexocytotic release mechanism. In conclusion, the application of nicotine during myocardial energy depletion increases overflow of noradrenaline by both calcium-dependent exocytotic release and calcium-independent nonexocytotic release mechanisms.
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PMID:Dual effect of nicotine on cardiac noradrenaline release during metabolic blockade. 770 41

Epidemiological studies have reported that cigarette smoking may protect from neurodegenerative diseases such as Parkinson's disease. These protective effects are thought to be mediated by nicotine. Recent data showed that nicotine significantly decreases respiratory control ratio (RCR) and superoxide anion generation of brain mitochondria. Thus, we investigated nicotine effects on rat brain in two experimental models: first, an in vitro anoxia/reoxygenation experiment and secondly, an in vivo rotenone-induced Parkinson-like syndrome. Anoxia/reoxygenation impaired mitochondrial respiration by 43.68% whereas in the presence of nicotine, it was less impaired, by 31.1% at 10(-7) M. In rats chronically administered rotenone (3 mg/kg/day), we observed profound mitochondrial damage: the RCR decreased by 50.36% and the superoxide anion generation and the membrane anisotropy increased by 56.03 and 13.43%, respectively. All of these indications of mitochondrial damage were limited by chronic administration of nicotine. Nicotine developed mitochondrial effects in vivo and in vitro at very low concentration. All these results were in accordance with epidemiological studies, which report a protective effect of nicotine in neurodegenerative diseases. Thus, we propose that one effect of nicotine is to preserve mitochondrial functions of the rat central nervous system.
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PMID:Nicotine protects rat brain mitochondria against experimental injuries. 1266 50