Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Normobaric hyperoxia decreases heart rate (HR) in humans and animals. This study explored the mechanisms of hyperoxic bradycardia by examining its response time, autonomic neural mediation, and reversibility in conscious dogs. Five trained mongrel dogs breathed from a mask as the inspired gas was alternated between air and O2 for multiple cycles, and continuous time series records of HR and oxyhemoglobin saturation were recorded on a digital computer and analyzed by the technique of ensemble averaging. Hyperoxia decreased HR by 9% (P < 0.001), but only gradually, requiring 5 min to reach steady state. This delay was much longer than the time required for hyperoxic respiratory depression (10-20 s), a response known to be mediated by chemoreceptor reflexes. The bradycardia was sustained for > or = 30 min. On return to normoxia, HR gradually returned toward, but failed to reach, the baseline HR, suggesting incomplete reversibility of the response. However, in control experiments without hyperoxic challenge, HR showed a slow continuous downward trend that was sufficient to account for the apparent incomplete reversibility of hyperoxic bradycardia. Hyperoxic bradycardia was unaffected by beta-adrenergic blockade but was completely prevented by muscarinic cholinergic blockade. We conclude that 1) hyperoxia-induced bradycardia in conscious dogs is mediated by efferents of the vagus nerve; 2) its afferent pathway remains unknown, but its long response time suggests mechanisms other than chemoreceptor reflexes or other known neural reflexes; and 3) it is completely reversible.
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PMID:Response time, autonomic mediation, and reversibility of hyperoxic bradycardia in conscious dogs. 809 6

The activity of peripheral chemoreceptors was studied in 19 preterm very low birthweight infants at the postconceptional age of 36 and 40 weeks using the hyperoxic test. The infants were in a healthy condition and did not receive any extra oxygen or medication when tested. The inhalation of pure oxygen caused a decrease in mean (SE) ventilation by 16.1 (2.6)% and 15.1 (2.1)% at the 36th and 40th gestational week respectively. At the 36th gestational week the ventilatory response was significantly slower than at 40 weeks (10.9 (6) and 7.3 (3) sec). Six infants who had been on supplemental oxygen for more than 21 days (from 21 to 56 days) responded with significantly lower response to hyperoxia at the 36th gestational week (-7.9 (3.6)%) than those receiving oxygen treatment for a shorter period of time, 0 to 16 days (-19.9 (3.2)%). The 'low responding' group included three infants who had suffered from chronic lung disease. Those infants showed the lowest hyperoxic response (-4.3 (3.9)%). There was no difference in the response among healthy preterm infants (eight infants) and infants with respiratory distress syndrome. At the 40th gestational week the differences, even though showing the same characteristics, were not statistically significant. No statistically significant relationship was found between the strength of the ventilatory response to oxygen versus gestational, postnatal age, nor the time interval between the termination of supplemental oxygen treatment and the test. No relationship was found between the number of apnoeic/bradycardic spells and the strength of the ventilatory depression caused by hyperoxia. In conclusion we found that the very preterm infants, with the exception of those who received long periods of oxygen treatment, have stronger peripheral chemoreceptor responses than those reported for 2-4 day old full term infants. However, infants who had suffered from chronic lung disease show a depressed hyperoxic response.
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PMID:Hypoxic ventilatory defence in very preterm infants: attenuation after long term oxygen treatment. 815 20

The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia at end-tidal CO2 concentration (FETCO2) 6%, 8% and 10% applied for 1 min produced a significant depression in gastric tone and motility. Hypocapnia at 3% FETCO2 increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympathetic gastric efferent nerve activity but not vagal efferent nerve activity. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly attenuated the inhibitory gastric response to hypoxia. Similar attenuation of hypoxia-induced depression of gastric tone and motility was produced by bilateral gastric sympathectomy but not by vagotomy. In contrast, the inhibitory effect of severe hypercapnia and the facilitatory effect of hypocapnia upon gastric tone and motility were unaffected by arterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FETO2 had no effect on the gastric nerve activities, gastric tone or motility. It is concluded that in the rat hypoxia co-activates sympathetic and vagal efferent nerve activities to the stomach via an arterial chemoreceptor reflex, and that hypercapnia activates sympathetic gastric nerve activity via central chemoreceptors. Hypocapnia activates efferent vagal gastric nerve activity. All chemical stimuli except that of hyperoxia have a significant local effect on the gastric tone and motility.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats. 822 66

In anesthetized kittens (< 1 to 24 days old), the effects of GABAA receptor antagonism on phrenic, hypoglossal and cervical sympathetic discharges were examined by i.v. bicuculline infusions during hyperoxia and hypoxia. Administration of bicuculline during hyperoxia produced marked increases in the amplitudes of inspiratory nerve discharges. During hypoxic stimulation (10% O2), the amplitudes of inspiratory activities decreased towards or below those observed during hyperoxia; bicuculline reversed this depression and restored inspiratory discharges. Our results indicated that GABAA receptors were functional shortly after birth, acting to mediate influences shaping inspiratory activity during hyperoxic breathing and during conditions of increased chemical drive.
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PMID:Effects of GABAA receptor antagonism on inspiratory activities in kittens. 824 45

Flumazenil, a benzodiazepine antagonist, clearly reverses midazolam-induced sedation; reversal of ventilatory depression has not been as well demonstrated. Thirty-two subjects completed this randomized, double-blind, placebo-controlled study investigating the dose-response relationship and duration of flumazenil's effects on ventilatory depression and hypnosis induced by a continuous midazolam infusion. A computer-controlled infusion of midazolam was used to titrate the predicted midazolam plasma concentration to a level at which subjects were unresponsive to verbal commands and then to maintain that concentration. Measurements of ventilation and hypnosis were repeated at predetermined intervals: before midazolam administration, before test drug (flumazenil [1, 3, or 10 mg] or placebo), and 5, 30, 60, 120, and 180 min after test drug administration. Ventilation and tidal volume were measured during an isocapnic hyperoxia clamp at a PETCO2 of 46 mm Hg (VE46 and VT46, respectively). A pseudo-rebreathing technique was used to measure the hypercapnic ventilatory response (HCVR) slope and ventilation intercept at a PETCO2 of 58 mm Hg (VE58). Midazolam reduced VE46, VT46, and VE58, as well as hypnosis scores, in all test drug groups. The reduction in HCVR slope, however, was significant only when all 32 subjects were considered in aggregate. All three doses of flumazenil reversed hypnosis and also reversed the reduction in VE46 and VT46 within 5 min. The reduction in VE58, however, was reversed less consistently. Flumazenil's effect on VE46 and VT46 lasted at least 30 min after 1 mg and at least 60 min after 3 mg, paralleling the effect of these doses on hypnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of large-dose flumazenil on midazolam-induced ventilatory depression. 825 Mar 14

In animals with intact peripheral chemosensory afferents, hypoxia differentially affects upper airway (UA) and chest wall muscles. To determine the contribution of brain stem (BS) hypoxia to the response of UA and chest wall muscles during early life, we perfused the BS through a vertebral artery intermittently with blood from an extracorporeal circuit in nine newborn piglets (age 1-5 days). BS perfusions were performed with hypoxemic blood (arterial PO2 32 +/- 6 to 38 +/- 8 Torr) with different levels of BS PCO2 (28 +/- 2, 37 +/- 4, and 56 +/- 5 Torr) while systemic normocapnic hyperoxia was maintained (arterial PCO2 36 +/- 3 to 40 +/- 6 Torr, arterial PO2 345 +/- 73 to 392 +/- 37 Torr). Electromyograms (EMGs) of alae nasi (AN), external intercostal (EI), and diaphragm (DIA) were recorded. Normocapnic hypoxia of the BS induced a sustained increase in AN EMG (P < 0.01, analysis of variance) and depression of EI and DIA EMGs without a transient increase. These contrasting responses were also observed during hypocapnic and hypercapnic hypoxia of the BS and were not affected by inputs from the peripheral chemoreceptors or rostral cerebral structures that were not exposed to hypoxia. We conclude that, despite eliciting the known central respiratory depression, BS hypoxia causes an increase in the respiratory drive to an UA airway muscle. Thus, BS hypoxia elicits a selective rather than a generalized respiratory muscle depression. The respiratory muscles with high energy expenditure (DIA and EI) are depressed while UA muscles are stimulated or disinhibited. This response is independent of the level of BS arterial PCO2.
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PMID:Response of upper airway and chest wall muscles to selective brain stem hypoxia in the newborn. 833 79

The effects of neocortical spreading depression (SD) on the expression of immunoreactive c-fos protein were examined within the superficial laminae of trigeminal nucleus caudalis (TNC), a brainstem region processing nociceptive information. KCl was microinjected into the left parietal cortex at 9 min intervals over 1 hr, and SD was detected by a shift in interstitial DC potential within adjacent frontal cortex. The stained cells in lower brainstem and upper cervical spinal cord were counted on both sides after tissues were sectioned (50 microns) and processed for c-fos protein-like immunoreactivity (LI) using a rabbit polyclonal antiserum. C-fos protein-LI was visualized in the ventrolateral TNC, chiefly in laminae I and Ilo and predominantly within spinal segment C1-2 (e.g., -1.5 to -4.5 mm from obex) ipsilaterally. SD significantly increased cell staining within ipsilateral TNC. The ratio of cells in laminae I and Ilo on the left: right sides was 1.32 +/- 0.13 after 1 M KCl, as compared to 1.06 +/- 0.05 in control animals receiving 1 M NaCl instead of KCl microinjections (p < 0.01). The ratio was reduced to an insignificant difference after chronic surgical transection of meningeal afferents and recurrent SD (1.09 +/- 0.11). Pretreatment with intravenous sumatriptan, a 5-HT1-like receptor agonist that selectively blocks meningeal C-fibers and attenuates c-fos protein-LI within TNC after noxious meningeal stimulation, also reduced the ratio to an insignificant difference (1.10 +/- 0.09). Sumatriptan or chronic surgical transection of meningeal afferents, however, did not reduce the ability of KCl microinjections to induce SD. On the other hand, combined hyperoxia and hypercapnia not only reduced the number of evoked SDs from 6.3 +/- 1.0 to 2.5 +/- 1.2 after 0.15 M KCl microinjection, but also significantly (p < 0.01) reduced associated c-fos protein-LI in TNC. These data indicate that multiple neocortical SDs activate cells within TNC. The increase in c-fos protein-LI, observed predominantly ipsilaterally, was probably mediated by SD-induced stimulation of ipsilaterally projecting unmyelinated C-fibers innervating the meninges. If true, this is the first report demonstrating that neurophysiological events within cerebral cortex can activate brainstem regions involved in the processing of nociceptive information via trigeminovascular mechanisms.
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PMID:Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. 838 35

1. We investigated how a continuous infusion of dopamine (DA; 5 micrograms/kg per min), which is often used clinically, would affect the ventilation and carotid chemoreceptor neural activity in anaesthetized cats. 2. In anaesthetized, spontaneously breathing cats, tidal volume (VT) and respiratory frequency (f) were continuously monitored at five levels of inspired oxygen (PIO2 = 110, 130, 150, 170, 760 mmHg) during Da or saline infusion. VT and f were sampled for 1 min after 3 min exposure to each level of PIO2. Time control study was also performed. 3. DA infusion significantly lowered VT under both normoxia and hypoxia in seven of eight cats. Respiratory frequency was not affected by DA infusion. Depression of ventilation during post-hypoxic hyperoxia was augmented by DA infusion. Chemodenervation abolished the ventilatory response to hypoxia and DA did not further affect the ventilatory response to hypoxia. 4. In a second group of artificially ventilated cats, carotid chemoreceptor neural activity was recorded at five levels of arterial oxygen tension. DA infusion significantly depressed carotid chemoreceptor neural activity during normoxia and hypoxia in six of seven cats. 5. These findings suggest that changes in ventilation during low dosage of DA infusion closely correlate with carotid body neural output. A predominant effect of this dosage of DA (5 micrograms/kg per min) was depression in the ventilatory response to hypoxia due to an inhibition of carotid body neural output.
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PMID:Effects of a continuous infusion of dopamine on the ventilatory and carotid body responses to hypoxia in cats. 854 81

Effects of prolonged action of low-pressure oxygen (0.3 MPa, 5h) on the free-radical oxidation (FRO) intensity were investigated just after oxygen exposure and 1, 3, 7, days after that. The FRO increase against the background of the anti-radical systems depression was shown by means of blood plasma chemiluminescent analysis. Under these conditions SOD activity and the content of diene conjugates and Schiff's bases increase in erythrocyte membranes. The displacement of equilibrium between pro- and antioxidants and antioxidants contents towards the latter took place in blood plasma on the 1st day after oxygen exposure. The erythrocyte SOD activity was raised while catalase activity was diminished. The last one was accompanied with the decrease in erythrocyte membrane diene conjugates amount. The secondary blood plasma and erythrocyte membrane FRO elevation was observed on the 3rd day after the exposure and, it was held on the 7th day after hyperoxia. The FRO increase in post-hyperoxia period was established.
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PMID:[Free radical processes in the rat blood during hyperbaric oxygenation and in the posthyperoxic period]. 875 11

Exposure to hypoxia (10% O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (> 97% O2). These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 microM to 30 microM) infused during a 45-second period in an isolated, buffer-perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (> 97% O2 for 48 hours), (2) hypoxia (10% O2 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.
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PMID:Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism. 907 31


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