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)

Heart rate (fH) at 20-23 degrees C was recorded in six different developmental stages of the bullfrog, Rana catesbeiana (n = 104, body mass 40 mg to 90 g), at rest after normoxic acclimation, during acute changes in O2 availability, and after brief but intense activity. The effects of cholinergic blockade and combined cholinergic and beta-adrenergic blockade on the response to this experimental protocol were also assessed. Mild tonic vagal inhibition of fH was evident during larval development but disappeared after metamorphosis. There was no tonic sympathetic stimulation of fH at rest in any developmental stage. Intense activity produced a tachycardia in all developmental stages but newly hatched larvae. In adults, tachycardia during activity resulted from beta-adrenergic stimulation but in larvae may have resulted from the direct effects of increased venous return stretching the cardiac pacemaker. Neither acute hypoxia or hyperoxia affected fH in any developmental stage, with the single exception of a severe depression of fH occurring at a PO2 of 30 Torr in newly hatched larvae. These results indicate that, although the heart of the newly hatched larvae is essentially devoid of regulation, cholinergic and beta-adrenergic mechanisms for reflex regulation of fH appear early in larval development. These mechanisms, although most fully expressed in the adult bullfrog, are essentially intact before metamorphosis of the larva.
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PMID:Ontogeny of heart rate regulation in the bullfrog, Rana catesbeiana. 348 92

We evaluated the ability of endotoxin to protect against hyperoxic depression of plasma membrane fluidity in endothelial cells and fibroblasts in culture. Second- to-fifth passage porcine aortic endothelial cells and human newborn foreskin fibroblasts with 20 ng/ml of endotoxin or diluent in the culture medium were exposed to 20% O2 (control) or 95% O2 (hyperoxic) in 5% CO2 for 4 hours. After exposure, cells were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic core of lipid bilayer membranes, or transparinaric acid (TPA), a natural, conjugated fatty acid that orients parallel to fatty acyl chains of membrane phospholipids. Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropies (rs) for DPH and for TPA by using fluorescence spectroscopy. Reductions in membrane fluidity increase the value of rs. Addition of endotoxin to the culture medium of control endothelial cells and fibroblasts had no effect on rs for DPH or TPA. In hyperoxic endothelial cells, rs for DPH and rs for TPA were increased (p less than 0.001). Addition of endotoxin to the medium of hyperoxic endothelial cells prevented the increases in rs for DPH and TPA. Hyperoxia increased rs for DPH (p less than 0.003) but not rs to TPA in fibroblasts, and endotoxin failed to prevent this increase. These results indicate that hyperoxia decreases plasma membrane fluidity in endothelial cells and fibroblasts and demonstrate that endotoxin prevents the decrease in plasma membrane fluidity in endothelial cells, but not in fibroblasts. These membrane-protective effects may represent an alternative mechanism by which endotoxin protects against hyperoxic cellular injury, and this mechanism may be specific for hyperoxic injury to endothelial cells.
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PMID:Endotoxin protects against hyperoxic decrease in membrane fluidity in endothelial cells but not in fibroblasts. 351 21

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

White Leghorn chicken eggs were exposed to either 60% O2 or room air (21% O2) for the first 19 days of incubation. Chicks that hatched from these eggs were then tested in discrimination learning tasks in which keypecking was autoshaped to colored lights that were paired with either access to food (Experiment 1) or heat (Experiment 2). Chronic prenatal exposure to 60% O2 reduced hatchability but did not affect mean hatching time. Although previous research has shown that hyperoxic treatment accelerates growth in chick embryos until the 18th day of incubation, experimental chicks weighed either the same (Experiment 1) or less (Experiment 2) than controls at hatching. Prenatal exposure to hyperoxia depressed rate of acquisition, but not final performance level in both discrimination tasks. The initial performance deficit appeared to reflect a temporary depression of activity or arousal, possibly due to a relatively greater hypothermia in experimental chicks. This general pattern of results was attributed to premature depletion of essential nutrients within the egg as a result of oxygen-induced growth acceleration.
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PMID:Autoshaped discrimination learning in chicks incubated under normobaric hyperoxia. 371 63

The herbicide nitrofen was administered to pregnant Fischer-344 and Sprague-Dawley rats on Days 10-13 of gestation (po, 20 or 40 mg/kg daily) and its effects on cardiac structure and function were investigated in the offspring. In the 21-day fetuses, nitrofen did not influence intrauterine growth or basal heart rate. In contrast, the herbicide produced a marked depression of heart rate and abnormal electrocardiographic (ECG) profiles in the newborn rats, in conjunction with labored respiratory movements and a profound increase in postnatal mortality. A few animals displayed cardiac ventricular septal defects and diaphragmatic hernias but these malformations did not appear to be associated with the ECG changes. The chronotropic deficiencies seen in the nitrofen-treated pups were reversible by acute hyperoxia (40% oxygen). These results suggest that the teratogenic effects of nitrofen on cardiac physiology and on postnatal mortality cannot be accounted for solely by specific gross anatomical damages to the rat heart and diaphragm; rather, other more subtle morphological and physiological factors which contribute to improper systemic delivery and cellular utilization of oxygen may be involved.
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PMID:Effects of prenatal nitrofen exposure on cardiac structure and function in the rat. 376 34

We studied the influence of prolonged exposure to hyperoxia (O(2) > 98%) on protein synthesis and on the ultrastructure of the granular pneumocyte. To study protein synthesis, as indicated by l-[U-(14)C]-leucine incorporation into protein, lung slices were incubated with radioactive leucine and a surface-active fraction was obtained by ultracentrifugation of lung homogenates. We found that, following an initial depression in protein synthesis after 48 h of hyperoxia, protein synthesis in rats exposed to oxygen for 96 h rose to greater than control levels. This increase in protein synthesis was noted in whole lung protein and in protein present in the surface-active fraction. Stereologic ultrastructural analysis of granular pneumocytes revealed that the lamellar bodies occupy the same percentage of cytoplasmic volume in oxygen-exposed and control rats after 96 h; a previous study had shown lamellar bodies of oxygen-exposed rats to occupy less volume than those of control rats after 48 h of exposure at which time protein synthesis was also depressed. After 96 h of exposure there is a greater amount of rough endoplasmic reticulum in the granular pneumocytes of oxygen-exposed rats. These studies show that after 96 h of hyperoxia the lung has recovered its ability to synthesize protein including protein in the surface-active fraction and that these biochemical changes are associated with consistent ultrastructural alterations in the granular pneumocyte.
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PMID:Adaption to hyperoxia. Influence on protein synthesis by lung and on granular pneumocyte ultrastructure. 440 5

Preadaptation of adult rats to hypoxia (10% O2 for 5 days) results in tolerance to oxygen-induced lung injury (greater than 95% O2 for 2 days). This study investigated whether hypoxia preadaptation maintained an endothelial cell metabolic function, angiotensin-converting enzyme (ACE) activity, despite exposure to hyperoxia. Lung ACE activity was measured as the capacity of isolated, ventilated, perfused lungs to hydrolyze an ACE substrate, benzoyl-phenylalanyl-alanyl-proline (BPAP), after in vivo hypoxia, hyperoxia, or sequential hypoxia-hyperoxia exposure. The results indicated that (1) hyperoxia decreases BPAP hydrolysis in isolated lungs, (2) hypoxia preadaptation does not affect BPAP hydrolysis (measured at ambient PO2), and (3) hypoxia preadaptation prevents hyperoxia-induced depression of lung ACE activity. These data imply that lung microvascular endothelial cells participate in the development of oxygen tolerance in this model.
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PMID:Hypoxia preadaptation prevents oxygen-induced depression of lung angiotensin-converting enzyme activity. 608 27

The effects of progressively increasing hyperoxia from 0.22 to 1 on the ventilatory action of a ventilatory analeptic with a peripheral action, almitrine, were studied in six dogs under deep anaesthesia by Alfatesine administered at a constant flow rate. At FiO2 = o.22, almitrine partially corrected hypoventilation. From FiO2 o.30 to FiO2 0.50, initial hypoventilation was unaltered. At FiO2 = 1, it was worsened. This preliminary study will need to be completed by examination of the interference almitrine-FiO2 at different levels of anaesthesia and of respiratory depression, by study of the effects of different levels of FiO2 on the respiratory depression caused by Alfatesine and by study of the effects of the sudden administration of pure oxygen.
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PMID:[Effect of different FiO2 on the ventilatory action of almitrine in the anesthetized dog. Preliminary study]. 610 90

Treatment of newborns with 20 mg/kg/day chlorphentermine orally for 1 week increased incorporation of thymidine into lung DNA without an associated change in tissue morphology or cyclic AMP levels. An increase in chlorphentermine dose to 60 mg/kg resulted in an accumulation of alveolar hypertrophic macrophages and a rise in incorporation of thymidine into lung DNA; however, cyclic AMP levels were decreased. In contrast, 20 or 60 mg/kg/day for 1 week phentermine-induced depression in the incorporation of thymidine into pulmonary DNA was accompanied by a decrease in cyclic AMP but no apparent alteration in tissue morphology. Hyperoxia did not modify the phentermine-induced changes in cyclic AMP levels and pulmonary ultrastructure. In contrast, hyperoxia altered the responsiveness of newborns to 20 mg/kg chlorphentermine as evidenced by the presence of foam cells. Data suggest that the chlorphentermine-induced increase in DNA synthesis in newborn lung seems independent of changes in cyclic AMP and tha modification of drug-induced alterations by hyperoxia may be related to the chemical structure of a compound.
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PMID:Modification by hyperoxia of chlorphentermine- or phentermine- induced effects on newborn rat lung morphology and metabolism. 627 4

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76


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