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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Local brain tissue oxygen tension, temperature, and electrical potential were continuously and simultaneously measured at each of two different depths in anesthetized, paralyzed rat brain. Brain tissue temperature increases up to 1 degree C were recorded in response to direct electrical stimulation, spreading depression, PTZ-induced seizures, hypercapnia, and hypoxia. An increase in brain tissue temperature was also recorded during reoxygenation after hypoxia. Thus, we have shown that, in this preparation, increases in either blood flow or oxidative metabolism lead to transient warming of the brain.
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PMID:Brain tissue temperature: activation-induced changes determined with a new multisensor probe. 336 63

Auditory brainstem responses (ABRs) were studied in a child with congenital central alveolar hypoventilation showing marked depression of respiratory drive during sleep. During wakefulness and normoventilation no ABR abnormalities were found, either at the age of 14 months or five years. ABR recordings during sleep at 14 months of age showed marked wave V latency and wave I to wave V interpeak latency prolongation of about 0.4 ms both for periods of hypoventilation and normoxic hypercapnia. ABR findings of this and other studies carried out in sleep apneas are discussed with respect to brainstem dysfunction associated with varied sleep apnea syndromes.
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PMID:Auditory brainstem response (ABR) in congenital central alveolar hypoventilation. 356 8

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.
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PMID:Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease. 356 37

We have analyzed a variety of approaches in assessing fetal breathing parameters (VT, TI, Ttot, VT/TI, VI) in eight fetal sheep during a control period and during stimulation with 6 and 9% CO2. By using conventional analysis of data blocks varying from 100 to 1500 breaths, several different conclusions could be reached regarding the respiratory response to hypercapnia: stimulation, depression, or no change in all parameters studied. A new analysis based on piecewise linear regression used as a data grouping technique indicated that a simple mean +/- SD of the individual parameters was an inappropriate description of normal or stimulated fetal breathing. Based on tests for homogeneity of regressions of VT on TI for a completely random design, it is concluded that an estimate of fetal respiratory drive is only described adequately by two to four regression regimes. These regimes, estimated from the regression technique, could be combined to give a weighted mean value based on the proportion of time they were present. Using this new approach and an analysis of variance, we found (i) that frequency and VI were similar between animals during control and hypercapnia, (ii) that breathing frequency decreased during hypercapnia, and (iii) a positive relationship between VT and TI.
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PMID:A novel analysis of fetal breathing. 356 33

A thermal clearance technique for measuring cerebral blood flow is described and compared with the radiolabelled microsphere technique. The thermal technique involves measurement of the rewarming curve generated after bolus infusion of 4-5 ml of ice-cold saline into the common carotid artery with a subdural thermistor placed on the parietal cortex. Evaluation of the biexponential decay curves obtained with this technique demonstrated a close correlation with total hemispheric, parietal, and parietal gray blood flow determined by simultaneous microsphere measurement. Despite significant correlations (p less than 0.001), scatter in the data produced a broad 95% confidence interval, thus making interpretation of blood flow with the thermal clearance technique impossible. Furthermore, instrumentation with the thermal probe, which required opening of the dura, blunted the cerebral blood flow response to hypercapnia. We conclude that the major limitations of the thermal clearance technique include: nonhomogeneous clearance function, significant variability, and depression of CO2 reactivity. These limitations must be addressed before this technique can be used reliably in the laboratory.
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PMID:Comparison of thermal clearance measurement of regional cerebral blood flow with radiolabelled microspheres. 359 Feb 53

Previous studies have shown that the arousal threshold to hypoxia, hypercapnia, and tracheal occlusions is greatly depressed in rapid-eye-movement (REM) sleep compared with slow-wave sleep (SWS). The aim of this study was to compare the arousal thresholds in SWS and REM sleep in response to an upper airway pressure stimulus. We compared the waking responses to tracheal (T) vs. nasal (N) occlusion in four unanesthetized, naturally sleeping dogs. The dogs either breathed through a tracheal fistula or through the snout using a fiberglass mask. A total of 295 T and 160 N occlusion tests were performed in SWS and REM sleep. The mean time to arousal during N and T tests was variable in the same dog and among the dogs. The mean time to arousal in SWS-tracheal occlusion was longer than that in N tests in only two of the four dogs. The total number of tests inducing arousal within the first 15 s of SWS-nasal occlusion tests was significantly more than that of T tests (N: 47%; T: 27%). There was a marked depression of arousal within the initial 15 s of REM sleep in T tests compared with N tests (N: 21%; T: 0%). The frequency of early arousals in REM tests was less than that of SWS for both N and T tests. The early arousal in N occlusion is in sharp contrast to the well-described depressed arousal responses to hypoxia, hypercapnia, and asphyxia. This pattern of arousal suggests that the upper airway mechanoreceptors may play an important role in the induction of an early arousal from nasal occlusion.
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PMID:Arousal responses to airway occlusion in sleeping dogs: comparison of nasal and tracheal occlusions. 359 57

To investigate the effect of intravenous dopamine on the chemical regulation of ventilation, we studied the ventilatory responses to hypercapnic hypoxia during dopamine infusion. Intravenous dopamine (3 micrograms X kg-1 X min-1) was administered to six healthy human subjects. Two hypoxic challenges (PETO2 = 52.5 +/- 2.5 mm Hg, SaO2 = 88.8 +/- 2.2%; mean +/- SD) were administered at three CO2 levels (PETCO2 = 40.8 +/- 0.5, 45.6 +/- 0.2, 49.8 +/- 0.3 mm Hg) to each subject. The ventilatory responses were quantified by calculation of slopes and intercepts of the relationship between minute exhaled ventilation (VE) and arterial hemoglobin saturation (SaO2), and by the relationship between this slope (delta VE/delta SaO2) and carbon dioxide tension. Dopamine caused a 77% reduction in delta VE/delta SaO2 (hypoxic sensitivity) during eucapnia, a 39.5% reduction in hypoxic sensitivity at PETCO2 = 46 mm Hg, and 38% reduction at PETCO2 = 50 mm Hg (P less than 0.05). Dopamine also reduced normoxic ventilation at all carbon dioxide levels. There was a greater depression in VE during hypercapnia (25.7% reduction) than during eucapnia (12% reduction). This indicates that dopamine depresses the normoxic ventilatory response to carbon dioxide. Intravenous dopamine reduces the ventilatory response to both hypoxia and hypercapnia but preserves the augmentation of hypoxic ventilatory drive by hypercapnia.
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PMID:Effect of dopamine on hypoxic-hypercapnic interaction in humans. 360 70

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low flow oxygen therapy dramatically improved the apnoea score, probably by relieving hypoxic brain depression. Slow waves also disappeared with oxygen therapy. Aminophylline was effective on apnoea score and duration (p less than 0.001). This beneficial effect could be explained by an improvement of the normal oscillations of respiration at the onset of sleep, a change in arousability or a stimulation of the ascending reticular system. These findings suggest a possible role of hypoxic depression in the manifestations of central sleep apnoeas and demonstrate the beneficial effect of low flow oxygen and aminophylline in treating certain central sleep apnoeas.
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PMID:Effect of aminophylline and relief from hypoxia on central sleep apnoea due to medullary damage. 360 31

Our purpose was to examine the influence of steady-state changes in chemical stimuli, as well as discrete peripheral chemoreceptor stimulation, on abdominal expiratory motor activity. In decerebrate, paralyzed, vagotomized, and ventilated cats that had bilateral pneumothoraces, we recorded efferent activity from a phrenic nerve and from an abdominal nerve (cranial iliohypogastric nerve, L1). All cats showed phasic expiratory abdominal nerve discharge at normocapnia [end-tidal PCO2 38 +/- 2 Torr], but small doses (2-6 mg/kg) of pentobarbital sodium markedly depressed this activity. Hyperoxic hypercapnia consistently enhanced abdominal expiratory activity and shortened the burst duration. Isocapnic hypoxia caused inhibition of abdominal nerve discharge in 11 of 13 cats. Carotid sinus nerve denervation (3 cats) exacerbated the hypoxic depression of abdominal nerve activity and depressed phrenic motor output. Stimulation of peripheral chemoreceptors with NaCN increased abdominal nerve discharge in 7 of 10 cats, although 2 cats exhibited marked inhibition. Four cats with intact neuraxis, but anesthetized with ketamine, yielded qualitatively similar results. We conclude that when cats are subjected to steady-state chemical stimuli in isolation (no interference from proprioceptive inputs), hypercapnia potentiates, but hypoxia attenuates, abdominal expiratory nerve activity. Mechanisms to explain the selective inhibition of expiratory motor activity by hypoxia are proposed, and physiological implications are discussed.
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PMID:Hypoxia inhibits abdominal expiratory nerve activity. 362 26

Sedative drugs have been found to depress the respiratory activity of upper airway muscles more than that of the diaphragm. To determine whether CO2 at narcotic levels has a similar action, we recorded phrenic and hypoglossal nerve activities in decerebrate, vagotomized, paralyzed cats. T5 or T6 external intercostal nerve activity was also recorded in some animals. End-tidal CO2 concentration was raised progressively to over 30% or until depression of nerve activity was apparent. Respiratory frequency was reduced by severe hypercapnia in most cats. Hypoglossal nerve activity was consistently decreased more than that of the phrenic nerve. In most cases intercostal nerve activity was also more susceptible than phrenic nerve activity to hypercapnic depression. The results indicate that CO2 at narcotic levels interferes both with the central pattern generator for breathing movements and with the expression of the pattern in specific motor nerves.
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PMID:Influence of extreme hypercapnia on respiratory motor nerve activity in cats. 367 97


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