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)

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48

Inhalation of the equimolecular mixture N2O - O2 rapidly achieves good analgesia in cases of coronary occlusion. This mixture was used with 51 patients (37 to 85 years old) with beneficial results on pain in 4 cases out of 5. This effect can be improved by giving a small amount of pethidine with the inhalation. In this way the respiratory depression of the full dose of narcotic analgesics is avoided. In halation of the mixture does not produce undesirable cardio-circulatory or respiratory changes. The oxygen content of the mixture increases patients' PaO2 without the risk of hyperoxia.
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PMID:[Nitrous oxide analgesia in myocardial infarction (author's transl)]. 60 76

Dopamine is present in the carotid body and has been postulated to be an inhibitory neurotransmitter. The purpose of this study was to determine the effects of dopamine on ventilation in man and to examine its mechanism of action. Dopamine (0.5-10 mug/kg per min) was infused in eight normal men at different levels of arterial chemoreceptor activity, produced by varying the inspired Po(2). During normoxia dopamine produced a small decrease in minute ventilation (Ve) and an increase in arterial Pco(2). When arterial chemoreceptors were stimulated by hypoxia, infusion of dopamine produced a marked initial depression of Ve followed by a sustained although less pronounced decrease in Ve. An increase in Pa(co) (2) and a decrease in Pao(2) were also observed. When arterial chemoreceptor activity was suppressed by hyperoxia, infusion of dopamine did not affect ventilation. Subjects also breathed a hypercarbic, hyperoxic gas mixture. The hypercarbia produces hyperventilation by stimulating central chemoreceptors, whereas the hyperoxia suppresses peripheral chemoreceptors. Dopamine did not alter ventilation while the subjects were breathing this gas mixture. These studies suggest that dopamine suppresses ventilation in man through an action on the arterial chemoreceptor reflex. These findings support the hypothesis that dopamine is an inhibitory neurotransmitter in the carotid body, and that release of dopamine may modulate the sensitivity of peripheral arterial chemoreceptors.
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PMID:Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex. 64 Nov 49

Rats (200-260 g) were exposed in sealed, recycling chambers continuously for 2-30 days to gas mixtures designed to maintain the same alveolar PO2 in the presence or absence of inert gas. Mixtures with inert gas (N2, He, or Ne) were at ground level; those without inert gas (100 percent O2) were in an altitude chamber. The O2 categories were: I-100 percent O2 at 747 torr; II-74 percent O2 + 26 percent inert and 566 torr 100 percent O2; III-47 percent O2 + 53 percent inert and 381 torr 100 percent O2; IV-21 percent O2 + 79 percent inert and 197 torr 100 percent O2. One of the two room-air controls was "restricted-fed" to the level of the lowest intake group. Measurements included body, pituitary, and thyroid weight, food and water intake, plasma volume and hematocrit, pituitary and plasma TSH, and plasma PBI. Severe depression in all variables and over 50 percent mortality was seen in I by day 4. All variables were depressed in II, but there was no mortality to 20 days. Pituitary-thyroid function appeared to be particularly sensitive to depression by hyperoxia, with plasma TSH levels reduced between 42 and 60 percent in II and III. No effect was attributable to the inert gas, whether it was N2, He, or Ne, nor was any specific effect traceable to the presence or absence of inert gas.
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PMID:Pituitary-thyroid function of rats in hypobaric oxygen-inert gas environments. 80 43

The effect of oxygen (O2) exposure on the ability of the isolated, perfused rat lung to clear serotonin (5-hydroxytryptamine, 5-HT) from the perfusate was evaluated in normal or vitamin E-deficient Sprague-Dawley rats. Rats were exposed to 100% O2 at 1 ATA for 4-48 h. Lungs were subsequently isolated, artificially ventilated, and perfused in a recirculating system with Krebs-Ringer bicarbonate solution, pH 7.4 containing 3% bovine serum albumin and 0.25 muM [14C] 5-HT. 5HT clearance was calculated from the disappearance rate of [ 14C] 5-HT from the perfusate. In normal rats exposed to 100% O2, there was a progressive reduction in the clearance of 5-HT with increasing duration of O2 exposure. Compared to lungs from air-exposed controls, clearance was depressed 20% (P less than 0.01) after 18 h, 22% (P less than 0.01) after 24 h, and 35% (P less than 0.001) after 48 h. With vitamin E-deficient rats, the reduction in 5-HT clearance occurred after a shorter exposure time and was of greater magnitude than in rats on a normal diet. Depression of 5HT clearance by the lungs is an early alteration of lung function fue to hyperoxia and is potentiated by vitamin E deficiency. The most likely mechanism for the depression of 5-HT clearance is interference with the transport properties of lung endothelium.
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PMID:Depression of serotonin clearance by rat lungs during oxygen exposure. 83 74

Clearance of 5-hydroxytryptamine (5-HT) by the lungs of normal and vitamin E-deficient rats was evaluated following a 60-min exposure to 100% oxygen (O2) at 4 ATA (HBO). After exposure, lungs were isolated, ventilated, and perfused, with a recirculating system used for measurement of 5-HT clearance. Control lungs were obtained from rats exposed to air at 1 ATA. In control normal rats, fractional clearance of 5-HT was 0.78+/-0.03 (mean+/-SE). Following HBO 5-HT clearance was 0.55+/-0.04 (P less than 0.01). In control vitamin E-deficient rats. 5-HT clearance was 0.85+/-0.05 and was decreased to 0.46+/-0.03 (P less than 0.001) following HBO. To evaluate the effect of recovery time after HBO on 5-HT clearance, separate groups of rats were killed at varying intervals post-HBO. In normal rats, 5-HT clearance had returned to control levels by 3-4 after HBO; in vitamin E-deficient rats, clearance remained unchanged 4 h after HBO and was only 74% (P less than 0.001) of control values 24 h post-HBO. These results indicate that depression of pulmonary 5-HT clearance occurs in rats due to hyperoxia and is potentiated by vitamin E deficiency. This represents a reversible alteration of lung function which requires vitamin E for complete recovery.
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PMID:Effect of hyperbaric oxygen exposure on pulmonary clearance of 5-hydroxytryptamine. 89 79

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1-5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P'CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P'CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4-7). HVR was independent of test SaO2 (range 60-90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented hypoxic ventilatory response in men at altitude. 150 56

The influence of aging on the ventilatory response to hypoxia was studied in the halothane-anesthetized male Wistar rats of various ages (1.5-20 months). The magnitude of increase in ventilation (normalized for body weight) during hypoxia in isocapnic conditions was attenuated in parallel with advancing age. However, ventilation in hyperoxia, normoxia or mild hypoxia did not differ among various age groups when the ventilatory volume was normalized for O2 consumption. Furthermore, threshold end-tidal PO2 for ventilatory depression in deeper hypoxia became progressively lower with advancing age. The results suggest that the age change in ventilatory response to hypoxia depends largely upon the progressive reduction in basal O2 requirement (consumption) with age.
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PMID:Changes in ventilatory response to hypoxia in the rat during growth and aging. 152 17

A new in vivo model for studying brain metabolic and haemodynamic oscillatory phenomena during ischaemia is described. In this model acute or chronic occlusion of one or two carotid arteries in the rat is performed. Due to the partial ischaemia developed, oscillations in the level of intramitochondrial pyridine nucleotides (NADH) as well as flavoproteins (Fp) were recorded from the brain by monitoring the fluorescence of these respiratory chain components. The two fluorescent signals (NADH and Fp) were measured by using the time sharing or DC fluorometer/reflectometer. The changes in the reflected light at the excitation wavelengths (366 and 450 nm) were recorded simultaneously. Bilateral carotid artery occlusion induced immediate oscillations (6-9 waves per min) in the mitochondrial redox state as well as in tissue blood volume in both hemispheres. To verify the accuracy of the NADH monitoring system, including the correction technique for haemodynamic and other artifacts, we used the intracarotid artery saline bolus injection approach. The results could be summarized as follows: (1) unilateral carotid artery occlusion resulted in delayed development of oscillations, particularly in the ipsilateral hemisphere; (2) the oscillation phenomenon was reversible if recirculation restarted within 5 min. Occlusion for more than 30 min resulted in irreversible oscillations; (3) the oscillation appearances and intensities were affected by various physiological conditions. Vasoconstriction, induced by hyperoxia, stimulated the oscillations while vasodilation, induced by hypercapnia, depressed them. Anoxia, hypoxia and spreading depression (SD) abolished the oscillations. Glucose injection was not effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oscillations of cortical oxidative metabolism and microcirculation in the ischaemic brain. 167 46

The ventilatory stimulating effects of hypoxia occurring at carotid bodies are potentiated by exercise. However, hypoxia also has central ventilatory depressive effects; the potential interactions between this hypoxic depression and exercise have not been studied. We examined the ventilatory response to a 20 min period of isocapnic hypoxia (end-tidal O2, PETO2, of 50 mm Hg), preceded and followed by a 5 min period of isocapnic hyperoxia in seven normal adult males at rest and during moderate exercise (45-75 W). When hypoxia was introduced at rest (PETO2 = 42 mmHg), ventilation initially increased from 13.73 +/- 3.04 (mean +/- SD) to 23.69 +/- 5.48 1.min-1 and then slowly declined to 19.01 +/- 4.68 1 min-1. The increase was caused by increases in tidal volume and respiratory frequency, but the decline was solely in tidal volume. During a background of moderate exercise (PETCO2 = 46 mmHg), introduction of hypoxia caused ventilation to increase from 30.84 +/- 6.31 to 56.44 +/- 10.58 1.min-1. Ventilation subsequently did not decline; at the end of the hypoxic period, ventilation was 57.06 +/- 12.59 1.min-1. The increase was also associated with an increase in tidal volume and respiratory frequency, as seen as rest, but with much larger magnitudes. Despite the absence of ventilatory decline, there was still a decline in tidal volume, but it was compensated by an increase in respiratory frequency. We conclude that exercise potentiated the acute ventilatory response to hypoxia by modifying both tidal volume and respiratory frequency but that exercise abolished or greatly reduced hypoxic decline by increasing respiratory rate.
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PMID:Ventilatory response to sustained hypoxia during exercise. 188 80


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