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

Bilateral carotid occlusion (BCO) was performed in pentobarbital anesthetized adult rats neonatally treated with capsaicin (50 mg/kg, sc, CNT rats). Pressor and ventilatory responses to BCO in CNT rats were compared with those of littermate controls injected with a same volume of solvent (olive oil, 0.1 ml). Capsaicin was used in order to produce partial degeneration of unmyelinated C fibres related to baroreflexes and peripheral chemoreflexes. In control rats, BCO provoked in less than 5 s, hyperventilation, hypocapnia and hyperoxia. Systemic arterial hypertension and tachycardia developed more slowly. They were maximum at 65 s. At this time, ventilation was returned to control values. Hyperventilation results from the stimulation of the carotid chemoreceptors by stagnant asphyxia generated by the blood flow stop. Hypertension and tachycardia are provoked by an increase in the orthosympathetic outflow when carotid baroreceptors are unloaded. In a first time, chemoreceptors stimulation tends to oppose to the increase of heart rate in normal rats. In a second one, development of hypertension is autolimited by the stimulation of the aortic baroreceptors particularly effective in rats. Simultaneously the hyperoxic inhibition from aortic chemoreceptors, the central hypocapnia and the reperfusion of the carotid bodies lead to the suppression of hyperventilation. As hyperventilation decreases when hypertension develops, even in rats with vago-sympathetic section at low cervical level, the part of aortic baroreceptors effects is probably reduced except for the fibres travelling through superior laryngeal nerves. Carotid bodies reperfusion seems to predominate. Before any manipulations, CNT rats had lower heart rate and systemic blood pressure than controls. During BCO, initial hyperventilation was moderately prolonged as hypertension slowly developed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral carotid occlusion in the rat neonatally treated with capsaicin]. 800 42

The effect of a previous exposure to hyperbaric oxygen (HBO) on the synthesis capacity of prostaglandin (PG) and thromboxane (TX) was investigated in the brain of male rats. Three groups of rats were used: 1. Neurotoxic HBO (n = 11): The rats were exposed to sixfold the atmospheric pressure (101.3 kPa), i.e., 6 absolute atmospheres (ATA), of pure O2 up to the first convulsion (6 ATA O2); 2. Mild hyperoxia (n = 10): The rats were exposed to compressed air at the same absolute pressure and for a similar time than that of the neurotoxic HBO group (here PO2 is 1.26 ATA); 3. Normoxia at atmospheric pressure (PO2 is 0.21 ATA) for control. There was no convulsion in groups 2 and 3. Decompression of the high pressure groups lasted 15 min. After decapitation, samples of the frontal cortex and the striatum were taken, weighed, washed, and then incubated in Krebs-Ringer bicarbonate for 1 h. The release of eicosanoids in the medium was determined by enzyme immunoassay. Mild hyperoxia only significantly reduced in the striatum the release of 6-keto-PGF1 alpha (1.3 +/- 2.4 vs 10.9 +/- 6.6 pg/mg wet tissue, p < 0.001; mean +/- SD) and PGE2 (3.2 +/- 2.7 vs 7.8 +/- 6.5 pg/mg wet tissue, p < 0.05), whereas TXB2 did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of hyperbaric oxygen on prostaglandin and thromboxane synthesis in the cortex and the striatum of rat brain. 829 21