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)

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.
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PMID:Effects of positive end-expiratory pressure on gas exchange in dogs with normal and edematous lungs. 33 16

Our purpose was to reexamine the relationship of the fall in cardiac output and blood pressure which occurs during positive end-expiratory pressure (PEEP) to changes in transmural right atrial and left atrial filling pressures. Closed-chest dogs, half with pulmonary edema, were studied during spontaneous breathing and inspiratory positive-pressure breathing (IPPB) with 0-15 cmH2O PEEP. Mean esophageal pressure accurately reflected changes in pericardial pressure and was used to estimate extracardiac pressure. We found that cardiac output fell approximately 50% and blood pressure fell 20% during 15 cmH2OPEEP in spite of well maintained transmural right atrial and left atrial (or pulmonary artery wedge) pressures suggesting a primary or reflex depression of atrial or ventricular function.
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PMID:Cardiovascular effects of positive end-expiratory pressure in dogs. 34 58

Three patients presented with severe congestive cardiomyopathy of unknown cause. All three had a profound depression of serum phosphorus levels resulting from the chronic ingestion of large quantities of a phosphorus-binding antacid. Results of physical examination and echocardiograms were consistent with cardiomegaly and severe myocardial dysfunction, and chest films showed enlargement of the cardiac silhouette with interstitial pulmonary edema. Serum phosphorus was restored to normal levels, and within 2 to 5 weeks the results of physical examination and echocardiogram of each patient returned to normal. We conclude that these patients had reversible hypophosphatemic cardiomyopathy and show the importance of inorganic phosphorus in myocardial metabolism and function. Serum phosphorus measurements should be a part of the routine evaluation of patients with congestive cardiomyopathy because, at least in some patients, hypophosphatemia appears to be a reversible cause of this disorder.
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PMID:Reversible severe congestive cardiomyopathy in three cases of hypophosphatemia. 634 61

The evaluation of pharmacologic effects in perinatal medicine is dependent on our clinical methods for measurement and monitoring of the mother, the fetus, and the newborn infant. The development of a noninvasive continuous method of measuring PO2, the transcutaneous PO2 electrode, has greatly enhanced the ability to assess effects of drugs on the cardiorespiratory system. During labor, diazepam and meperidine have been documented to cause respiratory depression and significant decreases in PO2. The advantageous effect of epidural anesthesia on the oxygen-cardiorespirogram of mothers in labor has also been demonstrated. Both fetal and maternal tcPO2 have been successfully assessed during the administration of peridural catheter anesthesia (carticaine) and during suppression of labor with fenoterol. In the newborn infant, monitoring of tcPO2 has been helpful in assessing the residual effects of drugs administered during labor and delivery, in prescribing the appropriate and safe dose of oxygen, and in defining the effects of theophylline on the oxygen-cardiorespirogram. We have also demonstrated the effect of furosemide on PO2 in the treatment of pulmonary edema accompanying bronchopulmonary dysplasia and of indomethacin for the management of patent ductus arteriosus. Use of tcPO2 measurements for clinical pharmacologic evaluation is a promising addition to our research techniques.
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PMID:Transcutaneous oxygen measurement to evaluate drug effects. 38 58

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.
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PMID:Renal effects of left atrial distension in dogs with chronic congestive heart failure. 43 20

1 The antidysrhythmic, haemodynamic and metabolic effects of intravenously administered disopyramide phosphate (1 to 5 mg/kg) have been studied in greyhounds, anaesthetized with trichloroethylene. 2 In doses of 2.5 and 5.0 mg/kg, disopyramide significantly reduced the ventricular dysrhythmias that occur in the initial 30-min period following acute coronary artery ligation. None of the disopyramide-treated animals developed ventricular fibrillations. 3 The metabolic consequences of coronary artery ligation, assessed by local coronary venous sampling from the ischaemic area, were not modified by disopyramide except that K+ egress was prevented. 4 There was evidence for substantial disopyramide-induced myocardial depression (decreased cardiac output and left ventricular dP/drmax with elevated ventricular filling pressure and pulmonary oedema and shunting) and it is suggested that great care be taken when the drug is administered intravenously in conditions where cardiac function is already compromised. Disopyramide also reduced myocardial blood flow. 5 In chloralose-anaesthetized mongrel dogs, disopyramide (2.5 mg/kg) significantly reduced the ST-segment elevation (assessed from epicardial recordings) that resulted from short (3 min) coronary artery occlusions. This could indicate a reduction in the extent and severity of myocardial injury or simply reflect decreased K+ efflux (since locally administered K+ itself increased ST-segment elevation).
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PMID:The effects of disopyramide phosphate on early post-coronary artery ligation dysrhythmias and on epicardial ST-segment elevation in anaesthetized dogs. 46 77

Cattle consuming only Kochia scoparia in a pasture southeastern Colorado became ill. Clinical signs were lacrimation, depression, anorexia, nystagmus, head pressing, and recumbency. Some cattle died acutely, with the only clinical signs being recumbency, nystagmus, and occasionally opisthotonos. Pathologic findings were pulmonary edema and congestion, hepatic necrosis and fibrosis, necrosis of proximal convoluted tubular epithelium in the kidneys, epidermal necrosis of lightly pigmented areas, and laminar cerebrocortical necrosis. When the cattle were removed from the pasture, the problem ceased.
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PMID:Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle. 50 Apr 79

We have presented three patients with epiglottitis who developed pulmonary oedema during the course of treatment with nasotracheal intubation and antibiotics. The exact mechanism for the development of pulmonary oedema in these patients is not known. Possible mechnisms are changed in the physical factors controlling the movement of fluids across the capillary-alveolar membrane, transitory bacteraemia and endotoxinaemia, or myocardial depression by the antibiotics and the anaesthetic agent. The pulmonary oedema had a benign course and responded to mechanical ventilation and increased airway pressure.
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PMID:Epiglottitis and pulmonary oedema in children. 66 67

The effectiveness of immunodepressants in lingering exudative processes, their inhibitory action in the proliferative phase of inflammation, depression of the phagocytic activity of leucocytes, as well as suppressive influence on the development of a toxic pulmonary edema and upon generalized anaphylaction reaction was demonstrated in tests staged on rats and mice. The antiphlogistic action of immunodepressants was not abolished during the first hours after their administration by specific metabolites, but was suppressed at the peak of the cytostatic effect together with the latter. The phlogolytic effect was not mediated through the hypophysis-adrenal system and did not include the lienic factor.
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PMID:[Mechanism of the anti-inflammatory action of immunodepressants]. 92 80


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