Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steady-state CO2-ventilation response curves with hyperoxia (end-tidal PO2 greater than 200 Torr) and mild hypoxia (end-tidal PO2 approximately equal to 60 Torr) were compared in five carotid body-resected (BR) patients and five control patients. The data were analyzed by fitting a linear equation, V = S(PETCO2-B), where V is minute ventilation S is the response curve slope. PETCO2 is end-tidal PCO2, and B is the response curve threshold. S slightly increased from hyperoxia to hypoxia in both BR and control groups. On the other hand, B moderately increased with hypoxia in BR patients, whereas it slightly decreased in controls. These changes were all not significant. However, in accordance with the change in B, the response curve to hypoxia at V of 10 1/min was significantly shifted in opposite directions in the two groups, i.e., rightward and leftward shift in BR and control groups, respectively. Thus the average magnitude of V calculated at PETCO2 of 40 Torr in hypoxia was significantly lower in BR patients than in controls (P less than 0.01). We conclude that this hypoxic depression of the CO2-ventilation response found in BR patients may have resulted, at least in part, from modulation of the brain stem neural mechanisms that were elicited by loss of afferent discharges from the carotid body.
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PMID:Evidence for hypoxic depression of CO2-ventilation response in carotid body-resected humans. 190 55

Reactive astrocytosis is a process by which astrocytes respond to brain injury by showing an increase in glial fibrillary acidic protein (GFAP) staining that is associated with hypertrophy and/or hyperplasia of these cells. Because spreading depression (SD) is a perturbation uncomplicated by neuronal necrosis and is seen in both in vivo and in vitro neural structures, we sought to determine whether SD was a sufficient stimulus to induce enhanced GFAP staining. SD was elicited in anesthetized rats by application of KCI to parietal cortex for 3 hr; equimolar NaCI was applied to contralateral cortex. SD was confirmed by monitoring DC potentials in frontal neocortices. Animals were allowed to recover for 48 hr, and their brains were processed for semiquantitative and computer-based analyses of GFAP staining intensity. Experimental GFAP staining was referenced to contralateral control levels. Neocortical SD (13-37 SDs) was associated with a significant (p less than 10(-4)), 43% increase in GFAP staining intensity, which remained statistically greater than normal for more than 2 weeks. If SD was inhibited by combined hyperoxia and hypercarbia, only a nonsignificant (p greater than 0.20), 7% increase in GFAP staining was seen. Thus, SD may be a useful physiologic process with which to begin to explore the cellular mechanisms that induce the transformation of normal astrocytes into reactive species.
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PMID:Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein. 190 91

This study assessed the effects of experimentally elevated plasma catecholamine levels on gill ventilation in rainbow trout (Oncorhyncus mykiss) exposed to various external ventilatory stimulants. Trout were exposed to hypoxia (water PO2 (PwO2) = 90 Torr) or hypercapnia (water PCO2 (PwCO2) = 4.5 Torr) for 30 min. These conditions caused gill ventilation volume (Vw) to increase by 2.3- and 1.5-fold, respectively, but did not stimulate release of catecholamines into the blood. While the stimulus (hypoxia or hypercapnia) was maintained, fish were given a bolus injection (0.3 ml), followed by intra-arterial infusion (0.6 ml.h-1), of a catecholamine mixture (2 x 10(-5) mol.l-1 adrenaline + 5 x 10(-6) mol.l-1 noradrenaline) to mimic the physiological concentrations and ratios of these catecholamines observed under more severe hypoxic or hypercapnic conditions. In hypoxic fish, this treatment caused a significant, but transient (5 min) depression of ventilation while during hypercapnia, the administration of exogenous catecholamines caused a more prolonged hypoventilatory response. These hypoventilatory responses occurred despite a catecholamine-induced blood acidosis (a potential ventilatory stimulant). To assess the importance of initial Vw and/or blood respiratory status on catecholamine-mediated hypoventilation, these experiments were repeated under hyperoxic (PwO2 = 640 Torr) hyperoxic hypercapnic (PwO2 = 510 Torr, PwCO2 = 4.8 Torr) or normoxic (PwO2 = 151 Torr) conditions in which Vw was either depressed (3.9-fold during hyperoxia) or unaffected. Intra-arterial infusion of catecholamines did not affect Vw under either of these experimental conditions. These results demonstrate that during a respiratory challenge, such as hypoxia or hypercapnia, physiologically relevant levels of circulating catecholamines can depress Vw and therefore do not support a stimulatory role for circulating catecholamines in the control of ventilation in fish.
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PMID:The effects of catecholamines on ventilation in rainbow trout during hypoxia or hypercapnia. 190 29

Exposure to hyperoxia causes loss of alveolar macrophage cell function. Toxicity was measured as suppression of the respiratory burst stimulated by phorbol myristate acetate subsequent to exposure (43.5% depression by 2-h exposure to 5 atm absolute O2 vs. controls). The presence of extracellular glutathione significantly protected these cells (7% loss). gamma-Glutamyl transpeptidase, a membrane enzyme with its active site directed outward, was necessary for use of extracellular glutathione. This was demonstrated using the gamma-glutamyl transpeptidase inhibitor, serine-borate complex, which significantly blocked both protection of cells by extracellular glutathione and extracellular glutathione-dependent synthesis of glutathione. The principal use of glutathione in antioxidant defense is as a substrate for glutathione peroxidase. The apparent Km for glutathione of glutathione peroxidase of rat alveolar macrophages was determined to be 2 mM; however, rat alveolar macrophages have approximately 1.3 mM intracellular glutathione, which is insufficient for maximal enzymatic activity. During hyperoxic exposure, this deficit would probably be more significant. Thus the ability of extracellular glutathione along with gamma-glutamyl transpeptidase activity to provide amino acids for de novo glutathione synthesis appears to be a potentially important component of antioxidant defense.
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PMID:Protection of alveolar macrophages from hyperoxia by gamma-glutamyl transpeptidase. 197 90

A study was made of the blood and tissue oxygen regime in patients with vibratory disease (VD) induced by local vibration and of the importance of lipid peroxidation (LPO) in oxygenation disorders. Venous hyperoxia, a decrease of the arteriovenous difference according to oxygen, the percentage of oxygen utilization by tissues, shift of the acid-base balance towards metabolic acidosis were established, attesting to tissue hypoxia that increased with the gravity of VD. The importance of a steady activation of LPO and depression of the antioxidant system in the pathogenesis of hypoxia associated with VD was supported by the correlation analysis data on oxygen balance and LPO, the functional and metabolic characteristics of red blood cells (according to the viscosity of red blood cell suspension and the content in the cells of SH-groups, lipoproteins and histidine) and platelets (according to aggregation in response to ADP and thrombin) as well as by the level of blood serum fluorescence. The authors provide evidence for the use of antioxidants (a complex of alpha-tocopherol with ascorbic acid and methionine and calcium antagonists of the nifedipine group), giving a membranostabilizing effect, in multimodality treatment of patients afflicted with VD.
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PMID:[Cell-membrane aspects of the pathogenesis of hypoxia in vibration disease induced by local vibration]. 204 32

Oxygen consumption rate (MO2) of hen eggs was measured on incubation day 16 (37.8 degrees C, 55% humidity) during acute exposure (90 min) to ambient hyperoxia (FI02 = 0.42) or hypoxia (FIO2 = 0.105). During the last part of these exposures, an H2 washout method was used to estimate relative changes in chorioallantoic membrane (CAM) blood flow, taking as an index the net change in the H2 washout rate constant between any experimental condition and the circulation arrested egg. Doubling normoxic FIO2 increased MO2 to an asymptotic value which was 4% above the normal (P less than 0.05; MO2 in normoxia = 890 mumols/h) even after correcting for the normoxic increase in MO2 with time during development (delta MO2/delta t = 21.5 mumols/h2; P less than 0.001). Halving FIO2 reduced MO2 calculated in the same way to 388 mumols/h. The estimate of the CAM blood flow, relative to normoxia, was 1.12 in hyperoxia (not significant, P = 0.05) and 0.68 in hypoxia (P less than 0.001). The limited changes in CAM blood flow and MO2 during hyperoxia indicate that they are both already close to their maximal values in normoxia. During acute hypoxia the 16 day embryo behaves as an oxygen-conformer; however, the small relative decrease in MO2 per unit of the flow index observed during hyperoxia suggests that the embryo can regulate its CAM blood flow to a small extent. The survival of the embryo and its recovery from hypoxia without a detectable O2 repayment suggest small if any anaerobic regulatory pathways and indicate a true metabolic depression.
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PMID:Oxygen uptake and chorioallantoic blood flow changes during acute hypoxia and hyperoxia in the 16 day chicken embryo. 205 58

Chemical control of respiration in cats after chronic normobaric hyperoxia (NH; inhalation of 100% O2 for 60-67 h) was compared with that of control rats, anesthetized with pentobarbital. After chronic hyperoxia, induction of moderate hypoxia (PaO2 = 50-60 Torr) increased inspiratory time (TI) often without increasing tidal volume (VT). More intense hypoxia (PaO2 = 40-50 Torr) depressed tidal volume and further increased TI, diminishing the respiratory drive (VT/TI). Hypercapnia, on the other hand, increased tidal volume and shortened respiratory cycle time; but these responses were subnormal. The normal stimulatory effects of intravenous nicotine and inhibitory effect of dopamine on carotid chemo-receptor activity and ventilation were preserved in the NH cats. Cyanide, however, did not stimulate carotid chemoreceptor activity and ventilation. Thus, the changes in the carotid and aortic chemosensory activities elicited appropriate reflex ventilation responses, indicating that the central component of the chemoreflex was not impaired. The ventilatory depression during hypoxia despite an active chemosensory input is consistent with the lack of carotid chemosensory response to and a central depressant effect of hypoxia in the NH cats, and was presumably associated in part with an increased responsiveness of airway reflexes. We conclude that chronic hyperoxia selectively attenuated carotid chemosensory and chemoreflex responses to hypoxia.
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PMID:Chemical respiratory control in chronically hyperoxic cats. 207 96

After voluntary hyperventilation, normal humans do not develop a significant ventilatory depression despite low arterial CO2 tension, a phenomenon attributed to activation of a brain stem mechanism referred to as the "afterdischarge." Afterdischarge is one of the factors that promote ventilatory stability. It is not known whether physiological stimuli, such as hypoxia, are able to activate the afterdischarge in humans. To test this, breath-by-breath ventilation (VI) was measured in nine young adults during and immediately after a brief period (35-51 s) of acute hypoxia (end-tidal O2 tension 55 Torr). Hypoxia was terminated by switching to 100% O2 (end-tidal O2 tension of first posthypoxic breath greater than 100 Torr). Brief hypoxia increased VI and decreased end-tidal CO2 tension. In all subjects, termination of hypoxia was followed by a gradual ventilatory decay; hyperoxic VI remained higher than the normoxic baseline for several breaths and, despite the negative chemical stimulus of hyperoxia and hypocapnia, reached a new steady state without an apparent undershoot. We conclude that brief hypoxia is able to activate the afterdischarge mechanism in conscious humans. This contrasts sharply with the ventilatory undershoot that follows relief of sustained hypoxia, thereby suggesting that sustained hypoxia inactivates the afterdischarge mechanism. The present findings are of relevance to the pathogenesis of periodic breathing in a hypoxic environment. Furthermore, brief exposure to hypoxia might be useful for evaluation of the role of afterdischarge in other disorders associated with unstable breathing.
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PMID:Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. 212 78

Seasonal affective disorders have recently been individualized by American authors. According to these authors, this subgroup of affective diseases deserve to be regarded as a clinical category owing to its specific symptoms, its epidemiological features and its response to treatment. They are characterized by the triad: hypersomnia, hyperoxia, weight gain, associated with usual symptoms of depression. Moreover, contrary to the bipolar manic-depressive psychosis, they seem to predominate among women. Finally, phototherapy, the various protocols of which are discussed here, is said to be effective. The influence of latitude combined with the effectiveness of phototherapy has led to original pathogenic hypotheses, among which the presence of a chronobiological disorder (abnormality of the season-induced circadian rhythm), although attractive and supported by a strict clinical study, has yet to be demonstrated. Also hypothetical is the role played by melatonin: is this hormone the principal "mediator" or an epiphenomenon?
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PMID:[Seasonal affective disorders, a new clinical category]. 213 39

1. Synchronization of spontaneous sympathetic discharge during the respiratory cycle was studied in the cervical and renal nerves of vagotomized, normotensive Wistar-Kyoto rats (WKYs) and age-matched spontaneously hypertensive rats (SHRs). Phrenic nerve discharge was used as an index of central inspiratory activity. 2. In normotensive Wistar-Kyoto rats depression of sympathetic activity appeared at the onset of inspiration reaching a minimum at mid-inspiration. Peak maximal sympathetic discharge corresponded to postinspiratory phase; a second increase sometimes appeared in late expiration. Variations of respiratory frequency over wide range of experimental conditions by hypoxia, hyperoxia, hyper- or hypocapnia and transection of carotid sinus nerves did not affect this pattern. 3. In SHRs the respiratory-phase-related timing of sympathetic discharge was variable. In normoxia, the maximal sympathetic activity occurred in late inspiration, preceded by short depression at early inspiration and followed by postinspiratory depression. A second increase in sympathetic activity was observed in mid-expiration. 4. The pattern of respiratory phase modulated sympathetic activity in SHRs was altered by hypoxic stimulation of the peripheral chemoreceptors. The early inspiratory depression of sympathetic activity was substantially prolonged and the maximal sympathetic discharge was shifted from inspiration to early expiration. This effect was abolished after carotid sinus nerves had been cut. 5. Hypercapnic stimulation of central chemoreceptors in SHRs with carotid sinus nerves cut did not influence the timing of the sympathetic activity in relation to the respiratory phase, though the magnitude of rhythmical sympathetic discharges was increased. 6. We discuss the possibility that altered synchronization between central respiratory drive and sympathetic neuronal system may contribute to the neurogenic mechanisms of arterial hypertension in SHRs.
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PMID:Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat. 223 3


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