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)

Substances that are inhaled for the purpose of recreational self-intoxication include aliphatic hydrocarbons, alkyl halides, alkyl nitrites, aromatic hydrocarbons, ethers, and ketones. All have the ability to cause asphyxia, arrhythmias, cardiovascular depression, neurologic dysfunction, and mucosal, pulmonary, and skin irritation following acute exposure and permanent neurologic damage with chronic exposure. The acute effects of alkyl halides and alkyl nitrites also include carbon monoxide poisoning and hepatorenal toxicity, and methemoglobinemia, respectively. Chronic exposure to aromatic hydrocarbons and ketones can result in liver, kidney, and bone marrow injury; myopathy, rhabdomyolysis, metabolic acidosis, and electrolyte abnormalities are further complications of chronic aromatic hydrocarbon inhalation.
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PMID:Volatile substances of abuse. 220 21

The basis for management of all complications is early recognition, preparation, and a problem-solving approach. Some anesthetic complications, such as equipment malfunction and injuries from endotracheal intubation or misplaced drug injections, are common to all animals and can be prevented almost entirely by careful management. Other problems, such as pulmonary dysfunction and cardiovascular depression, seem to occur more often in healthy horses than in healthy members of other domestic species. Postoperative myopathy-neuropathy, sometimes a devastating complication, seems to be peculiar to the horse, and its incidence has been linked to hypotensive inhalant anesthesia. Careful positioning and padding, monitoring of anesthetic depth, and treating of cardiovascular depression may prevent most cases of postanesthetic myopathy. Idiosyncratic drug reactions, such as MH, are entirely unpredictable and can be rapidly fatal unless recognized early and treated vigorously and specifically.
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PMID:Anesthetic complications in the horse. 228 54

Tissue and plasma levels of thiobarbituric acid reactive substances (TBARS) were measured in rats treated chronically with doxorubicin. In addition, heart creatine phosphokinase and antioxidant defenses were examined. Male rats received doxorubicin (DXR) 2 mg/kg or vehicle weekly subcutaneously for 13 weeks and were sacrificed at 14 and 19 weeks, 1 and 6 weeks after the last dose, respectively. Histological evaluation in DXR-treated rats at 14 and 19 weeks found significant and progressive cardiac and renal lesions as compared to controls. Heart TBARS were unchanged from controls. Plasma and kidney levels of TBARS were elevated above controls at both 14 and 19 weeks. Lung levels of TBARS were significantly elevated above controls at 14 weeks. Liver levels of TBARS were elevated at 19 weeks. Heart creatine phosphokinase activity was significantly depressed from controls at both 14 and 19 weeks. Heart glutathione peroxidase and superoxide dismutase activities were unchanged from controls. Heart glutathione, glutathione reductase, glucose-6-phosphate dehydrogenase, and catalase were elevated above controls at both 14 and 19 weeks. The lack of change in heart TBARS suggests that changes in TBARS in other organs may be secondary processes. The depression of creatine phosphokinase suggests that levels of adenosine triphosphate may be insufficient to sustain the myocardial function and this may partly be responsible for DXR-induced cardiac myopathy.
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PMID:Effects of chronic administration of doxorubicin on myocardial creatine phosphokinase and antioxidant defenses and levels of lipid peroxidation in tissues and plasma of rats. 259 35

The effects of four Ca2+ binding protein modulators (bepridil, perhexiline, calmidazolium and trifluoperazine) on cardiac myofibrillar ATPase activity in Triton-purified myofibrils prepared from normal dogs, normal hamsters and age/sex (male, 16-20 weeks)-matched myopathic hamsters (BIO 14.6) have been quantitated. When compared with normal hamsters, myopathic hamster myofibrils have a markedly depressed maximum MgATPase activity (178 +/- 2 vs. 119 +/- 3 nmol/mg per min, respectively) and a slightly increased requirement of Ca2+ for half-maximal activation (ED50; 0.66 vs. 0.75 microM free Ca2+, respectively). Calmidazolium, trifluoperazine and bepridil lower the ED50 for Ca2+ in myopathic myofibrils. Moreover, bepridil and trifluoperazine increase maximum myofibrillar MgATPase activity in myopathic hamster myofibrils. In contrast, calmidazolium depresses maximum and stimulates basal MgATPase activities in myopathic and normal hamster myofibrils. Qualitatively, different effects are apparent when these agents are examined in canine myofibrils. Thus, the pharmacological effects of Ca2+ binding protein modulators on cardiac myofibrillar ATPase activity are dependent upon species and/or pathological state. It is possible to directly enhance a pathological consequence of cardiac myopathy, depression in maximum myofibrillar MgATPase activity, with pharmacological agents.
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PMID:Differential effects of pharmacological modulators of cardiac myofibrillar ATPase activity in normal and myopathic (BIO 14.6) hamsters. 296 69

A case is presented of a young female with a paraneoplastic subacute cerebellar degeneration, parkinsonian syndrome, autonomic disturbance, profound depression, myopathy and cardiomyopathy. Her paraneoplastic affection preceded the actual detection of carcinoma of the breast by nine months. Block dissection of the carcinoma resulted in alleviation of her muscle weakness and a return of the electrocardiogram to normal.
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PMID:Neurological and cardiac complications of carcinoma of the breast. Case report. 300 85

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
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PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87

Premature uterine contractions were treated by intravenous beta-mimetics in 190 patients during a 2-year period. History and physical examination were directed toward identification of patients with cardiac problems. Unexpected cardiac pathology was discovered in 14 patients, all of whom exhibited severe and continuous nausea, retrosternal pain, or dyspnea during beta-mimetic administration. Treatment was immediately discontinued in the presence of S-T depression, supraventricular tachycardia, nonspecific T wave changes, and sinus tachycardia with right axis deviation. Further investigation revealed obstructive cardiac myopathy in one case and atrial septal defect in another. Such changes might be identified earlier by more extensive screening procedures (such as electrocardiogram) before drug administration. Administration of beta-mimetic agents may uncover previously unexpected cardiac pathology. Continuation of ritodrine in such cases is contraindicated and potentially hazardous.
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PMID:Unexpected cardiac pathology in pregnant women treated with beta-adrenergic agents (ritodrine). 668 69

Day-old white Leghorn chicks were fed P. citrinum-contaminated corn at 3.88, 7.75, 31, or 62% levels in the ration for a period of 5 weeks. High treatment levels (31 and 62%) of contaminated corn in the ration caused severe growth depression, high mortality, and significant decreases in feed consumption. Necrosis of periportal and centrilobular hepatocytes, glomerular atrophy and hyperplasia, degeneration and necrosis of tubular cells, lymphoid depletion, suppression of hematopoiesis, necrosis of pancreatic acinar cells, and a cardiac and skeletal myopathy were observed microscopically in chicks fed 31 and 62% contaminated corn in the rations. Low levels of contaminated corn in the ration (3.88 and 7.75%) caused few clinical effects; however, liver and kidney changes were observed microscopically. Ultrastructural observation of affected tissues showed swelling of mitochondria, dilatation of the endoplasmic reticulum, increased numbers of autophagic vacuoles and paramyelin figures, and lipoprotein peroxidation of organelles. The toxin (s) present in the P. citrinum contaminated ration have not been identified.
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PMID:Noncitrinin toxicity of Penicillium citrinum contaminated corn. 713 17

A patient with hyperkalemic periodic paralysis experienced the gradual onset of additional and unexpected neurologic abnormalities in middle age, suggestive of progressive supranuclear palsy. Although the concurrence of these findings may be coincidental, these features may evade recognition in other patients by being misattributed to chronic myopathy or depression.
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PMID:Progressive supranuclear palsy and hyperkalemic periodic paralysis. 738 97

A patient with a coup de sabre lesion of the forehead developed progressive ipsilateral limitation of ocular motility, primarily involving adduction and depression. Investigation disclosed no other explanation for the ocular motility disturbance, which we suspect represents restrictive myopathy maximally involving ocular muscles immediately subjacent to the area of linear scleroderma.
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PMID:Restrictive ophthalmopathy associated with linear scleroderma. 755 Sep 36


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