Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of normobaric hyperoxia on carotid body chemosensory function in the cat were studied. The hypothesis was that carotid body chemosensory function would be affected by chronic exposure to 100% O2 at sea level. It was based on the assumptions that carotid body tissue is exposed to high PO2 because of its high blood flow and that its O2 chemosensing mechanism is sensitive to O2 radical-induced reactions. Twelve cats were exposed to 100% O2 for 60-67 h, and 10 control cats were maintained in room air at sea level. They were anesthetized with pentobarbital sodium (Nembutal), and chemosensory afferents from a cut carotid sinus nerve were isolated and identified. The responses of single or a few clearly identifiable chemoreceptor afferents to isocapnic hypoxia and hypercapnia during hyperoxia and to the bolus injections of cyanide, nicotine, and dopamine were studied. We found that chronic hyperoxia severely blunted or eliminated the O2-sensitive response of the carotid chemoreceptors while augmenting the hypercapnic response. The response to cyanide but not to nicotine and dopamine were attenuated. Thus the hypoxic and hypercapnic responses that normally interact were separable. The lack of the cyanide response was consistent with the lack of the hypoxic response, suggesting a possible shared mechanism of carotid chemoreceptor response. Qualitatively normal responses to dopamine and nicotine indicated that the respective receptors were relatively intact after chronic exposure to hyperoxia and that the sensory nerves themselves were not affected by the prolonged O2 exposure.
 ...
PMID:Carotid body chemosensory function in prolonged normobaric hyperoxia in the cat. 311 Jan 24

The relation between arterial O2 tension (PaO2) and the firing rate of sympathetic preganglionic neurons (SPN) of the cervical sympathetic trunk was studied during graded isocapnic hypoxia and hyperoxia in unanesthetized acute C-1 spinal cats. In the PaO2 range between 40 and 400 Torr there was no relation between the two variables. Below 40 Torr firing rate increased as PaO2 decreased, reaching an average peak value of ten times control at a PaO2 of 20 Torr. Mean arterial blood pressure (MABP) was also independent of PaO2 between 40 and 400 Torr and increased by an average of 25% at PaO2 values below 40 Torr. Intravenous administration of hexamethonium or phentolamine abolished the MABP response but not the SPN response to hypoxia. Pentobarbital (5-60 mg/kg iv) did not modify the SPN response to hypoxia, although normoxic SPN background firing was considerably depressed. The excitatory effect of hypoxia seems independent of excitatory afferent input and appears to be a general property of SPN.
 ...
PMID:Hypoxic responses of sympathetic preganglionic neurons in the acute spinal cat. 730 56