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)

Continuous positive pressure ventilation (CPPV) is an established therapy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic pressure, inducing a decrease in cardiac output (CO) and oxygen delivery (DO2). Alternatively, mechanical ventilation with prolonged inspiratory to expiratory duration ratio (inversed ratio ventilation IRV) has been successfully used in ARF. No data are available about IRV in acute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (positive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiration to expiration duration ratio [I:E] = 3.0) were studied in nine dogs (body weight 29.9 +/- 4.3 kg) before and after induction of myocardial ischaemia. METHODS. Continuous intravenous anaesthesia and muscle paralysis were provided by 1.2 mg.kg-1 x h-1 piritramide and 0.08 mg.kg-1 x h-1 pancuronium, and the animals were ventilated with intermittent positive pressure ventilation (IPPV) as reference method. Cardiocirculatory performance was determined by means of heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and left ventricular end-diastolic pressure (LVEDP). Cardiac output (CO) was determined by thermodilution method. Systemic vascular resistance (SVR) was calculated. Pulmonary function was assessed by arterial and mixed venous blood gas tension for oxygen (PaO2, PvO2) and carbon dioxide (PaCO2). Functional residual lung capacity (FRC) was measured by means of the foreign gas wash-in method using helium as inert gas, and determination of extravascular lung water (EVLW) using the thermal-dye indicator technique. CPPV and IRV were studied in random sequence in the control phase and 60 min after induction of acute left ventricular ischaemia, which was achieved by occlusion of the ramus interventricularis anterior. RESULTS. During the control phase CPPV induced an increase in MPAP (P < 0.05), CVP (P < 0.05) and PAOP (P < 0.05). HR and MAP remained unchanged, whereas CO decreased by 16% (P < 0.05). FRC was elevated by 25 ml.kg-1 (P < 0.01), but not EVLW (9.1 +/- 3.5 ml.kg-1). There was no improvement in oxygenation; instead, oxygen delivery (DO2) decreased (P < 0.05). During inversed ratio ventilation MPAP, CVP, PAOP increased, but less than during CPPV. FRC was elevated mu 7.0 ml.kg-1 (P < 0.05), which was significantly less than during CPPV (P < 0.05). EVLW revealed no differences. During IPPV in the ischaemia phase cardiopulmonary performance deteriorated significantly. CO decreased by 19% (P < 0.05), whereas HR, MPAP, CVP and PAOP increased (P < 0.05). PaO2 was lower (P < 0.05) and alveolo-arterial PO2 gradient (PAaO2) increased (P < 0.05). All animals revealed moderate pulmonary oedema (EVLW = 15.1 +/- 8.4 ml.kg-1) (P < 0.01) and a lower FRC. Mechanical ventilation with PEEP significantly improved oxygenation and FRC; however, DO2 was slightly lower than during IPPV (not significant). IRV elevated PaO2, FRC and DO2, since CO was not depressed when compared with IPPV. CONCLUSIONS. CPPV and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ventilation, oxygenation was improved without apparent changes in EVLW. Haemodynamic performance was more impaired during CPPV, and no improvement of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typically induces an infarction of 35% of left ventricular muscle mass; however, non-ischaemic myocardium reveals an unchanged or increased contractility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounced during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventCntCo
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PMID:[Cardiopulmonary effects of CPPV (continuous positive pressure ventilation) and IRV (inverse ratio ventilation) in experimental myocardial ischemia]. 848 92

Aspirin overdose may result in acid-base disturbances, electrolyte abnormalities, pulmonary edema, chemical hepatitis, seizures, and mental status alteration, but myocardial depression has not been reported following aspirin overdose in children. In addition to these more typical features, the 13-month-old boy reported here developed clinical, radiographic, and echocardiographic evidence of myocardial impairment with pulmonary edema and moderately severe global left ventricular dysfunction (estimated shortening fraction of 23%). Complete resolution of the myocardial dysfunction was demonstrated on follow-up echocardiography as the child recovered from the aspirin intoxication. This case suggests that myocardial dysfunction can occur as a result of toxic aspirin ingestion, and that it may contribute to salicylate-induced pulmonary edema.
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PMID:Transient myocardial dysfunction in a child with salicylate toxicity. 853 Jul 86

Acrolein is a highly toxic, reactive, and irritating aldehyde that occurs as a product of organic pyrolysis, as a metabolite of a number of compounds, and as a residue in water when used for the control of aquatic organisms. It is an intermediate in the production of acrylic acid, DL-methionine, and numerous other agents. Its major direct use is as a biocide for the control of aquatic flora and fauna. It is introduced to the environment from a variety of sources, including organic combustion such as automobile exhaust, cigarette smoke, and manufacturing and cooking emissions, as well as direct biocidal applications. Organic combustion from both fixed and mobile sources is the significant source of acrolein in the atmosphere; it represents up to 8% of the total aldehydes generated from vehicles and residential fireplaces and 13% of total atmospheric aldehydes. This reactive aldehyde also occurs in organisms as a metabolite of allyl alcohol, allylamine, spermine, spermidine, and the anticancer drug cyclophosphamide, and as a product of UV radiation of the skin lipid triolein. Furthermore, small amounts are found in foods; when animal or vegetable fats are overheated, however, large amounts are produced. Most human contact occurs during exposure to smoke from cigarettes, automobiles, industrial processes, and structural and vegetation fires. Besides cigarette smoke, occupational exposures are a common mode of human contact, particularly in industries that involve combustion of organic compounds. Firefighters, in particular, are exposed to extremely high levels during the extinguishment and overhaul phases of their work. Water may contain significant levels of the herbicide. It has been found in paper mill and municipal effluents at 20-200 micrograms/L, and at 30 micrograms/L as far as 64 km downstream from the point of application. The USEPA-recommended water quality criteria for freshwater are only 1.2 micrograms/L (24-hr avg) and 2.7 micrograms/L (maximum ceiling). Acrolein is highly reactive, and intercompartmental transport is limited. However, it is eliminated from aqueous environments by volatilization and hydration to beta-hydroxypropanal, after which biotransformation occurs, with a half-life of 7-10 d. The Koc for acrolein is 24, and it is not likely to be retained in soil; activated carbon adsorbs only 30% from solution. Thus, the aldehyde is either leached extensively in moist soil or volatilizes quickly from dry soil. It is eliminated from air by reaction with .OH (half-life, 0.5-1.2 d), NOx (half-life, 16 d), and O3 (half-life, 59 d), as well as by photolysis and wet deposition. As expected from its high water solubility, bioaccumulation is low. Acrolein is highly toxic by all routes of exposure. The respiratory system is the most common target: exposure causes localized irritation, respiratory distress, pulmonary edema, cellular necrosis, and increased susceptibility to microbial diseases. Additionally, acute inhalation studies verify that it is a severe respiratory irritant that affects respiratory rates. Respiratory rate depression may have a protective effect by minimizing vapor inhalation, thereby explaining the subadditive effect of acrolein when combined with the other toxic combustion by-products CO and HCHO. Liquid contact with the skin and eyes causes severe irritation, opaque or cloudy corneas, and localized epidermal necrosis, but no allergic contact dermatitis. The cardiovascular system is affected, resulting in increased blood pressure, platelet aggregation, and quick cessation of beating in perfused rat hearts. It may also inhibit mitochondrial oxidative phosphorylation in the myocardium. Acute LD50s and LC50s are low. Levels are 7-46 mg/kg and 18-750 mg/m3, respectively, in rats; aquatic organisms are affected above 11.4 micrograms/L.(ABSTRACT TRUNCATED)
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PMID:Fate and effects of acrolein. 859 34

(S)-10-[(S)-(8-Amino-6-azaspiro[3,4]octan-6-yl)]-9-fluoro-2, 3-dihydro-3-methyl-7-oxo-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxyli c acid hemihydrate (CAS 151390-79-3, DV-7751a) a new quinolone antibacterial agent, was examined for LD50 value, phototoxicity and convulsion inducing potential in laboratory animals. A single oral administration of DV-7751a induced soft stool in rats at 1000 and 2000 mg/ kg and in monkeys at 250 mg/kg and vomiting in monkeys at 500 mg/kg or more. A single intravenous administration caused a decrease in locomotor activity, respiratory depression, convulsion, pulmonary edema and death in rats and mice. The LD50 values with oral administration were more than 2000 mg/ kg for rats and mice and more than 250 mg/kg for monkeys, and those with intravenous administration were 164.3 mg/kg for rats of both sexes at an injection rate of 2 ml/min, 118.8 mg/kg for male rats and 104 to 125 mg/kg for female rats at 0.5 ml/min, and 184.7 mg/kg for male mice and 187.4 mg/kg for female mice. DV-7751a showed very weak phototoxicity in mice after single oral administration of 600 mg/kg, followed by UVA irradiation, but no convulsion after oral administration of 200 or 1000 mg/kg in combination with 4-biphenylacetic acid at 400 mg/kg.
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PMID:LD50 value, phototoxicity and convulsion induction test of the new quinolone antibacterial agent (S)-10-[(S)-(8-amino-6-azaspiro[3,4]octan-6-yl)]-9-fluoro-2, 3-dihydro-3-methyl-7-oxo-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxyl ic acid hemihydrate in laboratory animals. 876 55

The haemodynamic and gas exchange abnormalities occurring in neurogenic pulmonary oedema (NPO) were examined retrospectively in 20 patients admitted to the Intensive Therapy Unit (ITU) over a 45-month period (February 1992 to November 1995). In 12 patients, where vasoactive therapy with dobutamine was employed, its effect on haemodynamics was examined. Cardiac index (CI median 2.2 l min-1 m-2) and left ventricular stroke work index (LVSWI 20 g.m.m-2) were markedly depressed, while pulmonary artery wedge pressure (PAWP 17 mmHg), mean pulmonary artery pressure (MPAP 30.5 mmHg), systemic vascular resistance index (SVRI 2852 dyne.s.cm-5.m2) and pulmonary vascular resistance index (PVRI 393 dyne.s.cm-5.m2) were substantially elevated above normal values. Mean arterial pressure (MAP 82.5 mmHg) and heart rate (HR 102 bpm) were within normal limits. The poor oxygenation is indicated by a median PaO2/fiO2 ratio of 18.0 kPa. Patients treated with dobutamine showed significant increases in CI and LVSWI and significant falls in SVRI and PAWP at 2 and 6 h after institution of therapy, and there was a significant rise in PaO2/fiO2 ratio to 27.8 kPa at 6 h. NPO was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine.
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PMID:Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. 884 33

Combination vaccines containing viral and bacterial antigens are commonly used in veterinary practice and have been associated with adverse reactions. A group of young Simmental calves developed fever and depression following administration of a mixed vaccine, and 1 died with pulmonary edema, suggesting that endotoxins or other bacterial components may interact synergistically with some adjuvants to cause an enhanced pathologic inflammatory response in some individuals.
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PMID:Systemic adverse reactions in young Simmental calves following administration of a combination vaccine. 899 86

Acclimatisation to environmental hypoxia initiates a series of metabolic and musculocardio-respiratory adaptations that influence oxygen transport and utilisation, or better still, being born and raised at altitude, is necessary to achieve optimal physical performance at altitude, scientific evidence to support the potentiating effects after return to sea level is at present equivocal. Despite this, elite athletes continue to spend considerable time and resources training at altitude, misled by subjective coaching opinion and the inconclusive findings of a large number of uncontrolled studies. Scientific investigation has focused on the optimisation of the theoretically beneficial aspects of altitude acclimatisation, which include increases in blood haemoglobin concentration, elevated buffering capacity, and improvements in the structural and biochemical properties of skeletal muscle. However, not all aspects of altitude acclimatisation are beneficial; cardiac output and blood flow to skeletal muscles decrease, and preliminary evidence has shown that hypoxia in itself is responsible for a depression of immune function and increased tissue damage mediated by oxidative stress. Future research needs to focus on these less beneficial aspects of altitude training, the implications of which pose a threat to both the fitness and the health of the elite competitor. Paul Bert was the first investigator to show that acclimatisation to a chronically reduced inspiratory partial pressure of oxygen (P1O2) invoked a series of central and peripheral adaptations that served to maintain adequate tissue oxygenation in healthy skeletal muscle, physiological adaptations that have been subsequently implicated in the improvement in exercise performance during altitude acclimatisation. However, it was not until half a century later that scientists suggested that the additive stimulus of environmental hypoxia could potentially compound the normal physiological adaptations to endurance training and accelerate performance improvements after return to sea level. This has stimulated an exponential increase in scientific research, and, since 1984, 22 major reviews have summarised the physiological implications of altitude training for both aerobic and anaerobic performance at altitude and after return to sea level. Of these reviews, only eight have specifically focused on physical performance changes after return to sea level, the most comprehensive of which was recently written by Wolski et al. Few reviews have considered the potentially less favourable physiological responses to moderate altitude exposure, which include decreases in absolute training intensity, decreased plasma volume, depression of haemopoiesis and increased haemolysis, increases in sympathetically mediated glycogen depletion at altitude, and increased respiratory muscle work after return to sea level. In addition, there is a risk of developing more serious medical complications at altitude, which include acute mountain sickness, pulmonary oedema, cardiac arrhythmias, and cerebral hypoxia. The possible implications of changes in immune function at altitude have also been largely ignored, despite accumulating evidence of hypoxia mediated immunosuppression. In general, altitude training has been shown to improve performance at altitude, whereas no unequivocal evidence exists to support the claim that performance at sea level is improved. Table 1 summarises the theoretical advantages and disadvantages of altitude training for sea level performance. This review summarises the physiological rationale for altitude training as a means of enhancing endurance performance after return to sea level. Factors that have been shown to affect the acclimatisation process and the subsequent implications for exercise performance at sea level will also be discussed. Studies were located using five major database searches, which included Medline, Embase, Science Citation Index, Sports Discus, and Sport, in
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PMID:Physiological implications of altitude training for endurance performance at sea level: a review. 929 50

An 81-year-old man underwent percutaneous transluminal gallbladder drainage. As the drain was accidentally removed six days later, he received cholecystectomy. After the operation, he developed hypotension, hypoxemia and ST level depression on ECG. He received artificial ventilation and cathecholamines. His chest CT showed marked pulmonary edema, and total protein of the edema-fluid was 3.3 g.dl-1. These findings suggested permeability pulmonary edema. He received postural drainage of the edema-fluid, and the pulmonary oxygenation was gradually improved. He was weaned from artificial ventilation on the 6th ICU day and discharged the next day.
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PMID:[The efficacy of postural drainage in a case of pulmonary edema following cholecystectomy]. 940 37

Our investigation was carried out in subjects intoxicated with heroin or heroin mixtures to find out the time interval during which delayed life-threatening complications become manifest, such as pulmonary oedema or relapse into respiratory depression or coma after naloxone treatment. We studied prospectively all drug intoxications between 1991 and 1992. Of the 538 intoxications, we assessed in detail 160 outpatients who lived within the catchment area of our hospital. The outcome variables studied were (1) rehospitalization for pulmonary oedema, (2) relapse into coma, and/or (3) death and cause within 24 h after release from hospital. Deaths occurring outside our hospital have to be reported, as decreed by law, to the Institute for Forensic Medicine. The results of our investigation showed no rehospitalization owing to pulmonary oedema or coma, but one death, outside the hospital, owing to delayed pulmonary oedema. This delayed complication had an incidence of 0.6% (95% confidence interval 0-3.8%). A reintoxication could be excluded in this patient. Based on reliable report, the pulmonary oedema occurred between approximately 2 1/4 and 8 1/4 hours after intoxication. In the literature, only two cases of delayed pulmonary oedema have been reported with reliable time statements (4 and 6 h after hospitalization). We therefore conclude that surveillance for at least 8 h is essential after successful treatment to exclude delayed pulmonary oedema in patients intoxicated with heroin or heroin mixtures.
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PMID:Patients intoxicated with heroin or heroin mixtures: how long should they be monitored? 942 91

A case is presented of a fatal drug interaction caused by ingestion of clozapine (Clozaril) and fluoxetine (Prozac). Clozapine is a tricyclic dibenzodiazepine derivative used as an "atypical antipsychotic" in the treatment of severe paranoid schizophrenia. Fluoxetine is a selective serotonin reuptake inhibitor used for the treatment of major depression. Clinical studies have proven that concomitant administration of fluoxetine and clozapine produces increased plasma concentrations of clozapine and enhances clozapine's pharmacological effects due to suspected inhibition of clozapine metabolism by fluoxetine. Blood, gastric, and urine specimens were analyzed for fluoxetine by gas chromatography/mass spectrometry (GC/MS) and for clozapine by gas-liquid chromatography (GLC). Clozapine concentrations were: plasma, 4.9 micrograms/mL; gastric contents, 265 mg; and urine, 51.5 micrograms/mL. Fluoxetine concentrations were: blood, 0.7 microgram/mL; gastric contents, 3.7 mg; and urine 1.6 micrograms/mL. Norfluoxetine concentrations were: blood, 0.6 microgram/mL, and none detected in the gastric contents or urine. Analysis of the biological specimens for other drugs revealed the presence of ethanol (blood, 35 mg/dL; vitreous, 56 mg/dL; and urine 153 mg/dL) and caffeine (present in all specimens). The combination of these drugs produced lethal concentrations of clozapine and high therapeutic to toxic concentrations of fluoxetine. The deceased had pulmonary edema, visceral vascular congestion, paralytic ileus, gastroenteritis and eosinophilia. These conditions are associated with clozapine toxicity. The combined central nervous system, respiratory and cardiovascular depression of these drugs was sufficient to cause death. The death was determined to be a clozapine overdose due to a fatal drug interaction.
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PMID:A fatal drug interaction between clozapine and fluoxetine. 972 31


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