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

Caesarean sections were performed on 18 Romney ewes on day 144 of pregnancy. Anaesthesia was induced in 9 ewes with CT 1341 and in 9 ewes with thiopentone and maintained in both groups with halothane administered with oxygen. Surgery was performed with the ewes in lateral recumbency, with respiration unassisted. Blood samples were collected from the intact umbilical artery at the time of delivery and analysed for PO2, PCO2, pH (base deficit was derived). The intervals between ewe induction and lamb delivery (lD), delivery and the onset of breathing (TSR), and delivery and the lamb standing were recorded. Lambs in the CT 1341 group both breathed and stood sooner than lambs in the thiopentone group. Significant linear relationships were only found in the CT 1341 group between TSR interval and PCO2 and pH. No significant correlations were found between the lD interval and any of the biochemical characteristics. The results of this study suggest that lateral recumbency does not interfere with uteroplacental circulation, that CT 1341 (2.2 mg/kg) is associated with less neonatal depression than thiopentone (10 mg/kg) and that severe neonatal hypercarbia may delay the onset of respiration in lambs with minimal drug depression.
 ...
PMID:The effects of CT1341, thiopentone and induction- delivery time on the blood gas and acid-base status of lambs delivered by casesarean operation and on the onset of respiration. 58 79

Single-unit activity was monitored extracellularly from medullary respiratory neurons and nonspecified neurons of decerebrate cats which were paralyzed, vagotomized, and artificially ventilated. Hypercapnia consistently resulted in increased discharge frequencies and decreased modal interspike intervals for respiratory units; peak integrated phrenic discharge heights increased concomitantly. Although isocapnic hypoxia usually resulted in comparable changes, the firing frequency of some respiratory units was depressed. Moreover, this depression was frequently observed simultaneously with a hypoxia-induced increase in phrenic discharge. Nonrespiratory unit discharge was mainly unaltered by hypercapnia or hypoxia. Following bilateral carotid sinus nerve section, hypercapnia-induced increases in respiratory neuronal and phrenic activities were still obtained; hypoxia depressed these activities. It is concluded that central chemoreceptor afferent influences are ubiquitously distributed to the medullary respiratory complex whereas peripheral chemoreceptor afferents produce only a discrete and unequal excitation of respiratory units. Hypoxia-induced ventilatory changes are further concluded to be the net result of peripheral chemoreceptor excitation of respiratory units and a direct depression of the brain stem respiratory complex by hypoxia.
 ...
PMID:Response of medullary respiratory neurons to hypercapnia and isocapnic hypoxia. 59 74

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.
 ...
PMID:Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex. 64 Nov 49

The ventilatory responses mediated by the central and peripheral chemoreceptors were separately assessed in eight healthy volunteers before and after the oral ingestion of ethanol in a dose of 0.75 ml/kg. No significant depression of the central response was observed, but a significant depression of the peripheral response was observed at 25 and 95 minutes after the consumption of ethanol. The peripheral chemoreceptor stimulus was the simultaneous increase of hypoxia and hypercapnia and this novel method is described.
 ...
PMID:The effect of ethanol on the ventilatory responses mediated by the peripheral chemoreceptors in man. 65 90

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.
 ...
PMID:Excessive polycythemia of high altitude: role of ventilatory drive and lung disease. 70 89

Avian respiratory pacemaker activity is dependent on some form of peripheral input but it may be inhibited by both central and peripheral stimulation. At present the results of central nervous stimulation are difficult to interpret but, aside from cortical influences, diving apnea appears to be maintained, in the face of increasing chemoreceptor input, by noxious stimulation of the upper respiratory tract and depression of the output of medullary respiratory neurons by advancing hypercapnia. If this is so, an obvious problem for future research is what initiates the prompt onset of hyperpnea when the animal surfaces and breathes. It is known that post-dive hyperpnea is little affected by either carotid body or pulmonary denervation, so peripheral chemoreceptors are unlikely to play a major role in this response.
 ...
PMID:The control of breathing in birds with particular reference to the initiation and maintenance of diving apnea. 77 99

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
 ...
PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

In 5 normal subjects we measured ventilation and P0.1, the pressure generated by the first 0.1 sec of inspiratory effort against a closed airway, in response to hypercapnia and hypoxia with and without added inspiratory resistance before and after oral meperidine (1.1 to 1.3 mg per kg). CO2 responses were studied in the steady state, whereas progressive hypoxia was used to elicit hypoxic responses. In general, resistance decreased ventilatory responses to hypercapnia but increased P0.1 responses to both hypoxia and hypercapnia. Meperidine depressed both ventilatory and P0.1 responses, more so in hypoxia than in hypercapnia. The combination of resistance and merperidine was additive in depressing responses to hypercapnia but in hypoxia produced little more depression than did meperidine alone. In both hypercapnia and hypoxia, meperidine decreased the augmentation of P0.1 that was associated with increased resistance. Normal subjects responded to acute increases of inspiratory resistance by increasing inspiratory motor output; this increase was distinctly blunted by meperidine.
 ...
PMID:Effect of meperidine on occlusion pressure responses to hypercapnia and hypoxia with and without external inspiratory resistance. 97 24

The respiratory frequency, tidal volume and ventilization responses of 20 conscious cats to hypoxia, at controlled levels of alveolar CO2, revealed a characteristic steady state response in the majority of animals which indicated a negative interaction of stimuli on tidal volume and minute volume of ventilation, but a positive interaction on frequency. Another series of studies, conducted on seven conscious cats, sought to identify hypoxic response thresholds and depression thresholds, by determining responses over a wide range of hypoxic stimulus intensities, and at different controlled alveolar PCO2. Response threshold was at about 65 torr PAO2. Under eucapnic conditions, ventilation began to fail at PAO2 about 30 torr due to failure of tidal volume. The frequency continued to increase even in the lowest range of PAO2. With hypocapnia no failure of ventilation, frequency, or tidal volume was seen even at the lowest PAO2, but with hypercapnia, the tidal volume began to fail at PAO2 about 50 torr. The minute volume however, continued to increase into the lowest range of PAO2, because the frequency continued to respond at a rate greater than the tidal volume was failing. The results are discussed in terms of interactive depression manifest through the coupled responses of peripheral and central mechanisms.
 ...
PMID:Hypoxia and carbon dioxide as separate and interactive depressants of ventilation. 101 31

Although morphine depresses respiration the mechanism of this depression remains unknown. Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects. This procedure produced resting hypoventilation manifested as a peak rise in alveolar carbon dioxide tension from 42.9 plus or minus 1.7 to 45.4 plus or minus 1.5 mm Hg (plus or minus S.E.M.) at 30 minutes ( greater than 0.01). Hypoxic ventilatory drive, measured by an index of the relation between ventilation and hypoxia (parameter A), decreased from a control of 108 plus or minus 17.6 to 42.8 plus or minus 5.3 at 60 minutes after morphine (p greater than 0.01); Hypercapnic ventilatory drive, measured as the slope of the ventilatory response to hypercapnia, also decreased from 1.69 plus or minus 0.24 to 0;98 plus or minus 0.20 (p greater than 0.01) 75 minutes after morphine. Decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.
 ...
PMID:Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man. 112 55


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>