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

Carotid body chemosensory response to hypoxia is attenuated as a result of prolonged normobaric hyperoxia (NH) in the cat. The effect of NH is likely to be due to high cellular PO2 and O2-related free radicals. Accordingly, the effect would be less if O2 delivery to the chemoreceptor tissue could be compromised. The aortic bodies, which appear to have less of a circulatory O2 delivery, as suggested by their vigorous responses to a slight compromise of O2 flow compared with those of the carotid body, could provide a suitable testing material for the hypothesis. We tested the hypothesis by studying both aortic and carotid body chemoreceptors in the same cats (n = 6) which were exposed to nearly 100% O2 for about 60 h. These chemoreceptor organs were also studied in 6 control cats which were maintained in room air at sea-level. The cats were anesthetized and their carotid and aortic chemosensory fibers were identified by the usual procedure, and their responses to hypoxia and hypercapnia and to bolus injections (i.v.) of cyanide and nicotine were measured. In the NH cats, the carotid but not aortic chemosensory responses to hypoxia and cyanide were attenuated and to hypercapnia (both onset and steady state) augmented. The aortic chemoreceptors were stimulated by hypoxia, hypercapnia, cyanide and nicotine both in the NH and the control cats similarly. The results support the hypothesis that it is presumably a higher tissue blood flow and hence a higher concentration of O2-related free radicals which ultimately led to the specific attenuation of O2 chemoreception in the carotid body.
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PMID:Aortic and carotid body chemoreception in prolonged hyperoxia in the cat. 178 Jun 2

Respiratory muscle EMG responses to transient, specific carotid body excitation (NaCN, hypoxia) and inhibition (dopamine, hyperoxia) were studied in 7 unanesthetized standing dogs while intact (N = 7) and during bilateral cold block of the vagi (N = 3). In all dogs carotid body excitation augmented the EMG activities of both expiratory muscles (triangularis sterni, TS; transversus abdominis, TA) and the (inspiratory) crural diaphragm (CR); carotid body inhibition significantly reduced phasic EMG activities in all muscles. With vagal blockade the response of the TS to carotid body stimulation was increased; that of the TA was essentially unchanged from the intact state. In all dogs expiratory muscle recruitment in response to carotid body excitation/inhibition could either precede or follow that of the CR. We conclude that in response to specific, transient carotid body excitation or inhibition: (1) Changes in CR, TS and TA EMGs are qualitatively similar. (2) Vagal feedback is strongly inhibitory to TS and excitatory to TA. (3) Changes in expiratory muscle EMGs do not require preceding changes in the CR. Carotid body stimulation contributes significantly to the generation of phasic expiratory activity during eupnea.
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PMID:The influence of carotid body chemoreceptors on expiratory muscle activity. 227 Mar 59

We tested the following hypothesis: if carotid body blood flow, and hence the relationship of the frequency of discharge in chemoreceptor afferent fibres to arterial PO2, were affected by atherosclerotic change, then a modification of the control of the respiratory and cardiovascular systems might result. Carotid body reflexes were therefore studied in conscious atherosclerotic rabbits and a control group of normal animals breathing 100% O2, three hypoxic gas mixtures to which was added sufficient CO2 to maintain the arterial PCO2 constant, and 2% and 4% CO2 in 21% O2 and N2. When breathing room air, the atherosclerotic rabbits breathed at a higher respiratory frequency and lower tidal volume than the normal animals, although there was no difference in the respiratory minute volume. The respiratory and cardiovascular responses to hyperoxia, isocapnic hypoxia and hypercapnia were essentially the same in both groups of animals. Serial sections of the carotid bodies showed pathological changes including interstitial fibrosis in the caudal part with interstitial haemorrhages. The proximal part of the ascending pharyngeal artery, the vessel supplying the organ, and its origin from the external carotid, and the arterioles in the caudal part of the carotid body were nearly always occluded to a varying extent by atheromatous plaques. The capillaries appeared normal under light microscopy. The rostral-caudal lengths of the carotid bodies were similar in the two groups. We conclude that the peripheral arterial chemoreceptor responses in atherosclerotic rabbits are relatively normal even though the arteries to, and arterioles within, the carotid body are partly occluded.
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PMID:Carotid chemoreceptor function and structure in the atherosclerotic rabbit: respiratory and cardiovascular responses to hyperoxia, hypoxia and hypercapnia. 259 Sep 27

We studied the interaction of O2 and CO2 at the peripheral chemoreceptors in 6 two-week-old awake lambs. The method used, which selectively tested the peripheral chemoreceptors, measured the immediate ventilatory (VE) response to pure O2 and then to O2 + CO2. From room air, the animal was switched abruptly to either pure O2 or O2 + 5% CO2, O2 + 7.5% CO2, or O2 + 10% CO2. VE was measured before and 8-10 sec after a step change in the inspired gas. In response to pure O2, VE/kg dropped 131 +/- 30 ml/min.kg (38%). Repeat O2 tests performed with the addition of CO2 showed that CO2 interacted to blunt the response to pure O2; the VE change from pre-test baseline to 8-10 sec being -77 +/- 42, -18 +/- 25, and +8.5 +/- 60 for 5%, 7.5%, and 10% added CO2 respectively. Carotid body denervation eliminated the immediate VE responses to O2 and CO2. We conclude that in the 2-week-old awake lamb, (1) hyperoxia suppresses the O2 drive output of the peripheral chemoreceptors, (2) during hyperoxia O2 and CO2 still interact at the chemoreceptor level, and (3) despite hyperoxia, the peripheral chemoreceptors retain a substantial graded response to incremental transient CO2 challenge.
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PMID:Peripheral chemoreceptor CO2 response during hyperoxia in the 14-day-old awake lamb. 314 Mar 31

Carotid body afferent contributions to activity of the intermediate area of the ventral medullary surface (IVMS) following transient hypoxia and hyperoxia were examined in 6 spontaneously breathing, pentobarbital-anesthetized cats. Two tidal breaths of 100% N2, 100% O2, or room air, were randomly administered before and after carotid sinus denervation (CSD). Images of scattered light from the IVMS showed that activity increased with hypoxia (10.1 +/- 2.4%), and decreased with hyperoxia (4.8 +/- 1.8%). CSD significantly increased the magnitude and delayed the onset of the hypoxic response, but reversed the initial component of the hyperoxic response. We conclude that carotid body afferents modulate the magnitude and timing of IVMS responses to transient respiratory challenges.
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PMID:Ventral medullary surface responses to hypoxic and hyperoxic transient ventilatory challenges in the cat. 760 4

We used extracorporeal perfusion of the vascularly isolated carotid sinus region to determine the effects of specific carotid body chemoreceptor hypocapnia-alkalosis on ventilatory control in the unanesthetized dog. Eight female dogs were studied during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid eye movement (REM) sleep. Carotid body perfusions lasted from 1 to 2 min, and each trial was preceded by a 1-min control period. Two levels of carotid body hypocapnia were employed, approximately 7 and 14 Torr below eupneic levels in a given dog. We found that 1) During wakefulness and NREM sleep, carotid body hypocapnia caused reduced tidal volume (VT) but not apnea or expiratory time prolongation. 2) The inhibition of ventilation in response to carotid body hypocapnia was graded below normocapnia, showing the highest sensitivity at carotid body PCO2 near 7 Torr below eupneic values. Inhibition reached a maximum near 14 Torr below the eupneic level; VT, inspiratory minute ventilation (VI), and VT-to-inspiratory time ratio fell 31, 23, and 27% in wakefulness and 30, 23, and 30% in NREM sleep. 3) Reductions in ventilation in response to carotid body hypocapnia are lessened but still persist throughout perfusion (up to at least 130 s) despite significant systemic hypercapnia. 4) During REM sleep, carotid body hypocapnia had no consistent inhibitory effect on ventilation until carotid body PCO2 was reduced to values near 14 Torr below the eupneic level, at which point ventilation was similar to wakefulness and NREM. 5) Moderate carotid body hypocapnia was as effective as carotid body hyperoxia in reducing VT and VI. We conclude that carotid body hypocapnia-alkalosis can significantly inhibit eupneic VT and ventilation during wakefulness and NREM sleep and, if the hypocapnia is severe enough, during REM sleep.
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PMID:Ventilatory effects of specific carotid body hypocapnia in dogs during wakefulness and sleep. 856 4

Hypoxic ventilatory and phrenic responses are reduced in adult rats (3-5 months old) exposed to hyperoxia for the first month of life (hyperoxia treated). We previously reported that hypoxic phrenic responses were normal in a small sample of 14- to 15-month-old hyperoxia-treated rats, suggesting slow, spontaneous recovery. Subsequent attempts to identify the mechanism(s) underlying this spontaneous recovery of hypoxic phrenic responses led us to re-evaluate our earlier conclusion. Experiments were conducted in two groups of aged Sprague-Dawley rats (14-15 months old) which were anaesthetized, vagotomized, neuromuscularly blocked and ventilated: (1) a hyperoxia-treated group raised in 60 % O2 for the first 28 postnatal days; and (2) an age-matched control group raised in normoxia. Increases in minute phrenic activity and integrated phrenic nerve amplitude (integral Phr) during isocapnic hypoxia (arterial partial pressures of O2, 60, 50 and 40 +/- 1 mmHg) were greater in aged control (n = 15) than hyperoxia-treated rats (n = 11; P < or = 0.01). Phrenic burst frequency during hypoxia was not different between groups. To examine the central integration of carotid chemoafferent inputs, steady-state relationships between carotid sinus nerve (electrical) stimulation frequency and phrenic nerve activity were compared in aged control (n = 7) and hyperoxia-treated rats (n = 7). Minute phrenic activity, integral Phr and burst frequency were not different between groups at any stimulation frequency between 0.5 and 20 Hz. Carotid body chemoreceptor function was examined by recording whole carotid sinus nerve responses to cessation of ventilation or injection of cyanide in aged control and hyperoxia-treated rats. Electrical activity of the carotid sinus nerve did not change in five out of five hyperoxia-treated rats in response to stimuli that evoked robust increases in carotid sinus nerve activity in five out of five control rats. Estimates of carotid body volume were lower in aged hyperoxia-treated rats (4.4 (+/- 0.2) x 10(6) microm3) compared to controls (17.4 (+/- 1.6) x 10(6) microm3; P <0.01). We conclude that exposure to hyperoxia for the first month of life causes life-long impairment of carotid chemoreceptor function and, consequently, blunted phrenic responses to hypoxia.
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PMID:Life-long impairment of hypoxic phrenic responses in rats following 1 month of developmental hyperoxia. 1182 78

Reactive oxygen species (ROS) induce DNA damage with the ensuing activation of the chromosomal repair enzyme poly(ADP-ribose) polymerase (PARP). ROS also interact with the function of carotid body chemoreceptor cells. The possibility arises that PARP is part of the carotid chemosensing process. This study seeks to determine the presence of PARP and its changes in response to contrasting chemical stimuli, hypoxia and hyperoxia, both capable of generating ROS, in cat carotid bodies. The organs were dissected from anesthetized cats exposed in vivo to acute normoxic (PaO2 approximately 90 mmHg), hypoxic (PaO2 approximately 25 mmHg), and hyperoxic (PaO2 > 400 mmHg) conditions. Carotid body homogenate was the source of PARP and [adenine 14C] NAD was the substrate in the assay. Specimens of the superior cervical ganglion and brainstem were used as reference tissues. We found that PARP activity amounted to 27 pmol/mg protein/min in the normoxic carotid body. The activity level more than doubled in both hypoxic and hyperoxic carotid bodies. Changes of PARP in the reference tissues were qualitatively similar. We conclude that PARP is present in the carotid body but the augmentation of the enzyme activity in both hypoxia and hyperoxia reflects DNA damage, induced likely by ROS and being universal for neural tissues, rather than a specific involvement of PARP in the chemosensing process.
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PMID:Poly(ADP-ribose) polymerase activity in the cat carotid body in hypoxia and hyperoxia. 1236 43

Carotid body chemoreceptors undergo significant maturational changes in the post-natal period over a period of days to weeks. This is likely initiated by the rise in Pa(O2) at the time of birth and reflects the changing value of "normoxia" from 25 Torr to near 100 Torr. Chemoreceptors in the newborn period have a lower absolute discharge frequency and the dynamic response to acute hypoxia is less compared to the adult. This maturation change appears due to changes occurring presynaptically to the afferent nerve fibers. Hypoxia-induced secretion from the glomus cell (catecholamine and other constituents of dense cored vesicles) is enhanced whilst constitutive (non-hypoxia-dependent) release is reduced with age. On the post-synaptic side, the number of afferent synaptic sites increases four- to five-fold in the post-natal period and there may be an increase in afferent nerve excitability. Both of these changes are subject to environmental perturbations in which post-natal exposure to chronic hypoxia or hyperoxia leads to significantly reduced organ sensitivity and function. Thus, developmental changes and environmental factors may significantly change the ability of an animal to detect and respond to hypoxic insults, perhaps leading to periods of heightened vulnerability to hypoxic stresses.
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PMID:Development of carotid body/petrosal ganglion response to hypoxia. 1601 11

Carotid body chemoreceptors respond to a decrease in arterial partial pressure of O(2) with an increase in sinus nerve action potential (AP) activity which initiates a number of protective reflexes. The spike generation process is unresolved but is generally considered to be caused by a synaptic depolarizing potential (SDP) in the nerve endings caused by release of an excitatory transmitter from the glomus cell, which is a secretory cell that is presynaptic to the nerve terminals. To detect the purported SDPs, stimulating electrodes were placed at sites within the carotid body from which orthodromic APs could be evoked at low threshold currents. The probability of AP generation as a function of stimulus current was fitted well to a Boltzmann distribution. Subthreshold electrical stimuli which were expected to summate with subthreshold SDPs, failed, in all instances, to evoke APs at the expected probability. When the stimulus was gated to the occurrence of a spontaneous AP, no change in electrical threshold was observed as the delay between the spontaneous AP and electrical stimulus was increased, despite the presumed disappearance of an SDP in the post-AP period. Decreases in spontaneous AP generation rate, caused by hyperoxia, were associated with only slight changes in the mean orthodromic stimulus threshold, but with a significant increase in slope of the Boltzmann function, suggesting a decrease in the variance of nerve terminal excitability during hyperoxia. These results suggest that AP generation is not due to SDP events; rather, AP generation is likely to be due to a process endogenous to the nerve terminals that modulates the variability of nerve terminal excitability.
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PMID:Orthodromic spike generation from electrical stimuli in the rat carotid body: implications for the afferent spike generation process. 1723 2


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