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)

Four experiments were carried out with 10 to 12 day old leghorn chicks weighing approximately 93 to 101 g. The chicks were injected intraperitoneally with sterigmatocystin (STG) dissolved in olive oil. The LD50 values as established in the first two experiments were 10.0 and 14.0 mg/kg body weight with most of the deaths occurring between 9 and 21 h following injection. Histopathological studies demonstrated that there was hemorrhage, foci of degeneration and necrosis with fibroblastic proliferation in sinusoids of the liver while the kidneys showed tubular degeneration and necrosis. Biochemical analysis of blood sera demonstrated that STG caused a marked elevation in the activities of lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase, and a depression of creatine kinase, but no effects on gamma-glutamyl transferase, amylase and lipase. Free and conjugated bilirubin were elevated in the sera while total protein, albumin, glucose, potassium, chloride and phosphorous concentrations were depressed. In addition, total white blood cells and circulating agranulocytes were depressed while circulating granulocytes were elevated. STG did not significantly affect the concentration of uric acid, cholesterol, triglycerides, calcium, magnesium and sodium in blood.
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PMID:Acute toxicity of sterigmatocystin to chicks. 356 71

A young woman taking tranylcypromine for depression was hospitalized with severe chest pain and hypertension after eating cheese. Electrocardiography initially showed arrhythmias and precordial ST segment depression. Myocardial creatine kinase values were elevated, and echocardiography showed regional ventricular dysfunction, suggestive of focal cardiac myonecrosis. The cardiovascular pathophysiology of tyramine hypertensive crisis and related catecholamine excess states, including pheochromocytoma and clonidine withdrawal, is reviewed. Cardiac myonecrosis is a potential adverse effect of the hypertensive crisis associated with monoamine oxidase inhibitor use. Psychiatric indications for monoamine oxidase inhibitors may be expanding, but clinicians should continue to exercise caution in the use of these agents.
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PMID:Cardiac myonecrosis in hypertensive crisis associated with monoamine oxidase inhibitor therapy. 357 43

Two growth experiments were conducted to evaluate in broiler chicks the compatibility between lasalocid medication in the feed (at 90 or 125 ppm) and a long-term administration of chloramphenicol either via the feed (500 ppm) or via the drinking water (500 mg/liter). The simultaneous administration of lasalocid and chloramphenicol generally caused severe growth depression, decreased feed intake and impaired feed conversion. Several chicks showed evident symptoms of intoxication, such as ataxia, leg weakness and paralysis. The development and frequency of these symptoms were dependent on the dosage of lasalocid and on the duration of the simultaneous administration. Biochemical examinations (Experiment 2) revealed in the affected chicks significant changes in several parameters, in particular a markedly increased activity of creatine kinase and GOT in the plasma. It confirmed that the observed leg weakness and paralysis were caused by myodegeneration.
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PMID:Incompatibility between lasalocid and chloramphenicol in broiler chicks after a long-term simultaneous administration. 359 Jun 19

Various experimental models were utilized to determine the in vivo cardiac actions underlying the presumptive therapeutic benefit of the naturally occurring adenine nucleoside, inosine. 1. In pentobarbital-anaesthetized dogs coronary vasodilator responses to arterial hypoxia were augmented and postanoxic depression of cardiac contractile force was prevented by i.v. infusion of inosine (5 mg X kg-1 X min-1). 2. Thermographic observations demonstrated in the in situ dog heart a significant inosine-induced epicardial warming (coronary flow increase) which was resistant to P1-purinergic blockade (aminophylline). 3. Following total cardiopulmonary bypass and cardioplegic cardiac arrest of 90 min duration in the dog, inosine administration (5 mg X kg-1 X min-1) evoked a lasting increase in myocardial contractile force and cardiac output. 4. In Langendorff perfused guinea pig hearts subjected to normothermic ischaemia of 1 hour duration and treated with inosine (0.05 mg X min-1), the release of cytoplasmatic enzymes (CK-MB, alpha-HBDH) and myoglobin was significantly less than in untreated ischaemic controls. In the two latter series of experiments (3 and 4) the inosine action was contrasted by the deleterious effect of catecholamines (noradrenaline and isoproterenol) administered in moderate or small doses, respectively. It was concluded that inosine has cardioprotective actions partly related to and partly independent of its influence on coronary blood supply, suggesting that administration of the nucleoside may be useful in various surgical attempts directed to myocardial salvage.
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PMID:Inosine increases anoxic tolerance and postischaemic restitution of the heart: experimental studies on possible mechanism(s) of action. 359 Nov 70

In 70 consecutive patients (pts) with acute transmural inferior infarction, 58 had significant precordial ST depression (group A) and the remaining 12 had no ECG changes in precordial leads (group B) on admission. At the time of hospital discharge, the persistence of anterior ST depression was observed in 13 pts (group A1), normalization in 45 (group A2). Infarct size was significantly greater (p less than 0.05) in group A than in group B (37.6 vs. 23.8 CK-MB gEq). The largest infarct (51.5 CK-MB gEq) and the most serious clinical course was observed in group A1. No significant differences were noticed in the frequency of reinfarction and episodes of acute coronary insufficiency during hospitalization and one-year follow-up between groups. Persistent precordial ST depression is a simple ECG marker of extensive infarction, left ventricular dysfunction and a worse clinical course.
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PMID:Significance of anterior precordial ST-segment depression in acute inferior myocardial infarction. 359 51

To determine the significance of the direction of ST segment deviation on admission of patients who evolved non-Q wave myocardial infarction (MI), 97 patients with initial ST segment depression were compared to 207 patients with initial ST segment elevation. Patients with ST segment depression developed smaller infarcts than those with ST segment elevation (creatine kinase MB isoenzyme 8.2 vs 13.3 gmEq/m2, p less than 0.002), but had a lower left ventricular ejection fraction on admission (44% vs 51%, p less than 0.001), more in-hospital complications, and a higher cumulative 1-year mortality (29% vs 11%, p less than 0.001) that could be accounted for by an excess of adverse baseline characteristics. Although a severity index (combining magnitude and extent of the initial ST segment deviation) was not useful for discriminating prognosis of patients with non-Q wave MI who presented with ST segment depression, it was useful in identifying a subgroup of patients with ST segment elevation with an adverse prognosis. The poor outcome of patients with non-Q wave MI presenting with either ST segment depression or severe ST segment elevation on admission suggests that patients in these subgroups should receive close surveillance and should possibly be considered for aggressive therapy.
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PMID:High-risk subgroups of patients with non-Q wave myocardial infarction based on direction and severity of ST segment deviation. 367 77

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.
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PMID:Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size. 367 99

Reciprocal ST segment changes are frequent during acute inferior myocardial infarction, yet their significance remains controversial. In order to investigate the implications of these changes, the ECG obtained on admission for 83 patients with acute inferior myocardial infarction was compared with the clinical course and the results of angiographic and coronary arteriographic studies performed an average of 3 weeks after the onset of symptoms. Group 1 consisted of 59 patients with at least 1 mm of horizontal on downsloping ST segment depression in at least 1 of leads V1 to V4. Groups 2 consisted of 24 patients without precordial ST depression in this area. Group 1 patients were generally older than group 2 patients (59.6 +/- 6.4 versus 54 +/- 5.3 yr, P less than 0.01) had higher total creatine kinase (CK) levels and MB fractions (1835 +/- 940 versus 875 +/- 305, P less than 0.01, 269 +/- 102 versus 95 +/- 35 for MB fraction) and more complications during the hospital course (80% versus 38% P less than 0.01) and greater left ventricular dysfunction (ejection fraction 52.2 +/- 6% for group 1 versus 59.2 +/- 7% for group 2; cardiac index 2.75 +/- 0.41 min-1 m-2 for group 1 versus 3.25 +/- 0.31 min-1 m-2 for group 2 P less than 0.005). No difference was observed on biplane angiography as far as left ventricular wall kinesis was concerned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reciprocal ST segment changes in acute inferior myocardial infarction: clinical, haemodynamic and angiographic implications. 369 49

The hypothesis that the toxic effects of imidocarb mediated by reduced cholinesterase activity might be intensified by hypomagnesaemia was tested in calves. Hypomagnesaemia was induced in 12 males (50 kg) using an artificial milk based on a commercial nondairy coffee creamer. Although plasma magnesium levels reached 0.33 mmol litre-1 in two weeks no clinical signs were detected. In 12 control calves a daily magnesium supplement of 0.6 g was inadequate although the published requirement is 0.45 g; it was raised to 1.2 g to keep plasma magnesium normal. Lighter calves developed hypomagnesaemia more readily and fast-growing calves had lower plasma urea concentrations. Plasma calcium, but not plasma magnesium, showed significant positive correlation with plasma albumin. The only statistically significant effects of hypomagnesaemia were slight elevations of white cell count and plasma sodium. The hypomagnesaemic and normomagnesaemic calves were divided into two equal groups and treated with 3.3 mg kg-1 of imidocarb dipropionate or a placebo. The drug produced the expected clinical signs of mild toxicity and depression of cholinesterase but no other adverse effects. Transient slight depressions of plasma calcium and potassium concentration, a transient rise of plasma sodium and elevation of creatine kinase occurred. None of the effects of imidocarb treatment was intensified by hypomagnesaemia except, perhaps, constriction of the pupils; generally, hypomagnesaemic animals were affected less.
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PMID:Effect of induced hypomagnesaemia on the toxicity of imidocarb in calves. 370 46

The relations between reciprocal ST segment depression in the electrocardiogram and infarct size and 10 year prognosis were studied in 315 patients who survived for at least 28 days after a first anterior or inferior myocardial infarction. ST depression was more common in inferior infarcts (72%) than in anterior (37%) ones. It occurred more frequently in complicated infarcts and in the presence of considerable ST elevation. Patients experiencing second or third degree heart block were significantly more likely to show reciprocal changes. The rise in peak cardiac enzyme concentration was higher in patients showing ST depression. In patients with ST depression, peak creatine kinase concentration was 46% higher, aspartate aminotransferase was 39% higher, and lactate dehydrogenase 29% higher after correction for site and complications. A discriminant function analysis selected infarct site, peak aspartate aminotransferase, and magnitude of ST elevation as predictors of the occurrence of ST depression. Age, severity, and smoking status did not significantly improve discrimination. Despite larger increases in peak enzyme concentrations patients with ST depression had marginally fewer subsequent episodes of unstable angina or fatal or non-fatal infarction and a marginally lower 10 year death rate. Neither difference was statistically significant. ST depression occurring early in the acute phase of myocardial infarction is likely to be a reflection of electrophysiological changes taking place at the site of the infarct that is manifested in the contralateral surface of the heart. Other causes, however, such as transient ischaemia at the site of the reciprocal changes or extension of the infarct to contiguous areas cannot be excluded in all cases.
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PMID:The aetiology and prognostic implications of reciprocal electrocardiographic changes in acute myocardial infarction. 370 82


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