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

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.
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PMID:Hypoxia and carbon dioxide as separate and interactive depressants of ventilation. 101 31

Buprenorphine was studied to determine the respiratory depressant effect in a double blind comparison with morphine. Buprenorphine produced a more prolonged displacement of the carbon dioxide response curve than morphine. Because of the marked difference in the time effect curves the relative potency was determined at the time of peak effect--3 hours post-administration for buprenorphine (0.15 and 0.3 mg) and 1 hour post administration for morphine (5 and 10 mg). The data from the subjects who received higher doses of buprenorphine (0.6 and 1.2 mg) showed that there was a linear relationship over the dose range 0.15-1.2 mg in terms of respiratory depression.
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PMID:A double blind comparison of buprenorphine and morphine in conscious subjects following administration by the intramuscular route. 103 70

The inverse relationship between blood lead concentration and aminolevulinic acid dehydrase (ALAD) is well known. Recently, it has been suggested that a similar relationship exists between carboxyhemoglobin (COHb) and ALAD activity. This study was undertaken to examine more closely the possible effect of carbon monoxide on ALAD. Blood from 19 human volunteers was analyzed for both carboxyhemoglobin and ALAD activity. Smokers had significantly lower concentrations of ALAD than nonsmokers and a rise in carboxyhemoglobin concentration was assocaited with a fall in ALAD activity. The in vitro bubbling of carbon monoxide into human blood did not significantly effect ALAD activity. Four groups of rats (10 per group) wre exposed to carbon monoxide or dietary lead acetate according to the following design: (I) Control--no Pb or CO; (II) 500 ppm Pb acetate in diet; (III) 250 ppm CO four hours/day X 5 days/week X 4 weeks; (IV) Both Pb and CO. Analysis of the rat data showed a significant depression of ALAD by lead. The activity of ALAD in the rats exposed to CO was significantly increased suggesting the possibility of an adaptive phenomenon.
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PMID:Experiments on the effect of carbon monoxide on aminolevulinic acid dehydrase (ALAD). 103 10

The effect on respiration of diazepam, haloperidol and chloropromazine in patients with chronic airways obstruction was studied on ten patients by the modified rebreathing method of ventilatory response to carbon-dioxide. The two parameters of the ventilatory response studied were: (a) the slope expressed as litres/minute/mmHg CO2 and (b) minute ventilation at a computed pCO2 57 mmHg (VE 57). A significant decrease in either of these parameters indicated respiratory depression. Following administration of 10 mg diazepam intramuscularly to ten patients a significant depression of respiration was observed in five patients. Administration of 50 mg chloropromazine intramuscularly to eight patients significantly depressed respiration of three patients. A significant depression of respiration was not observed in any of the ten patients given 5 mg haloperidol intramuscularly. These results indicate that the lack of significant respiratory depression from an intramuscular injection of 5 mg of haloperidol to patients with severe chronic airways obstruction makes it a safer drug, for the management of acute psychotic episodes in such patients, than 50 mg of chloropromazine or 10 mg of diazepam given intramuscularly.
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PMID:Effect on respiration of diazepam, chloropromazine and haloperidol in patients with chronic airways obstruction. 107 41

Respiratory depression induced by tilidine was compared with that of morphine in a crossover study in 6 healthy subjects. Increments of tilidine, 150 mg/70 kg, and morphine, 10 mg/70 kg, were given intravenously and displacement of each subject's CO2 response curve was measured after each dose increment. Both tilidine and morphine caused dose-related displacement of the CO2 response curves to the right. Approximately 80 to 120 mg of tilidine can be expected to induce the respiratory depression of morphine, 10 mg, when given intravenously. Subjective effects after tilidine were qualitatively similar to those of morphine but were of longer duration with nausea and vomiting more frequent. The respiratory depression of both drugs was effectively antagonized by naloxone.
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PMID:Comparative respiratory depression of tillidine and morphine. 109 12

The effect of breathing 100 ppm of carbon monoxide versus compressed, purified air for 1 h on maximal treadmill exericse was studied (double-blind crossover design) in 10 middle-aged, healthy nonsmokers. The mean venous carboxyhemoglobin level significantly increased from 1.67% to 3.95% after breathing carbon monoxide (P less than 0.001) and significantly decreased from 1.63% to 1.30% after breathing compressed, purified air (P less than 0.001). The mean exercise time until exhaustion significantly decreased from 697.7 to 662.7 s after breathing carbon monoxide (P less than 0.001) and insignificantly increased from 694.9 s to 703.4 s after breathing compressed, purified air. Ischemic S-T segment depression larger than or equal to 1.0 mm after exercise occurred in 1 of 10 subjects after exercise following carbon monoxide inhalation. Increased carboxyhemoglobin levels of the magnitude encountered after smoking or heavy atmospheric pollution impair exercise performance in normal persons.
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PMID:Effect of carbon monoxide on maximal treadmill exercise. A study in normal persons. 110 62

A double-blind trial has been performed to investigate the respiratory effects of low oral doses of benzoctamine, and to compare them with diazepam and a placebo. The displacement of the carbon dioxide response curves indicated that whilst diazepam caused respiratory depression, benzoctamine had a variable effect. Some volunteers showed depression, but most showed stimulation. Peak respiratory effects were seen 1 hr after oral administration, returning to normal 2-3 hr after administration. It is suggested that oral drugs given for premedication need to be administered at least 2 hr before operation to obtain maximum sedative effects at a time when respiratory effects are returning to normal. In animal experiments it has been shown that the analgesic actions of morphine are diminished by concurrent administration of benzoctamine, and that the depression of respiratory rate caused by morphine is enhanced.
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PMID:Benzoctamine-a study of the respiratory effects of oral doses in human volunteers and interactions with morphine in mice. 110 19

It is well known that hypoxia, acting mainly through peripheral chemoreceptors, is an important ventilatory stimulus. It is also known that under certain circumstances hypoxia can lead to ventilatory depression, perhaps through its effect on the central nervous system. This study, utilizing dogs, was carried out to determine the degree of hypoxia required to produce ventilatory depression and to study the effects of chloralose anesthesia, variations in blood carbon dioxide tension, and peripheral chemoreceptor denervation on hypoxic ventilatory depression. In the awake, intact dog, ventilatory depression did not occur until the Pao2 = 18.6 plus or minus 0.8 mmHg (SEM). This value was not significantly different from that observed in chloralose anesthetized dogs, Pao2 = 18.7 plus or minus 0.43 mmHg. Hyper- and hypocapnia had no significant effect on the Pao2 at which ventilatory depression occurred. Denervation of either aortic or carotid chemoreceptors produced a very small change in the Pao2 of ventilatory depression, increasing it from 18.6 plus or minus 0.58 to 20.8 plus or minus 0.93 mmHg. Denervation of both aortic and carotid chemoreceptors produced a further small increase (Pao2 = 21.8 plus or minus 0.76 mm Hg). In peripheral chemoreceptor-denervated animals, hypoxia produced no significant change in ventilation until the ventilatory depression point was reached. These studies indicate that in the dog hypoxic ventilatory depression occurs only during severe hypoxia and ventilatory depression occurs only during severe hypoxia and is uninfluenced by chloralose anesthesia, hyper- or hypocapnia, and only slightly affected by chemoreceptor denervation.
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PMID:Hypoxic ventilatory depression in dogs. 111 Feb 30

Although chronic lithium therapy has been associated with a defect in the urinary concentrating mechanism, short-term renal effects of lithium have received little attention in the intact animal. Solute-free water reabsorption (T-cH2O) and free water clearance (CH2O) were measured in primates of the genus Galago under control conditions and while animals were receiving either 0.5 mmol/kg-h or 1.0 mmol/kg-h lithium chloride (135 mM) intravenously. CH2O was unchanged by lithium infusion (P greater than 0.10), whereas T-cH2O was significantly depressed at all levels of osmolal clearance (P smaller than 0.01). Spontaneous recovery of near-normal T-cH2O was documented in two animals within 1 wk following acute lithium infusion. In addition it was observed that lithium-induced depression of T-cH2O could be partially prevented by pretreatment with intravenous amiloride. These results suggest that alterations in the renal concentrating mechanism can occur rapidly following the onset of lithium administration. They also imply that impairment of the renal concentrating mechanism by lithium is due at least in part to antagonism of the action of vasopressin on the collecting duct.
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PMID:Acute effects of lithium on the renal concentrating mechanism in a primate. 111 55

The effects of 1.0 per cent end-tidal halothane-oxygen anesthesia on spontaneous ventilation, ventilatory deadspace, functional residual capacity (FRC), and alveolar-arterial oxygen difference (A-aD-O-2) were measured in patients with chronic obstructive pulmonary disease and in normal patients of similar age. results obtained were compared with values obtained preoperatively from the same patients. The following were measured: 1) ventilation and ventilatory deadspace, breathing room air and breathing 100 per cent oxygen; 2) functional residual capacity (FRC) and alveolar-arterial oxygen tension difference (A-aD-O-2); 3) forced expiratory volume in 1 second (FEV1.0); 4) ventilatory response to exogenous carbon dioxide. Findings indicated that ventilation is depressed more during halothane anesthesia in patients with emphysema than in normal patients and that the extent of depression is best related to a preoperative measurement of FEV1.0 (P less than 0.001, r = 0.86). The depression in alveolar ventilation results primarily from a reduction in tidal volume. A-aD-O-2 and ventilatory deadspace-to-tidal volume ratio are increaded and FRC decreased with anesthesia in patients with COPD, but the changes are no greater than those found in normal patients.
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PMID:Anesthetic effects on ventilation in patients with chronic obstructive pulmonary disease. 111 64


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