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)

Shock is a well-known complication of iron poisoning. Its aetiology is multifactorial with hypovolaemia due to gastrointestinal blood loss and myocardial depression due to systemic acidosis contributing to its genesis. Primary myocardial dysfunction has not been considered to play a role. Our clinical experiences and autopsy findings in three fatal cases of iron poisoning support myocardial dysfunction and damage as contributing factors to their cardiovascular collapse. The three patients, all female, were 3 1/2, 16 and 28-years-old. Onset of shock occurred at 1, 2 and 5 days post-ingestion. There was no response to vigorous fluid replacement therapy and aggressive catecholamine infusions. Central venous pressures were elevated. Microscopic examination of postmortem tissue showed myocardial damage and the presence of stainable iron. It is speculated that the myocardial depression is mediated by lipid peroxidation of myocyte organelle membranes due to iron catalysed free radical generation. The presence of myocardial dysfunction has therapeutic implications. Patients with severe iron poisoning require early and serial measurements of arterial blood pressure, central venous pressure and cardiac output. If primary myocardial dysfunction is documented then fluid replacement, inotropic support and afterload reduction should be considered.
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PMID:Myocardial failure and shock in iron poisoning. 339 27

Chronic obstructive pulmonary disease (COPD) is a common and very debilitating disease in the United States. COPD is characterized by plugging of airways with secretions, impaired airway integrity with airway collapse with effort, bronchospasm, frequent infections, destruction of alveolar tissue, and ventilation-to-perfusion inequality. This results in abnormalities in pulmonary mechanics and respiratory gas exchange, all of which make hyperventilation much less effective. However, research has shown that the pulmonary patient can improve work capacity in an exercise training program. Training also alleviates the severe emotional problems of anxiety, depression, and social isolation frequently present in COPD sufferers. Even the lowest level patient can frequently improve in a training program, and guidelines for the implementation of such a therapeutic regimen are provided.
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PMID:Athletic training in chronic obstructive pulmonary disease. 352 97

Clonidine and doxepin alleviate the symptoms of the opiate withdrawal syndrome. Clonidine was slightly more effective in controlling sweating, hot flushes, palpitations and nausea, and doxepin was slightly more effective in relieving the craving for opiates, lassitude and depression. Adverse effects such as sedation, dry mouth and falls in blood pressure occurred in both groups. There were six cases of collapse during treatment with high doses of doxepin, whereas only one subjective circulatory effect occurred in the clonidine group. At these high doses, doxepin may cause orthostatic hypotension via a peripheral alpha-receptor blockade. Clonidine reduced pulse rate whereas doxepin, with its anticholinergic action and indirectly via its alpha-receptor blocking action, raised it. Several patients in the doxepin group hat fits, as opposed to only one in the clonidine group. It is possible that the use of barbiturates had reduced the convulsive threshold in some of our patients. Overall, clonidine and doxepin were equipotent at adequate individual dose levels, and both were well tolerated. In this trial, serious side-effects occurred less often in the clonidine group.
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PMID:A controlled comparison of clonidine and doxepin in the treatment of the opiate withdrawal syndrome. 352 50

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Adult female Wistar rats were injected with 1 mg/kg body weight of uranyl nitrate (UN). Evaluation of renal function, histopathology studies, and determination of plasma erythropoietin (Ep) titers after exposure to 456 mb for 16 h were performed at 1, 2, 7, 10, 15, and 21 days after drug injection. Plasma urea and creatinine concentrations markedly increased during the first seven days after injection, reaching maximal values on day 7 and decreasing thereafter. Significant increases in urine volume and significant depressions in urine osmolality also were observed; both alterations were most marked on day 7 after injection. A coagulative necrosis of the epithelium of proximal convoluted tubules, desquamation of the necrotic cells, and dilation or collapse of the tubular lumen were observed; the lesions were more marked on day 7. Plasma Ep levels in UN-treated rats exposed to hypobaria were markedly lower than in noninjected controls similarly exposed. Measurements were performed one, two, and seven days after UN injection, with maximal depression observed on day 7. These observations indicate that there is a correlation between the extent of both tubule damage and degree of renal dysfunction and plasma Ep production during exposure to hypoxia in UN-treated rats. This suggests that the renal Ep component is derived primarily from tubular cells.
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PMID:Relationship between severity of renal damage and erythropoietin production in uranyl nitrate-induced acute renal failure. 369 9

Haemorrhagic shock was induced in anaesthetized, open-chest dogs by controlled arterial bleeding, sufficient to reduce and maintain mean arterial blood pressure at 40 mmHg for 30 min. The blood volume was then restored to the pre-shock level by rapid, intravenous reinfusion of the blood shed during the shock period. Haemorrhagic shock produced significant haemodynamic changes, characterized by a marked depression of myocardial function. Cardiac output (1226 +/- 57 ml min-1), peak aortic blood flow (6030 +/- 383 ml min-1) and maximum rate of rise of left ventricular pressure (2708 +/- 264 mmHg s-1) were all reduced by more than 50%. The haemodynamic profile was markedly improved by reinfusion of shed blood but this improvement was not sustained. There was a gradual decline such that 50% of the untreated animals suffered complete circulatory collapse and death between 60 and 120 min following reinfusion. Neither haemorrhagic shock, nor reinfusion of shed blood produced any consistent or significant changes in the myocardial adenine nucleotide pool. The ATP, ADP and AMP levels were, respectively, 25.9 +/- 4.2; 15.6 +/- 1.0; 4.3 +/- 1.9 nmol g-1 protein, before haemorrhagic shock; 21.6 +/- 3.4; 21.5 +/- 2.5; 10.2 +/- 2.7 nmol g-1 protein, after 30 min haemorrhagic shock; and 29.9 +/- 3.9; 16.5 +/- 1.2; 4.2 +/- 1.1 nmol g-1 protein, 60 min following reinfusion of shed blood. Pretreatment with allopurinol (50.0 mg kg-1 i.v.), 60 min before inducing haemorrhagic shock, had no significant effect upon the haemodynamic response to shock, but did prevent the gradual decline seen following reinfusion in the untreated animals. All of the allopurinol-treated animals displayed significantly better haemodynamic profiles than the untreated animals, furthermore, there was a 100% survival rate in this group. 5 Allopurinol had no significant effect upon the myocardial adenine nucleotide pool either during haemorrhagic shock or following reinfusion of shed blood.
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PMID:The protective action of allopurinol in an experimental model of haemorrhagic shock and reperfusion. 380 69

Fifty-four cases of death from hyperosmolar comas were examined pathoanatomically together with the postmortem biochemical analysis of the CSF and blood. Brain of animals with disturbances of the blood and CSF osmolarity was studied electron cytochemically and autoradiographically. It was discovered that the hyperosmolar comas are manifested by excosis and brain collapse. The brain is reduced in volume due to deep cell-extracell dehydration and alteration of the hematoencephalic barrier with the irreversible depression of the neuronal and glial metabolism. In 7 patients dying with the purulent-necrotic changes of vessels resulting from the hyperosmolar effect of verografin used for the carotid angiography, numerous perivascular hemorrhages developed in the brain. Dysequilibrium syndrome in hemodialysis is manifested by an acute brain swelling or by a formation at a later period of symmetrical ischemic-hemorrhagic necrosis in the thalamus and occipital lobes of the large hemispheres.
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PMID:[Pathologo-anatomical characteristics of hyperosmolar and other comatous conditions]. 392 35

Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and anuria after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure, disseminated intravascular coagulation, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.
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PMID:Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax. 394 Jul 93

The blood flow to the left lower lobe (QL), and total (QT) pulmonary blood flow, were measured in 10 open-chest dogs using electromagnetic flowmeters. Ventilation of the left lower lobe with 7% oxygen in nitrogen produced a greater reduction in QL/QT (41%) than lobar ventilation with 7% oxygen in nitrous oxide (33%). Lobar collapse reduced QL/QT by 65%, but there was no change in QL/QT when 50% nitrous oxide was administered to the right lung. The i.v. infusion of lignocaine hydrochloride during ventilation of the lobe with 7% oxygen in nitrogen produced no change in QL/QT. However, lignocaine infusion during lobar ventilation with 7% oxygen in nitrous oxide produced a further reduction in QL/QT to a value which was not significantly different from that observed during ventilation with 7% oxygen in nitrogen. Lignocaine had no effect on QL/QT during lobar collapse whether the right lung was ventilated with 50% oxygen in nitrogen or 50% oxygen in nitrous oxide. It is concluded that lignocaine reverses the depression of hypoxic pulmonary vasoconstriction produced by lobar ventilation with nitrous oxide.
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PMID:Reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction by lignocaine hydrochloride during collapse and ventilation hypoxia of the left lower lobe. 395 25

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39


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