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)

Factors that contribute to the lethality of amitriptyline overdosage were studied in cats. Amitriptyline (50 mg/kg) given i.p. to unanesthetized cats produced convulsions in all of the animals and death in five of six animals; pretreatment with diazepam (5 mg/kg) protected against the convulsions and death. Respiratory depression contributed to the mortality when amitriptyline was given i.v. in cats anesthetized with pentobarbital as indicated by the finding that artificial respiration delayed the time of death induced by a continuous i.v. infusion of the drug. The i.v. infusion of amitriptyline in pentobarbitalized cats under artificial respiration produced death due to cardiovascular collapse. The latter was characterized by hypotension, bradycardia, depression of myocardial contractile force, atrioventricular block, intraventricular conduction delay and cardiac arrhythmias. These effects appear to be due to a direct membrane (quindine-like) cardiotoxic action of amitriptyline. Dopamine and dobutamine were effective in protecting the animals against the acute cardiovascular collapse induced by amitriptyline. The protection was associated with a diminution of the hypotension, the negative inotropic and chronotropic actions and the incidence of atrioventricular block produced by the tricyclic antidepressant drug. The results suggest that the positive chronotropic, inotropic and dromotropic actions of the amines may all be contributory factors in their protection action. Isoproterenol and norepinephrine were less effective than the other two amines.
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PMID:Protective action of diazepam and of sympathomimetic amines against amitryptyline-induced toxicity. 709 63

Thirty patients with variant angina pectoris (VAP) were analyzed for electrocardiographic features during episodes of VAP. Twenty-nine of these patients had cardiac catheterization, and an autopsy study was performed in one. The patients showed predominantly concave upright T-waves during pain. An increase of R wave amplitude (expressed as delta R) of more than 10% was seen in 17/30 patients (57%). The primary ST-T changes produced by the VAP episodes were conspicuous in two patients with pre-existent complete left and right bundle branch block. Serious dysrhythmias, including ventricular fibrillation (VF), ventricular tachycardia (VT), ventricular premature beats (VPBs) (more than five/min, multifocal and R on T phenomenon), and 2 degrees atrioventricular block were found in thirteen patients (43%). The development of dysrhythmias was related to the duration of VAP episodes. The average time to onset of dysrhythmias was 3.54 min. The dysrhythmias were not contingent upon pre-existing coronary artery anatomy (defined by Friesinger's coronary score), left ventricular ejection fraction or left ventricular segmental abnormalities. The location of the ST-segment elevation and the presence of dysrhythmias during the episodes of VAP (A-V blocks, ventricular tachycardia and fibrillation) were not predictive factors of the coronary anatomy. Eight patients (27%) developed myocardial infarction (MI). Five of them had nontransmural MIs and three developed transmural MIs. The development of MI was not related to the severity of the VAP attacks (appreciated by the magnitude of ST-segment elevation and R wave changes) but showed a relation to the development of an unstable pattern which preceded the infarction. Sixteen patients underwent exercise testing. In eight of them, the coronary arteriograms were normal (Group I); in the remaining eight, significant proximal coronary artery obstructive disease was found (Group II). Group I patients displayed a normal ST-segment response and functional aerobic capacity (FAI = 4.4 +/- 14) as well as normal heart rate (HR) and double product (SBP X HR) responses (HR = 154 +/- 21; SBP X 21; SBP X HR = 290 +/- 71). During exercise, a normal delta R was observed. With one exception, Group II patients showed an abnormal ST-segment response with an overall low exercise capacity (FAI = 57 +/- 17) and decreased hemodynamic response (HR = 27; SBP X HR = 130 +/- 40). FAI, HR, SBP X HR Group I vs. Group II = P less than .005/less than .02/less than .005. The abnormal ST-segment response included elevation in four patients and depression in three. During exercise, Group I with ST-elevation displayed a normal (negative) delta R response; while Group II with ST-depression displayed an abnormal delta R response (positive or no change). There was no difference in the coronary score between Group II patients with ST-segment elevation or depression.
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PMID:Prinzmetal's variant angina: electrocardiographic and angiographic correlations. 714 73

Factors influencing serum digoxin concentrations, and the relation of these levels to classical electrocardiographic (ECG) and clinical manifestations of toxicity, were assessed in a series of 463 consecutively hospitalized patients of mean age 58 years. The majority of patients were receiving beta-acetyldigoxin or beta-methyldigoxin. Age, sex, creatinine clearance, and weight-corrected dose collectively explained less than 7% of overall variability in serum digoxin concentrations; creatinine clearance, which declined significantly with age (r=-0.36, p less than 0.001) was the most important of these determinants. ST-segment depression was present in the majority of patients and became more common at higher serum digoxin concentrations. However, PR interval, QRS durations, QT interval, or the presence of AV block were not associated with serum levels. Among 75 patients with atrial fibrillation, ventricular rate did not decline with increasing digoxin concentrations. The presence of gastrointestinal, neuromuscular, or psychiatric symptoms classically attributed to digitalis toxicity was not associated with serum digoxin concentration. Serum levels of digoxin appear to be of limited value in assessing the degree of digitalization.
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PMID:Clinical implications of serum digoxin concentrations. 724 50

Effects of local anesthetics (procaine, lidocaine, prilocaine, mepivacaine and bupivacaine) on AV conductivity were studied using a direct perfusion technique of the canine AV node artery in situ. The agents induced dose-dependent depression of AV conductivity in doses between 100 microgram and 3 mg. The depression was assumed to have resulted from their direct action on the AV node, since it was not affected by prior administration of atropine or tetrodotoxin into the AV node artery. The order of potency to suppress AV nodal conductivity evaluated from ED50 for causing first to third degrees of AV block was bupivacaine greater than mepivacaine = prilocaine = lidocaine greater than procaine with a relative potency ratio of 5 : 2--2.5 : 1.
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PMID:Comparative study of the action of local anesthetics on AV conductivity of dog heart in situ. 728 50

The electrophysiologic effects of diltiazem, a calcium antagonistic agent, were studied in 30 subjects with various degrees of sinus or AV node dysfunction. After diltiazem was administered, sinus activity was not depressed in control subjects, whereas marked inhibition was observed in some of the patients with sick sinus syndrome. Ventricular automaticity was little affected by this drug. The AV conduction system was significantly depressed, and there was no difference in degree between controls and AV block patients. The depression of the AV conduction system became more marked as the basic atrial cycle length was shortened. The drug had no apparent effects on atrial refractoriness, atrial echo zone, or the accessory pathway system. Conclusively, diltiazem affects mainly sinus and AV conduction systems. Its effect on the sinus mode may provide a hazardous problem in patients with the sick sinus sysdrome patients, while its effect on the AV node will have therapeutic value in patients with AV nodal re-entrant arrhythmias.
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PMID:Electrophysiologic effects of diltiazem, a calcium antagonist, in patients with impaired sinus or atrioventricular node function. 744 77

Mibefradil (Ro 40-5967) is a novel calcium antagonist from a new chemical class and is the first that selectively blocks the T-type calcium channel. In this multicenter, double-blind, placebo-controlled, parallel designed study, its antianginal and antiischemic effects were evaluated in 126 patients with chronic stable angina pectoris. Exercise tests were performed after 1 week of placebo (baseline) and 2 weeks after randomization to 25, 50, 100, and 150 mg (once daily) or placebo. Highly significant dose-response relations were present across all treatment groups for exercise duration, time to angina, and time to ST-segment depression. They were associated with a dose-dependent decrease in heart rate and blood pressure and plasma concentrations > 300 ng/ml. Mibefradil was well tolerated. First-degree atrioventricular block (8%) and dizziness (7%) were the most frequently reported adverse events; however, the first-degree atrioventricular block was dose-related, and only one patient discontinued the trial because of dizziness. The excellent efficacy and adequate safety profile of mibefradil may be a consequence of T-type calcium-channel selectivity.
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PMID:Effects of the new calcium antagonist mibefradil (Ro 40-5967) on exercise duration in patients with chronic stable angina pectoris: a multicenter, placebo-controlled study. Ro 40-5967 International Study Group. 757 82

A 24-year-old man presented to the emergency department with nausea, vomiting, abdominal pain, and an acute confusional state of 6 hours' duration. Ten hours before admission, he had ingested a mixture of orange juice and six ground leaves, later identified as Nerium oleander (common pink oleander) leaves. His blood pressure was 100/80 mm Hg, and his pulse rate was irregular at 40/min. He was disoriented and his speech was dysarthric. Twelve-lead electrocardiography revealed a complete atrioventricular block, with a nodal escape rhythm of 40/min and diffuse ST depression. The presumptive diagnosis of acute oleander intoxication was confirmed by the detection of digoxin (1.0 nmol/L [0.8 ng/mL]) on radioimmunoassay. Despite intensive therapy, the patient's hemodynamic condition deteriorated. His blood pressure decreased to 70/40 mm Hg; he became oliguric and nonresponsive to external stimuli; and his potassium concentration rose to 6.8 mmol/L. Eighteen hours after admission, an empiric 480-mg dose of digoxin-specific Fab antibody fragments was administered intravenously over 30 minutes. Within minutes of the initiation of immunotherapy, the patient woke up; his blood pressure rose to 90/50 mm Hg; and he regained a sinus rhythm of 68/min with a prolonged PR interval. His potassium concentration decreased to 5.1 mmol/L within 15 minutes and normalized within 1 hour of therapy initiation. One day later, the 1 degree atrioventricular block disappeared, but the ST depression persisted for an additional 6 days. The value of digoxin-specific Fab antibody fragments in the treatment of plant glycoside and, in particular, oleander intoxication is discussed.
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PMID:Beneficial effect of digoxin-specific Fab antibody fragments in oleander intoxication. 757 73

The purpose of the present study was to clarify the characteristic findings of electrocardiogram (ECG) in 11 patients with acute myocarditis. ST elevation without reciprocal ST depression was one of the conspicuous findings in the acute stage. Total QRS amplitudes at the acute stage were significantly decreased as compared to those before illness and during the convalescent stage. Abnormal Q waves were present in 7 patients and disappeared in a short period. The number of leads showing Q waves was inversely correlated to left ventricular (LV) ejection fraction (r = -0.87, p < 0.01). Conduction disturbances were present in 7 patients. Second degree and advanced AV block was transient while bundle branch block remained over months. Corticosteroid treatment was effective for patients who had edematous myocardial thickening and AV conduction disturbances. As the serial ECG findings in acute myocarditis are so characteristic, and this help to differentiate it from acute myocardial infarction (AMI).
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PMID:Serial electrocardiographic findings in acute myocarditis. 784 77

Seven adult mares were used to determine the analgesic, CNS, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments. A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 micrograms/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (CEA). A dose of 30 micrograms of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (CSA). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal CEA and CSA extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 +/- 28.8 minutes vs 127.1 +/- 27.7 minutes). All mares remained standing. Both CEA and CSA induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, PCV, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values. Results indicate that use of detomidine for CEA and CSA in mares probably induces local spinal and CNS effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.
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PMID:Caudal analgesia induced by epidural or subarachnoid administration of detomidine hydrochloride solution in mares. 806 16

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5


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