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)

Energy requirements for uptake of 14-C labeled 5-hydroxytryptamine ([14-C]5-HT) were studied in isolated guinea pig lungs, ventilated with 95% O2-5% CO2 and perfused in a recirculating system with Krebs-Ringer-bicarbonate solution containing 4% bovine serum albumin and 5 mM glucose. After 14 min preincubation with various inhibitors, lungs were perfused for 30 min with 0.25 times 10- minus 6 M [14-C]5-HT. Aliquots of perfusate were analyzed for [14-C]5-HT and metabolic products. Control lungs had a fractional serotonin clearance of 0.57 plus or minus 0.04. The rate of removal of [14-C]5-HT was inhibited 96% by imipramine, 88% by chlorpromazine, and 65% by ouabain, but was unaffected by iproniazid. Anoxia and cyanide each inhibited uptake by 68%. Omitting glucose from the perfusate reduced uptake by 30%. 2-Deoxyglucose and iodoacetate decreased the rate of [14-C]5-HT removal by 44 and 70%, respectively. Uptake was not affected by lung weight gain nor by changes in lung mechanical properties produced by [14-C]5-HT. [14-C]5-HT uptake by guinea pig lung requires a metabolic source of energy providing additional evidence for transport by an active process.
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PMID:Depression of pulmonary 5-hydroxytryptamine uptake by metabolic inhibitors. 113 May 33

Experiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F2 alpha, and high K+. Under control conditions, these anoxic contractions were not prevented by alpha-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.
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PMID:Anoxic contractions in isolated canine cerebral arteries: contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry. 243 36

Anoxia has been shown to potentiate the constrictor effects of 5-hydroxytryptamine (5HT) in isolated vascular tissue. In the present study, canine coronary arterial rings were incubated with various treatments and exposed to 5HT (4 X 10(-7) M) and anoxia (95% N2 and 5% CO2). Developed tension was increased by 250 +/- 40 mg by 5HT alone and 2,000 +/- 90 mg by 5HT and anoxia. Calcium (5 mM) potentiated, while inorganic (lanthanum, 10(-2) M) and organic calcium antagonists (nifedipine, verapamil and diltiazem; IC50 = 7 X 10(-9), 7.3 X 10(-8) and 2.4 X 10(-7) M, respectively) blocked the anoxic potentiation. Anoxia alone decreased resting tension (RT). Methysergide 3 X 10(-5) M inhibited both the 5HT- and anoxia-potentiated responses. Nitroglycerin decreased RT and inhibited the anoxic response (IC50 = 7.6 X 10(-6) M), while dipyridamole decreased RT and did not affect the anoxic response. These data suggest that the potentiation of 5HT contraction by anoxia is dependent upon extracellular calcium influx and is linked to a 5HT receptor. In addition, inhibition of the anoxic response can be achieved at other sites and is not a property common to all coronary vasodilators.
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PMID:Effects of nitroglycerin, dipyridamole, nifedipine, verapamil and diltiazem on canine coronary arterial rings contracted with 5-hydroxytryptamine and anoxia. 309 50

Nicorandil, nitroglycerin and diltiazem effects on normoxic and anoxic contractile responses to 5-hydroxytryptamine (5-HT) and norepinephrine (NE) were compared in isolated miniature pig coronary artery strips. Anoxia augmented contractile responses of the strips to 5-HT and NE. Nicorandil and nitroglycerin inhibited the normoxic contractile responses to 5-HT and NE and the further contraction induced by subsequently imposed anoxia. Diltiazem inhibited only the responses to 5-HT and to subsequently imposed anoxia. Whereas nicorandil and nitroglycerin produced relaxation of both potassium- and lanthanum-induced contractions, diltiazem was an effective relaxant of the potassium-induced contraction. The present experiments demonstrate that anoxia can augment the contractions of isolated large coronary arteries to 5-HT and NE. Nicorandil as well as nitroglycerin attenuate normoxic and anoxic contractions to 5-HT and NE. This is probably accomplished by inhibition of intracellular Ca2+ mobilization.
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PMID:Effects of a new antianginal agent, nicorandil, on normoxic and anoxic contractions in isolated miniature pig coronary arteries exposed to 5-hydroxytryptamine and norepinephrine: comparison with nitroglycerin and diltiazem. 622 11

Anoxia augments contractions of isolated canine coronary arteries to 5-hydroxytryptamine and norepinephrine. Lidoflazine inhibits normoxic contractions to both monoamines and the further increases in tension seen with anoxia in rings exposed to 5-hydroxytryptamine; further increases in tension caused by anoxia in presence of norepinephrine were not affected by lidoflazine. These experiments demonstrate that anoxia can cause constriction of large coronary arteries and that lidoflazine depresses both anoxic and normoxic contractions of coronary smooth muscle.
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PMID:Effect of the Ca2+ antagonist lidoflazine on normoxic and anoxic contractions of canine coronary arterial smooth muscle. 739 61