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)

The respiratory effect of di-methadone administered subcutaneously was examined in awake, unsedated female Labrador retrievers in which a chronic tracheostomy had been established. Respiratory depression was determined from the change in ventilatory response to carbon dioxide. Two methods for assessing the response were evaluated and compared, namely the classical steady-state and rebreathing techniques. Maximal methadone-induced respiratory depression after administration of 2 mg/kg of dl-methadone occurred by 1 hr as detected by both methods, but the magnitude of the response as detected by the steady-state technique was significantly greater. At 8 hr significant respiratory depression was still detectable by the steady-state but not by the rebreathing technique. At comparable serum drug levels, the rebreathing method consistently detected a smaller degree of drug-induced respiratory depression. Methadone administration produced a decrease in slope of the ventilation-response curve which was significant at 1 and 2 hr for both methods. Slopes of the response curves obtained at pretreatment control measurements were markedly different for the two techniques, being significantly greater for the rebreathing method. Serum dl-methadone concentration was measured by radioimmunoassay. The mean serum half-life of methadone was 4.7 hr. There was excellent correlation between the logarithm of serum drug concentration and drug-induced respiratory depression as measured by either technique.
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PMID:Methadone-induced respiratory depression in the dog: comparison of steady-state and rebreathing techniques and correlation with serum drug concentration. 70 33

Bartoli et al. (1974) found in dogs with constant PaCO2 that an increase in PCO2 in the vascularly isolated lungs increased ventilatory drive by a vagal reflex. We have examined the range of lung PCO2 over which the reflex operates. In anaesthetized dogs we ventilated the lungs separately with O2, maintaining gas exchange with the right lung. When we occluded the left pulmonary artery, left lung PCO2 fell to 2--4 mm Hg, and phrenic nerve firing decreased significantly. Phrenic activity increased again when left lung PCO2 was raised in steps to 19, 32 and finally to 50 mm Hg. PaCO2 was unchanged. Phrenic responses were abolished by cutting the left vagus nerve or by cooling it to 7--8 degrees C. The largest increase in phrenic activity occurred when left lung PCO2 was increased from 2 to 19 mm Hg, and the smallest when PCO2 was raised from 32 to 50 mm Hg. Hence the significance of the pulmonary-CO2 ventilatory reflex may lie in depression of ventilatory drive when pulmonary CO2 falls below normal, rather than in stimulation of breathing when pulmonary CO2 increases above normal.
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PMID:I. Pulmonary-CO2 ventilatory reflex in dogs: effective range of CO2 and results of vagal cooling. 70 74

The popularity of the motorcycle, specifically trail bike riding, in the past several years has produced an increasing incidence of severe "clothesline" injuries to the larynx and trachea. Even at moderately high speed the impact of a horizontal cable with the neck of the rider causes a sudden hyperextension of the neck, and an avulsion of the larynx from the trachea, separating at the relatively rigid fibrous connective tissue between the cricoid cartilage and the first tracheal ring. Interruption of the strap muscles, the recurrent laryngeal nerves, laceration of the esophagus, and compression fracture of the cervical vertebral bodies can occur. The unseated rider requires immediate assistance, airway obstruction being his greatest problem. In the early minutes after the accident he must be transported to an emergency facility where tracheostomy and resuscitation can be provided. Mediastinal infection, tracheoesophageal fistula, subglottic stenosis, and intermittent depression many follow the initial repair. Rehabilitative measures include permanent tracheostomy, the use of neuromuscular pedicle graft, hyoid bone graft, intracordal injection of teflon paste, and carbon dioxide laser excision of webs and cicatricial tissue.
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PMID:Laryngotracheal separation. 73 96

Acute oral and inhalation toxicity of dichloromethane was investigated in both male and female Sprague-Dawley rats. Oral LD50 was found to be 1.72 ml/kg for males and 1.06 ml/kg for females. LC50 was found to be 18 100 PPM (1 X 6 hours) for both male and female rats. Acute oral intoxication is characterized by severe vascular changes and depression of the central nervous system accompanied by gastro-intestinal hemorrhagy. A similar CNS depression is also found in acute intoxication by inhalation. The nature of the symptoms as well as the sequence of physiological (hypotension, hypothermia) and biochemical events observed (high COHb level, etc.) indicate that the combined action of dichloromethane and its metabolite, carbon monoxide, are responsible for the development of vascular and CNS disturbances and subsequently the sudden death of the animals.
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PMID:[Toxicological studies on dichloromethane, a solvent simulating carbon monoxide poisoning (author's transl)]. 74 72

In five volunteers the sensitivity of the respiratory centre to carbon dioxide after naloxone and nalorphine injections was studied using "double blind" method and increments of doses. Alterations in the respiratory centre sensitivity were reflected by changes in respiratory minute volume, which was measured before and after drug injections, as well as after carbon dioxide stimulation. Comparison of results and their statistical verification showed that nalorphine alone causes respiratory depression and carbon dioxide stimulation is, beside the weak initial action, almost ineffective. Naloxone causes very small, if at all, respiratory depression and the respiratory centre answers efficiently to carbon dioxide stimulation.
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PMID:The sensitivity of the respiratory center and some circulatory and subjective responses after nalorphine and naloxone injections. 77 23

The effect of bumetanide on renal function has been compared with that of furosemide and a placebo in a double-blind study of 9 healthy young men. The sequence for oral administration of the drug was subjected to a random assignation based upon the Latin-square methodology under three different conditions. (1) Normal hydration: The administration of bumetanide (2 mg) produced within the next 4 hr a diuresis comparable to that induced by 80 mg of furosemide. Urinary excretion of sodium, potassium, chloride, calcium, and uric acid also followed comparable patterns. Phosphaturia occurred only under bumetanide. The effect of bumetanide seemed longer lasting. (2) Water loading: The effects of bumetanide and furosemide were comparable with the exception of the phosphaturic effect induced by bumetanide. The action of both diuretics on the diluting segment of the nephron was well demonstrated by the marked depression of CH2O. (3) Water deprivation: The effects of the two diuretics were comparable, including depression tCH20. In none of these conditions did the placebo produce any significant effect.
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PMID:Bumetanide, a new loop diuretic. 78 89

Five healthy rhesus monkeys were ventilated with intermittent mandatory ventilation and 20 torr positive end-expiratory pressure (PEEP) for 8 hours. PEEP was increased to 25 torr and the monkeys were ventilated for 4 more hours. Lactated Ringer's solution and human salt-poor albumin were used to expand plasma and extracellular fluid volume throughout the entire period of study. Homologous blood was administered to maintain hematocrit at control levels and maintenance fluids were infused to maintain transmural pulmonary capillary wedge pressure at 5 to 15 torr. Although cardiac output, mean aortic blood pressure, oxygen consumption, venous admixture, transmural pulmonary capillary wedge pressure, HCO3- and in-vivo base excess were not changed when intermittent mandatory ventilation was employed, cardiac output and blood pressure were significantly depressed by brief periods of controlled mechanical ventilation when alternated with intermittent mandatory ventilation. Sporadic increases in arterial-venous oxygen content difference occurred. Arterial carbon dioxide tension was elevated moderately, with a concomitant depression of arterial pH. No pneumothorax occurred. High PEEP was well tolerated with intermittent manditory ventilation, intravascular volume expansion, and careful cardiovascular monitoring.
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PMID:Cardiorespiratory effects of high positive end-expiratory pressure. 81 Nov 32

Chemical control of breathing was studied before and after the administration of the daily dose of methadone in 14 former heroin addicts who were enrolled in a methadone maintenance program and taking 60 to 100 mg/day. Two major groups were identified: group 1 in which subjects (n=6) had taken the drug for less than two months, and group 2 in which the subjects (n=6) had taken the drug from eight to 43 months. Prior to the daily dose of methadone, the levels of arterial carbon dioxide tension were significantly higher and ventilatory response to hypoxia significantly lower in group 1 than in group 2. Ventilatory responses to carbon dioxide (CO2) were also lower in group 1, but the difference was not statistically significant. Following the daily dose of methadone, the subjects in group 1 manifested significant reductions of ventilation and arterial oxygen tension, significant increases in arterial carbon dioxide tension and significant depressions of ventilatory responses to both CO2 and hypoxia in comparison to values before the administration of methadone. In contrast, subjects in group 2 manifested only a significant decrease in ventilatory responsiveness to hypoxia with no change in ventilation, arterial blood gas tensions or ventilatory responsiveness to CO2 following the daily dose. Two intermediate subjects (five and seven months) behaved as long-term subjects with regard to arterial carbon dioxide tension and CO2 responses but as short-term subjects with regard to responsiveness to hypoxia. Thus, during the first two months of methadone maintence, there is continual alveolar hypoventilation due to depression o both central (CO2) and peripheral (hypoxia) chemoreception. After five months, alveolar hypoventilation is abolished as the CO2-sensitive chemoreflex acquires full tolerance to methadone at the maintenance dose level. In contrast, tolerance of the hypoxia-sensitive chemoreflex is developed more slowly and is never complete.
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PMID:Control of breathing during methadone addiction. 84 54

The effect of dietary vitamin E on lipid synthesis from U-14 C-D-glucose and 1-14C-acetate was studied in rat lungs in vitro. One-month-old Sprague-Dawley male rats were fed either a basal vitamin E-deficient diet or one supplemented with 45 ppm vitamin E ad libitum for two months. Glucose oxidation to CO2 by lungs was significantly (p less than 0.05) decreased by the exclusion of vitamin E from the diet. Oxidation of acetate to CO2 was not affected by the presence of vitamin E in the diet. The extent of labeled carbons from both glucose and acetate incorporated into total lipids was significantly lower in the lungs of vitamin E-deficient animals than in those of the supplemented group. However, the relative amounts of phospholipids, neutral lipids are free fatty acids in total lipids, and of glyceryl moiety and fatty acids in total lipids and in phospholipid fraction were not significantly altered by the status of dietary vitamin E. The results suggest a general depression of lipid synthesis in the lungs of vitamin E-deficient rats.
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PMID:Effect of dietary vitamin E on lipid synthesis by rat lung in vitro. 84 45

The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.
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PMID:Respiratory influence on the total and regional cerebral blood flow responses to intracranial hypertension. 84 90


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