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)

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness. 225 47

Rates of protein synthesis were measured in vivo [corrected] in the lung and heart from fed rats exposed to hyperoxia (less than or equal to 95% O2) for either 6 or 24 h. Protein synthesis rates were depressed by 16-32% compared with normoxic controls in these tissues. The inhibition in both tissues was greatest after 24 h hyperoxic exposure. The decreased fractional rates of synthesis in both tissues were related to changes in ribosomal activity rather than capacity. The fall in synthesis rate per ribosome was greatest in both tissues when the exposure period was increased to 24 h. The possible mechanism(s) involved in hyperoxia-induced depression of protein synthesis are discussed.
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PMID:Effect of hyperoxic exposure on protein synthesis in the rat. 244 80

Effects on ventilatory responses to progressive isocapnic hypoxia of a synthetic potent progestin, chlormadinone acetate (CMA), were determined in the halothane-anesthetized male rat. Ventilation during the breathing of hyperoxic gas was largely unaffected by treatment with CMA when carotid chemoreceptor afferents were kept intact. The sensitivity to hypoxia evaluated by hyperbolic regression analysis of the response curve did not differ between the control and CMA groups. The reduction of ventilation after bilateral section of the carotid sinus nerve (CSN) in hyperoxia was less severe in CMA-treated than in untreated animals. Furthermore, the CMA-treated rats showed a larger increase in ventilation during the hypoxia test and a lower PO2 break point for ventilatory depression. Inhibition of hypoxic ventilatory depression by CMA persisted even after the denervation of CSN. We conclude that exogenous progestin likely protects regulatory mechanism(s) for respiration against hypoxic depression through a stimulating action independent of carotid chemoreceptor afferents and without a change in the sensitivity of the ventilatory response to hypoxia.
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PMID:Effect of a synthetic progestin on ventilatory response to hypoxia in anesthetized rats. 248 Sep 46

Cultured type II pneumocyte responses to in vitro normoxia (95% air:5% CO2) or hyperoxia (95% O2:5% CO2) were quantified. Normoxic culture (0 to 96 h) of rabbit type II cells resulted in enhanced cell-monolayer protein and DNA content. During this same time, cellular activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH Px) decreased. Compared to cultures maintained in normoxia, hyperoxic exposure of cultures resulted in decreased cell-associated protein and DNA content. Exposure to hyperoxia also resulted in cytotoxicity as demonstrated by elevated cellular release of DNA, lactate dehydrogenase (LDH), and preincorporated 8-[14 C]adenine. Cellular catalase and GSH Px activities in hyperoxic cells decreased similarly to normoxic controls. In contrast, cellular SOD activity in hyperoxic cells decreased less than in normoxic cultures. Cellular SOD activity in hyperoxic cultures, when normalized for cellular protein, but not DNA, was greater than normoxic values after 24 to 96 h of exposure. Unlike the decrease in cellular antioxidant enzymes during normoxic and hyperoxic culture, cellular LDH activity increased during both these exposures. Cellular LDH activity in 24 to 96 h hyperoxia-exposed cells increased to a lesser extent than normoxic controls. The extent of depression in LDH activity was dependent on whether the activity was normalized for cellular protein or DNA. Type II pneumocytes, which normally undergo hyperplasia and hypertrophy during hyperoxia in vivo, exhibited oxygen sensitivity in vitro. Exposure of type II cells to hyperoxia in vitro resulted in alterations in cellular SOD and LDH activities, but recognition of such changes were dependent on whether enzymatic activities were normalized for cellular DNA or protein.
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PMID:Responses of type II pneumocyte antioxidant enzymes to normoxic and hyperoxic culture. 250 12

1. Noradrenaline (NA;ED90) caused a contraction of the rat aorta which could be separated into two components, a rapid response mediated by release of intracellular Ca2+ and a more slowly developing contraction which relied principally upon Ca2+ influx. 2. Exposure to acute (30 min) hypoxia has been previously shown to reduce the NA-induced contraction (by 28.0 +/- 2.7%, n = 168) which recovered completely upon re-oxygenation (recovery response). In the present study, prolonged exposure to hypoxia (70 h) caused a more pronounced reduction (39.7 +/- 3.0%, n = 90) of the NA-induced contraction, but, re-oxygenation then produced incomplete recovery to 77.9 +/- 3.9% (n = 90) of the control response. 3. Prolonged exposure to 95% O2 caused a 36.5 +/- 3.1% (n = 42) reduction of NA-induced contractions, whereas prolonged exposure to 21% O2 only caused a small (12.6 +/- 3.4%, n = 6) depression of these responses. 4. The component of the NA-induced contraction mediated by release of intracellular Ca2+ is 39.8 +/- 1.3% (n = 83) of the NA contraction in Ca-containing Krebs solution and was previously found to be unaffected by acute hypoxia. However, following prolonged exposure to either hypoxia or 21% O2, this component only reached 30.7 +/- 2.2% (n = 32) or 28.3 +/- 0.9% (n = 6) of the control response, respectively. Prolonged exposure to 95% O2 caused a more pronounced reduction of this component of contraction which then reached 19.1 +/- 2.1% (n = 12) of the control response. 5. Verapamil (10nM-10 microM) produced similar concentration-dependent reductions of NA-induced contractions elicited during control conditions or acute hypoxia; under these conditions, 1 microM verapamil caused a 34.1 + 6.9% (n = 6) and a 41.8 + 2.9% (n = 18) reduction of these responses respectively. However, recovery responses caused by re-oxygenation of tissues exposed to acute hypoxia were more sensitive to verapamil which, at a concentration of 1 microM, caused a 59.2 + 2.7% (n = 18) reduction of these responses. Verapamil (10 nM-10 microM) also caused similar pronounced concentration-dependent reductions of contractions elicited during prolonged exposure to normoxia or hyperoxia and of recovery responses obtained following re-oxygenation of tissues exposed to prolonged hypoxia; 1 microM verapamil caused a 62.5 + 1.1% (n = 6), 77.2 + 3.8% (n = 12) and a 68.0 + 4.3% (n = 12) reduction of these responses respectively. In contrast, contractions elicited during prolonged hypoxia were less sensitive to verapamil which at a concentration of 1 microM only caused a 16.2 + 2.2% (n 12) reduction of these responses. 6. The present study indicates that prolonged exposure of the rat aorta to either hypoxic or oxygenated conditions causes attenuation of NA-induced contraction. However, these effects are also accompanied by changes in tissue Ca2+ handling which differ under each condition and might account for the observed modifications in tissue sensitivity to the calcium-entry blocker verapamil.
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PMID:The effects of verapamil upon noradrenaline-induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2. 261 85

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.
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PMID:Aminophylline effects on ventilatory response to hypoxia and hyperoxia in normal adults. 279 6

The effects of normobaric hyperoxia on both microsomal membrane fluidity and mechanism of phospholipid synthesis in rabbit liver and kidney have been studied. Hyperoxia induces in both organs an impairment of de novo synthesis of glycerolipids which could be due to an inactivation of acyltransferase activities involved in the initial formation of phosphatidic acid. The ability to replace phospholipid fatty acids by reacylation mechanism decreases slightly in the hyperoxic kidney, while it does not change in the hyperoxic liver. Concerning the effect of high arterial pO2 on microsomal membrane fluidity, the hyperoxic liver shows a more fluid environment within the membrane core of microsomes; however, no difference was shown in that of microsomal membrane core of hyperoxic kidney. An insight into the lipid composition of microsomes indicates that liver microsomal membranes have lower cholesterol content and higher unsaturation degree of phospholipid fatty acids, whereas hyperoxic kidney microsomes become more saturated and did not show any difference in their cholesterol content. In both hyperoxic liver and kidney microsomes, phospholipid content decreases in agreement with the depression of phosphatidic acid biosynthesis. These results are discussed in relation to the values of microsomal membrane microviscosity obtained.
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PMID:Lipid alterations in liver and kidney induced by normobaric hyperoxia: correlations with changes in microsomal membrane fluidity. 288 41

Recent work with isolated blood vessels has emphasized the importance of intact endothelium when the relaxation of vascular smooth muscle is induced by acetylcholine (ACh). However, the physiologic significance of this endothelial-dependent ACh response in a complete organ circulation is unclear. We questioned whether diminished ACh vasodilation would result from damage of lung vascular endothelium and whether this response could be used as an indication of endothelial injury. We therefore induced pulmonary endothelial cell injury in one rat model by repeated injections of alpha-naphthyl thiourea (ANTU) and in a second rat model by exposing rats for 52 h to 100% oxygen at a barometric pressure of 760 torr (hyperoxia). Rats injected with Tween 80, the solvent for ANTU, or exposed to ambient Denver air served as the respective control animals. The isolated lungs of these rats were perfused with a recirculating cell- and plasma-free, physiological salt solution to study the effect of ACh or NaCl infusion on pulmonary perfusion pressure and vascular responsiveness. ANTU-treated rats demonstrated an intact vasodilatory response after ACh infusion when compared with the solvent control animals. The immediate pulmonary vasodilation after ACh infusion was slightly enhanced in the hyperoxic rat lung when compared with the rats exposed to ambient air, but there was no difference between these groups in the prolonged depression of vascular responsiveness to hypoxia or angiotensin II. Thus, in both models of lung endothelial cell injury, the pulmonary vascular responses to ACh were intact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetylcholine-induced pulmonary vasodilation in lung vascular injury. 300 69

Ventilatory effects of propofol, used as a sole agent for the induction and maintenance of general anaesthesia, were studied in 14 healthy unpremedicated patients. Subarachnoid anaesthesia was established before induction of general anaesthesia. Induction was with propofol 2.5 mg kg-1 given while the patients breathed 100% oxygen. We intended to start an infusion of propofol 100 micrograms kg-1 min-1; maintain it for at least 25 min; make a first set of quasi-steady-state observations; double the infusion; and repeat observations after 25 min. The single induction bolus plus single rate infusion was not totally satisfactory: further boluses were usually needed. At induction there was apnoea in all but three patients, sometimes lasting more than 3 min; hyperventilation before induction, combined with hyperoxia, probably exaggerated this. Established ventilatory rates were generally 30% higher than awake. One patient became bradypnoeic. Tidal volume and minute ventilation, and the Tl:Ttot ratio, were reduced. Doubling the infusion rate had no clear effect on frequency or tidal volume, but it further reduced the Tl:Ttot ratio and caused an increase in PE'CO2 of 1 kPa. The ventilatory response to carbon dioxide was 58% of baseline awake control (95% confidence limits +/- 26%) at the lower infusion rate, with further slight depression when the infusion rate was doubled. Doubling the rate of infusion of propofol did not give twice the effect on ventilation, and probably is not giving twice the "depth" of anaesthesia. We cannot say if this is for pharmacokinetic or pharmacodynamic reasons.
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PMID:Some ventilatory effects of propofol as sole anaesthetic agent. 312 6

Hyperoxia and severe hypoxia are known to depress tracheal mucus flow in vivo. It is not clear, however, whether this is also seen in bronchial mucociliary transport system. The author attempted to ascertain acute effects of hyperoxia and moderate hypoxia on bronchial mucociliary clearance by analyzing the regional clearance of aerosolized radioactive tracers within the lung. Eleven healthy persons were exposed to pure oxygen or moderate hypoxia (mean end-tidal PaO2 57.5 mmHg) for 30 min. Twenty four patients with chronic pulmonary emphysema were studied for the chronic effect of hypoxemia on regional mucociliary clearance. They had slight hypoxemia (mean PaO2 76 mmHg). After inhalation of 99mTc-albumin aerosols, clearance of deposited aerosols was quantified as a function of time. The results were analyzed for whole right lung in the acute hyperoxic and hypoxic studies, and for 3 concentric areas representing central, mid, and peripheral regions of the right lung in the study of patients. In healthy subjects, breathing pure oxygen caused significant depression that started 30 min after the initiation of oxygen exposure and was kept up even after stopping the exposure. The clearance was significantly impaired during exposure to moderate hypoxia, though it seemed to be transient. The patients with chronic pulmonary emphysema had a significantly lower clearance in the central region than that in asymptomatic smokers (p less than 0.01). There was no significant correlation, however, between the degree of hypoxemia and the regional clearance. These results suggest that 1) acute exposure to pure oxygen and moderate hypoxia causes bronchial mucociliary dysfunction in humans, 2) the patients with chronic pulmonary emphysema have a lower clearance in the central region of the lung than asymptomatic smokers, and 3) chronic slight hypoxemia has no apparent effect on bronchial mucociliary clearance.
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PMID:[Influence of hyperoxia and hypoxia on bronchial mucociliary clearance]. 322 Apr 40


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