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)

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

The antifibrillatory and electrophysiologic actions of bepridil and butyl-methylenedioxyindene (BU-MDI), two intracellular calcium antagonists, were examined in anesthetized dogs. The administration of bepridil (1.0-10.0 mg/kg i.v.) significantly increased the electrical threshold for ventricular fibrillation determined during unobstructed coronary flow, and was associated with a significant decrease in ventricular excitability and a progressive depression in ventricular myocardial conduction. BU-MDI (3.0-30.0 mg/kg i.v.) did not significantly alter ventricular fibrillation thresholds during unobstructed coronary flow, nor did it significantly alter electrophysiologic properties such as ventricular excitability, conduction or refractoriness. The administration of either bepridil (10 mg/kg i.v.) or BU-MDI (30 mg/kg i.v.), however, resulted in significant increases in the ventricular fibrillation thresholds determined during transient myocardial ischemia, restoring the threshold values to corresponding non-ischemic levels. These results suggest that an inhibition of the action and/or availability of intracellular calcium may play a role in the antifibrillatory actions of BU-MDI and bepridil during transient ischemia.
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PMID:Antifibrillatory actions of bepridil and butyl-MDI, two intracellular calcium antagonists. 387 80

Pulmonary artery balloon counterpulsation was instituted in 10 pigs when right ventricular failure limited cardiac output. Global myocardial depression was produced by infusion of propranolol, and the left ventricle was fully supported by left heart bypass. A stable model of failure was achieved in six pigs. Following application of pulmonary artery balloon counterpulsation right atrial pressure decreased from 18.2 +/- 2.1 to 15.9 +/- 2.5 mm Hg (p less than 0.05). Cardiac output increased from 416 +/- 94 to 758 +/- 127 ml/min (p less than 0.001). Right ventricular stroke work increased from 0.29 +/- 0.07 to 0.65 +/- 0.12 gm X m. (p less than 0.05). There was no cardiac output before or after institution of balloon counterpulsation in four pigs studied during ventricular fibrillation or asystole. We conclude that pulmonary artery balloon counterpulsation improved cardiac output and right ventricular stroke work in a model of right ventricular failure where the pulmonary circulation was unaltered and the left ventricle supported by left heart bypass. Balloon counterpulsation was not effective during ventricular fibrillation or asystole. Pulmonary artery balloon counterpulsation should be considered when right ventricular failure limits cardiac output during left heart bypass.
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PMID:Pulmonary artery balloon counterpulsation in the management of right heart failure during left heart bypass. 396 9

A 61 year old male with left main coronary artery disease died suddenly during ambulatory Holter monitoring. The monitoring documented ST depression followed by ST elevation, followed by junctional and ventricular escape rhythms with no measurable blood pressure by cuff methods. The mechanism of sudden death in patients with left main coronary artery disease is thought to be a combination of ventricular fibrillation or bradyarrhythmia and electromechanical dissociation secondary to a sudden onset of severe pump failure.
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PMID:Sudden death during ambulatory monitoring in a patient with left main coronary artery disease. 408 77

1. In cats anaesthetized with chloralose, repeated injections of 20 mug ouabain were made either into the cerebral ventricles, or into the ventromedial nucleus of the hypothalamus (VMH), or intravenously whilst the electrocardiogram, arterial blood pressure and respiration were recorded.2. The injections produced cardiac arrhythmias preceded by sinus bradycardia, variable changes in arterial blood pressure and respiratory depression. Death occurred either from ventricular fibrillation or from cardiac arrest.3. The arrhythmias which occurred after the injections into the cerebral ventricles were not peripheral effects produced after absorption of the ouabain into the blood stream, because with intravenous injections larger amounts were required to produce the arrhythmias and to cause death than with intraventricular injections. The arrhythmias which resulted in death were due to an action on the VMH. With microinjections of ouabain into this region of the brain death occurred earlier and after smaller doses than after intraventricular injections.4. While sinus bradycardia was abolished by bilateral vagotomy other cardiac arrhythmias were prevented by acute cardiac sympathectomy and cervical cord transection. Thus both the sympathetic and parasympathetic nervous systems appear to be involved in the production of these arrhythmias.5. Since some of the cardiac arrhythmias obtained with ouabain in anaesthetized cats resemble the cardiotoxic effects seen in clinical practice during treatment with digitalis glycosides it is concluded that these effects, too, are, at least in part, central in origin, caused by an action on the VMH and mediated mainly via the sympathetic nervous system.
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PMID:Effects of microinjection of ouabain into the hypothalamus in cats. 504 46

1. Both MJ 1999 and AH 3474 protected guinea-pigs anaesthetized with urethane against ouabain-induced ventricular fibrillation.2. MJ 1999 had 1/90, and AH 3474 1/30, of the activity of procaine in reducing the height of the action potential of frog sciatic nerve.3. MJ 1999 and AH 3474 reduced the rate of rise of intracellularly recorded action potentials at concentrations in excess of 160 x 10(-6)M (50 mg/l.). It was concluded that direct depression of depolarization could have contributed little to the protection against ouabain-induced fibrillation.4. MJ 1999, but not AH 3474, greatly prolonged the duration of the action potential in acute experiments on isolated atrial and ventricular muscle, and prolonged the Q-Tc interval of the electrocardiogram in anaesthetized guinea-pigs. It is suggested that this effect contributes to anti-arrhythmic activity.5. At concentrations up to 80 x 10(-6)M AH 3474 had positive chronotropic and inotropic effects on isolated rabbit atrial muscle, but at higher concentrations these were superseded by negative effects. MJ 1999 was depressant at all concentrations studied, the threshold concentrations being 19 x 10(-6)M for chronotropic, and 162 x 10(-6)M for inotropic effects.
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PMID:A third class of anti-arrhythmic action. Effects on atrial and ventricular intracellular potentials, and other pharmacological actions on cardiac muscle, of MJ 1999 and AH 3474. 548 44

Mitral valve prolapse is usually a benign affection, and yet but rather seldom, severe rhythmic troubles and even a sudden death may happen. The authors relate an observation about a seventeen years old young man presenting syncopes caused by ventricular fibrillation fit. The existence of a mitral valve prolapse is demonstrated by phonomecanogram and specially by echocardiogram which shows a telesystolic depression of the small valve. The observation is followed by commentaries about the frequency and clinic of Barlow syndrome. The rhythmic troubles liable to accompany this mitral damage are analysed and so is the evaluation of the risk of a sudden death by ventricular fibrillation.
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PMID:[Mitral valve prolapse and severe rhythmic trouble (author's transl)]. 625

Changes in conduction times induced by ischemia (delta CT) have been shown to be quantitatively related to genesis of spontaneous ischemic ventricular fibrillation (VF). We studied conduction delay encountered by premature impulses in epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion in eight control and in eight verapamil treated dogs. Acute myocardial ischemia was produced by single-stage ligation of left anterior descending artery below second diagonal initially, and 30 minutes later below first diagonal branch. In treated dogs, verapamil was given, 0.15 mg/kg intravenous bolus, immediately after first ligation and was followed by an infusion of 7.5 micrograms/kg/min. Thus post-treated segment and pretreated segment were obtained in the same animal. delta CT was compared between control and treated dogs in four myocardial zones: (1) normal, (2) ischemic including pre- and post-treated segments, (3) reperfused, and (4) border of reperfusion or ischemia. Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium. In addition, in the border of ischemia retrograded conduction showed significantly less depression during ischemia and reperfusion. The protective effect of verapamil was impressive both in pretreated and post-treated segments of ischemic myocardium. We conclude that verapamil offers significant protective action with regard to ischemia-induced conduction delay. Since delta CT is quantitatively related to ischemic VF, verapamil can be antiventricular fibrillatory in myocardial ischemia.
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PMID:Effect of verapamil on conduction delay produced by myocardial ischemia and reperfusion. 626 20

In acute myocardial infarction depression of the ST segment in leads distant from those showing ST elevation has been considered to be "reciprocal" but might reflect local ischaemia. To examine this possibility 103 consecutive patients who underwent exercise testing early after myocardial infarction were reviewed. Treadmill exercise testing was performed a mean of 12 (range 5-30) days after infarction using a limited Naughton protocol. Thirty five (34%) of the patients had had reciprocal change, defined as greater than or equal to 1 mm ST depression in leads remote from the site of the infarct, within 48 hours of infarction. Twenty two (63%) of the 35 patients developed exercise induced ST depression in the leads previously showing reciprocal change. Coronary artery disease was assessed in 10 of these patients by arteriography and in four at necropsy: all but one had stenosis of greater than or equal to 50% in a coronary artery supplying the reciprocal territory in addition to the disease in the vessel to the infarct site. Of patients with reciprocal ST depression, 23.5% experienced nonfatal reinfarction, pulmonary oedema after discharge, or death compared with only 9.5% of patients without reciprocal ST depression. Eight (23.5%) patients with reciprocal depression had ventricular fibrillation while in hospital compared with only two (3%) patients without. Reciprocal ST depression in acute myocardial infarction may reflect ischaemia in territory distant from the site of infarction and is associated with a high risk of fatal arrhythmias and late morbidity.
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PMID:"Reciprocal" depression of the ST segment in acute myocardial infarction. 641 Dec 61

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
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PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79


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