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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, we demonstrated that chronic exposure to hyperoxia causes in vivo airway muscarinic receptor hyperresponsiveness in the developing rat [Am. J. Physiol. 262 (Lung Cell. Mol. Physiol. 6): L263-L269, 1992]. To test whether airway cholinergic hyperresponsiveness might result from intrinsic alterations in smooth muscle contractility, we measured the effect of in vivo hyperoxia on the contractile force elicited by acetylcholine (ACh) of isometrically mounted tracheal rings in vitro. Tracheal rings were obtained from 3-wk-old rats exposed to air or to > 95% O2 for 8 days. Muscarinic responses were determined by measuring the force elicited by exposure to increasing concentrations of ACh. Responses were normalized to the morphometrically determined tracheal smooth muscle cross-sectional area in a plane perpendicular to the axis of force generation. In vivo O2 exposure significantly increased maximal ACh-induced stress generation (response to 10(-3) M ACh: air, 15.92 +/- 1.37 g/mm2; O2, 21.78 +/- 1.52 g/mm2; P = 0.010). The ACh-induced stress generation of cylinders from hyperoxic rats was substantially reduced by both epithelial removal and treatment with the cyclooxygenase inhibitor indomethacin. We conclude that in vivo hyperoxic exposure increases tracheal smooth muscle contractile function in vitro and that epithelium-derived prostaglandin(s) contributes to the observed increase in maximal contractile responsiveness.
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PMID:Exposure of immature rats to hyperoxia increases tracheal smooth muscle stress generation in vitro. 817 85

Airway hyperreactivity is recognized as one of the long-term sequelae of bronchopulmonary dysplasia (BPD). Due to the improved care and prognosis of very low-birth weight infants, the incidence of BPD is increasing. There are data that suggest the increased survival of premature infants may be associated with the observed increased incidence of childhood asthma. The hyperoxia received as part of the treatment of respiratory distress syndrome is believed to be partly if not completely responsible for BPD. To gain insight into the potential role that hyperoxia might play in producing airway hyperreactivity, 4-day-old guinea pig pups were exposed to 70% oxygen or air for 96 h, and airway responsiveness to acetylcholine (ACh) was assessed both 2 and 9 days after the completion of the hyperoxia exposures. Unlike ozone, the mechanism for the persistently increased airway reactivity is not related either to the inhibition of neuronal acetylcholinesterase or inhibition of the neuronal M2 muscarinic receptor. A difference in antioxidant protection did not account for the increased response of the neonatal guinea pigs compared with hyperoxia-exposed rat pups. These data support the usefulness of the neonatal guinea pig as a model to study the mechanism responsible for hyperoxia-induced airway hyperreactivity.
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PMID:Airway hyperreactivity produced by short-term exposure to hyperoxia in neonatal guinea pigs. 922 25

The physiological response of two central nervous system neurotransmitter receptors to oxidative stress was studied using the rat model of hyperoxia. We show that hyperoxia leads to a decline in the ability of isoproterenol (ISO) to augment GABAergic responses in cerebellar Purkinje neurons in vivo. This effect is reversed by the N-tert-butylalpha-phenylnitrone (PBN). We also show that hyperoxia produces a decline in the ability of oxotremorine (OXO) to stimulate dopamine (DA) release in striatal slices. This effect is accompanied by an increase in hydroxyl radical levels in the CNS reflected in an increase in 2,3-DHBA, suggesting that the change is the result of an increased level of oxidative stress. We also show a time dependent effect of hyperoxia on both beta-adrenergic and muscarinic receptor function. We examined the interaction between age and hyperoxia exposure and found that in 12-month-old rats there is a decline in the baseline response prior to oxygen exposure that may interfere with observing a subsequent effect of hyperoxia. Differential effects were observed between the cerebellum and striatum with respect to the interaction of age and time of oxygen exposure. Overall, the data suggest that age and hyperoxia may be acting via a common mechanism because there was no synergistic effect of the two conditions.
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PMID:Effect of normobaric hyperoxia on two indexes of synaptic function in Fisher 344 rats. 1023 24

Chemotransduction of arterial hypoxemia by the cat carotid body is generally thought to begin with a hypoxia-induced depolarization of the glomus cells (GCs) of the carotid body (CB). This depolarization activates voltage-gated calcium channels with the subsequent entry of calcium, movement of transmitter-containing vesicles to the synaptic-like juncture between the GC and apposed sensory afferent neuron. The vesicles exocytotically release their transmitters which then proceed to the receptors on both the postsynaptic neuron and on the GCs themselves (autoreceptors). Action potentials and their modulation in the sensory fibers are the result, along with the modulation of further neurotransmitter release from the GCs. The purpose of the present study was to: (1) determine the parameters of an incubated cat CB preparation capable of releasing measurable amounts of catecholamines (CAs) in response to hypoxia; (2) determine the impact of muscarinic activities on CA release during the hypoxic challenge; (3) determine if the muscarinic activity preferentially modified the release of one CA more than another; (4) determine if there were any differences in the pattern of hypoxia-induced release of dopamine (DA) vs. norepinephrine (NE). CBs were harvested from deeply anesthetized cats. Cleaned of fat and connective tissue, they were incubated in Krebs Ringer bicarbonate solution at 37 degrees C, and bubbled with a hyperoxic mixture of gases (95% O(2)-5% CO(2)) for 30 min. The first series of experiments to address the CB's hypoxia-induced release of CAs explored the effects of incubating CBs for 2 h with hyperoxia vs. normoxia (21% O(2)-6% CO(2)) followed by a 30 min hypoxic challenge, with or without L-dihydroxyphenylalanine (L-DOPA). In the second series of experiments the CBs, after the first 30 min of hyperoxia, were next challenged with hypoxia (4% O(2)-5% CO(2)) for intervals of 3-20 min with intervening recovery periods of hyperoxia to determine the effect of the duration of the hypoxic exposure on CA release. In the third series of experiments the CBs, after the first 30 min of hyperoxia, were challenged with hypoxia for intervals of 10-40 min in the presence or absence of an M1 or M2 muscarinic receptor antagonist. CAs released into the incubation medium were analyzed by means of high performance liquid chromatography-electrochemical detection using standard procedures. Incubated cat CBs challenged for 2 h with hyperoxia followed by 30 min of hypoxia, released much more measurable amounts of CAs in the presence of 40 microM L-DOPA than without it. Moving from hyperoxia to hypoxia produced a better yield than moving from normoxia to hypoxia, and at least 10-20 min exposures were needed for measurable amounts of CAs. The M1 muscarinic receptor antagonist, pirenzepine, reduced the hypoxia-induced release of CAs during each exposure. Further, the reduction appeared to be dose-related. The M2 muscarinic receptor antagonist, methoctramine, enhanced the hypoxia-induced release of CAs during each exposure. These data support a role for acetylcholine (ACh) in the hypoxia-induced release of CAs, and suggest a significant, if modest, muscarinic dimension to it. And although hypoxia induced a greater release of DA than of NE, the muscarinic modulation of the release (both decreasing it and increasing it) may have had a greater impact on NE release than on DA release. Finally, the patterns of hypoxia-induced release of DA and NE from incubated cat carotid bodies are significantly different.
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PMID:Muscarinic modulation of hypoxia-induced release of catecholamines from the cat carotid body. 1182 Oct 6