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)

Drug-addicts frequently suffer from pulmonary diseases, particularly those who practice self-injection of the drugs intravenously. Emphasis is at present laid on the various excipients which are thought to induce acute alveolitis with subsequent acute pulmonary oedema in heroin-addicts. It has also been suggested that the deep ventilatory depression that precedes pulmonary oedema may play a part and this is interesting since the depression can now be prevented with naloxone. Infectious lesions, such as septic pulmonary embolism or endocarditis, are easier to explain. The ever increasing use of tablets crushed for injection is responsible for peri-arteriolar granulomas of the lung with possibly severe sequelae. Finally, the almost generalized consumption of marihuana in the United-States has led to the discovery of new properties of this drug, including ventilatory stimulation and broncho-dilatation. However, this is mostly of theoretical interest. The psychotropic effects of marihuana and its irritant effect on the bronchi when inhaled make it unlikely that it will be ever be used for therapeutic purposes.
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PMID:[Pneumopathies in drug addicts]. 663 69

Cases of fatal poisoning with cupric compounds are relatively rare in everyday life and are not covered much in forensic literature. A case was encountered of fatal poisoning with a blue vitriol solution introduced into the uterine cavity in order to interrupt a pregnancy. A 39-year-old woman brought to the hospital by ambulance complained of pain in the lumbar region and profuse bloody genital discharge, which had appeared 3 days earlier. She believed she was 2 months pregnant and denied artificial interruption of the pregnancy. Upon examination, her condition was grave: a weak pulse of 80; blood pressure 100/60. The abdomen was soft, the liver and spleen not enlarged. Pasternak symptom was negative. The uterus was soft, painless and enlarged to 9 weeks of pregnancy. The uterine cervix was clean, the orifice closed. Discharge was profuse and bloody. The diagnosis was that she was 9 weeks pregnant and had a missed criminal abortion. Scraping out the uterus and corresponding therapy to control bleeding were ineffective. An operation was performed--extirpation of the uterus. However, despite the steps taken, the bleeding did not stop, and the patient's condition continued to worsen. 10 hours after being admitted to the hospital, she died. During forensic investigation, diffused, violet-colored cadaverous spots were discovered. Extensive subcutaneous hemorrhage was detected around the areas of injection. The skin covering was edematous; when pressed with a finger, areas of depression remained. There was about 250 ml of watery blood in the abdominal cavity. Internal organs were anemic. There were multiple subpleural, subepicardial, subcapsular, intraorgan and intramuscular micro- and macro-punctate hemorrhages; bleeding into the mucosa of the gastrointestinal tract and urinary tracts; and cerebral and pulmonary edema. Forensic histological examination showed acute circulatory disturbance with perivascular and peridiapedetic hemorrhage; concentrations of aggregated and hemolyzed erythrocytes in the small vessels and capillaries; cerebral, pulmonary and stromatic edema. In the kidneys there was coaugmentation of renal glomeruli; epithelial necrosis of part of the coiled ducts; lower epithelium in places had pigment grains; primarily in openings of straight ducts there were pigment cylinders; extreme plethora of the surrounding area, and infiltration from annular cells and polynuclears. Forensic chemical analysis showed 12.8 mg of copper; 6.6 mg in the uterus and 5.6 mg in the kidneys. From data obtained it can be concluded that the patient died from cupric compound poisoning, complicated by interruption of the pregnancy and uterine hemolytic hemorrhage. It was later established that during the month before being admitted to the hospital the patient introduced a solution of blue vitriol into the uterine cavity to interrupt the pregnancy.
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PMID:[Fatal poisoning with blue vitriol]. 663 45

3-Methylindole (3MI), a ruminal fermentation product of tryptophan, is the causative agent in the development of acute bovine pulmonary edema (ABPE). The disease is dependent on the activation of 3MI by mixed function oxidases (MFO). Electron micrographs have revealed that the lamellar bodies of the type II cells are disrupted in structure and contain neutral lipids (NL) instead of surfactant phospholipids (PL). Goat lung slices were used to investigate the changes in PL metabolism induced by 3MI. Eighteen slices were cut from each lung and divided into control, 3MI (0.57 mM), and indole (0.57 mM) groups. After a 3-hr pretreatment with these compounds, the slices were incubated with [14C]acetate. The lipids were extracted and separated. 3MI inhibited the incorporation of [14C]acetate into all of the PL studied, but had little effect on its incorporation into NL. Indole displays the same effects on membranes as 3MI, but is not activated by the MFO system and does not induce lung injury. Indole pretreatment had little effect on acetate incorporation in any of the lipid fractions. These results indicate that metabolism of 3MI in lung slices is responsible for the depression of PL synthesis in vitro. Increasing the level of unlabeled choline in the medium from 10 microM to 10 microM had no effect on the depression of [14C]acetate incorporation into phosphatidylcholine (PC). This suggests that choline uptake is not limiting the synthesis of PC in the 3MI-treated lung slices.
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PMID:The effect of 3-methylindole on phospholipid synthesis in goat lung tissue slices. 669 67

Of 1,994 yearling and 2-year-old cattle in a winter feeding program, 117 died within 42 days of being fed toxic amounts of monensin sodium in a liquid protein supplement. Death losses commenced on the third day after ingestion of a toxic amount in the feed. Clinical signs in cattle that died in less than 9 days included anorexia, pica, diarrhea, depression, mild hindlimb ataxia, and dyspnea. Gross necropsy findings in cattle dying in the acute phase of the illness included hydrothorax, ascites, and pulmonary edema, as well as petechial hemorrhages, edema, and yellow streaking in skeletal and cardiac muscle. Cattle dying after 9 days had gray streaks in heart and skeletal muscle, generalized ventral edema, enlarged, firm, bluish discolored liver, and enlarged heart. Microscopic changes in cattle dying in the acute phase (less than 9 days) consisted of pulmonary edema, congestion, and hemorrhage. Cardiac and skeletal muscle had localized areas of edema, hemorrhage, and coagulative necrosis. In cattle dying after 9 days of illness, the changes included lymphocytic infiltration, sarcolemmal nuclear proliferation, and fibrosis in skeletal and cardiac muscle. Lungs contained increased alveolar macrophages and a few neutrophils. Centrilobular necrosis and mild fibrosis were found in the liver. Changes varied somewhat according to the area of heart or skeletal muscle that was affected. Active muscles, eg, those in the heart ventricles and diaphragm, were altered most severely. Intoxication appeared to be a result of sedimentation of monensin in the molasses carrier to give remarkable concentrations of the substance at the bottom of the holding tank.
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PMID:Accidental monensin sodium intoxication of feedlot cattle. 673 46

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.
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PMID:Acute monensin toxicosis in sheep: light and electron microscopic changes. 674 73

Pulmonary injury caused by alpha naphthylthiourea (ANTU) is characterized by alterations of the capillary endothelial barrier followed by lung edema. Because pulmonary uptake of 5-hydroxytryptamine (5-HT) is dependent upon active transcellular transport by lung endothelium, it may be an index of early impairment of endothelial function caused by ANTU. We studied the effect of a single intraperitoneal dose of 5 or of 10 mg/kg of ANTU on pulmonary uptake of 5-HT by isolated rat lungs. Four h after the administration of ANTU, when lung tissue structure and dry-to-wet-weight ratios were comparable to those of control animals, 5-HT uptakes were significantly reduced (p < 0.05). Twenty-four h after the administration of ANTU, when lung edema was present on histologic examination and by lung weights, 5-HT uptakes were further reduced. They returned to control values 14 days after the administration of ANTU. Depression of 5-HT uptake is an early and reversible alteration of lung endothelial cell function caused by ANTU. Uptake of 5-HT may provide a sensitive probe with which to detect and evaluate pulmonary endothelial cell injury caused by toxicants.
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PMID:Effect of alpha naphthylthiourea on uptake of 5-hydroxytryptamine from the pulmonary circulation. 677 86

We present a case of acute lithium ion intoxication in which the main clinical feature was respiratory failure secondary to pulmonary oedema possibly due to myocardial depression, associated with profound stupor. The initial lithium ion concentrations were 3.15 mmol/l in plasma and 27.6 mmol/l in urine. Under symptomatic treatment with oxygen, digitalis and diuretics, both the pulmonary and the neurological disorders reverted gradually, in parallel with the decreasing plasma lithium ion concentrations.
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PMID:Acute pulmonary oedema due to lithium intoxication. 680 41

Two patients are described who developed acute pulmonary oedema: the first following a grand mal epileptic seizure of idiopathic origin, the second following electric shock therapy (ECT) for depression. Neither patient had any detectable underlying cardiopulmonary disease. The first patient recovered spontaneously but the second patient died of fulminant pulmonary oedema. This is the first report of neurogenic pulmonary oedema following ECT.
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PMID:Acute pulmonary oedema following grand mal epilepsy and as a complication of electric shock therapy. 680 34

Heart failure is associated with a reduction in tissue norepinephrine concentration, catecholamine fluorescence, and tyrosine hydroxylase activity. We hypothesized that this attrition of sympathetic nerve function might also be associated with a reduction in the ability of the neuronal membrane to sequester catecholamines. Since the heart does not release epinephrine, the cardiac extraction of epinephrine should be an index of the membrane uptake system. In 12 patients with documented left ventricular failure (pulmonary edema) secondary to mechanical overload and in 10 patients with no history of heart failure, we measured simultaneous plasma catecholamine concentrations in the aorta, coronary sinus, and femoral vein. The aortocoronary sinus extraction of epinephrine was 43 +/- 17% in the group with no evidence of heart failure but 0 +/- 14% in the group with failure. Net norepinephrine outflow (release minus extraction) was significantly higher in the group with failure, possibly because of reduced extraction. There was neither a reduction in the ability of the lower limb to extract epinephrine nor an increased norepinephrine outflow from the limb. These findings suggest that the sympathetic neuronal membrane uptake system is also depressed in the failing heart and that if the mechanism of catecholamine sequestration in the heart is related to that in the lower limb, the ablation of sympathetic nerve function is specific to the heart and is not a result of a generalized depression of the peripheral sympathetic nervous system.
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PMID:Reduced aortocoronary sinus extraction of epinephrine in patients with left ventricular failure secondary to long-term pressure or volume overload. 686 2

Supplemental albumin added to a standard non-albumin resuscitation regimen has been shown to significantly impair heartwork in seriously injured patients. The role of calcium dynamics in this myocardial depression was analyzed in 94 injured patients who were in shock for an average of 32 minutes, received an average of 14.5 transfusions, 9.2 L crystalloid, 0.9 L plasma, and 20.9 mEq calcium prior to the end of operation. By random selection, 44 patients received an average of 31 gms of albumin during operation, 207 gms during the early postoperative period (mean = 30 hrs) of extravascular fluid sequestration, and 402 gm during the mobilization period. The albumin resuscitated patients had normal total protein and serum albumin levels and higher total calcium (TC) levels, however, they had a significantly lower Ca++ and Ca++/TC. The accumulative slope for heartwork/filling pressure was significantly depressed in albumin patients as was the mean work unit/filling pressure index. The level of Ca++ and the Ca++/TC ratio correlated directly with the calculated work unit index in both the albumin and non-albumin patients. This suggests that a supplemental albumin binds serum Ca++ causing an increase in TC but a reduction in Ca++ and Ca++/TC. The fall in Ca++ and Ca++/TC seems responsible, in part, for heart failure and pulmonary edema in albumin resuscitated patients.
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PMID:The cardiac effect of altered calcium homeostasis after albumin resuscitation. 721 93


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