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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report on the effects of propranolol, a beta-adrenergic blocking agent, on 10 patients with pathological panic states. Propranolol was effective in treating acute pathological panic, but modest doses of the drug administered for brief periods of time did not alleviate chronic panic attacks associated with agoraphobia. The drug suppressed panic associated with depressive syndromes but did not affect the depression and had no clear effect on anticipatory anxiety. The authors suggest that further study of these findings may clarify other clinical problems.
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PMID:The treatment of pathological panic states with propranolol. 98 38

Verapamil (Isoptin) caused a dose-dependent peripheral vasodilation, increase in myocardial contractility, and tachycardia in the anaesthetized dog. Propranolol pretreatment blocked the cardiac stimulation following verapamil but the vasodilation was unaltered. Inflation of a thoracic aortic balloon prevented the fall in intravascular pressure and reduced the tachycardia and positive inotropic responses. These experiments suggest that clinical doses of verapamil cause peripheral vasodilation which leads to a sympathetic reflex induced increase in heart rate and myocardial contractility. Verapamil also had a direct myocardial depressant action which became evident at doses above the range used clinically. The drug increased the PR interval in conscious dogs for up to 60 minutes. This effect was partly mediated through cholinergic stimulation and partly through a direct depression on atrioventricular conduction.
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PMID:Cardiovascular action of verapamil in the dog with particular reference to myocardial contractility and atrioventricular conduction. 99 Nov 62

1. Propranolol, when used for treating arterial hypertension, may influence determinants of both cardiac and vascular function; the consequent changes in cardiac performance may result from the interaction of different and possibly opposite effects. 2. Cardiac funtion was investigated in fifty-four primary hypertensive men in the pretreatment state and after 3 weeks of propranolol therapy at a daily dose of 320 mg. 3. beta-Receptor blockade caused depression of pre-injection left ventricular function, which was unrelated to the direction and the extent of changes in peripheral circulation. 4. The ejection left ventricular function could be either depressed or improved depending on the direction to which treatment shifted the vascular resistance, and consequently, the impedance to left ventricular ejection. 5. Withdrawal of the adrenergic support is probably the major factor responsible for the poor ventricular adaptation to an augmented impedance.
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PMID:Cardiac function in the treatment of arterial hypertension with propranolol. 107 80

Several agents used clinically in the treatment of angina pectoris were studied in an atherosclerotic rabbit model previously shown to be useful in differentiating antianginal drug activity. Intravenously administered isosorbide dinitrate afforded protection against pacing-induced S-T segment depression in a dose-related manner. Drugs with no protective effect included pentaerythritol tetranitrate, chromonar, and papaverine. Propranolol also did not prevent pacing-induced S-T segment depression, due in part to the overriding of the beneficial negative chronotropic effect of this drug by pacing.
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PMID:Effects of several antianginal agents on pacing-induced S-T Segment depression in the atherosclerotic rabbit. 112 7

The influence of acute myocardial depression on ventricular stiffness and on its elastic and viscous components was studied in 19 dogs. After the animals were placed on cardiopulmonary bypass, stiffness was measured by sinusoidally injecting volume changes of 0.5 ml (deltaV) at 22 Hz into paced, isovolumically (deltaP) of the sinusoidal pressure response. Stiffness was linearly related to pressure (P) throughout the cardiac cycle, so that deltaP/delta V = alpha P + beta, where alpha and beta are constants. Myocardial depression was induced in one of three different ways: by coronary artery ligation, by administration of propranolol (Inderal), or by administration of pentobarbital. All three interventions caused significant increases in the slope, alpha, of the stiffness-pressure relationship, while the intercept, beta, remained unchanged. Release of the coronary occlusion or administration of acetylstrophantidin partially reversed depression and the change in alpha; Approximation of the mechanical nature of the left ventricle in terms of a linear second-order mechanical system permitted the division of stiffness into its elastic and viscous components. Like total stiffness, both the elastic and the viscous components were linearly related to ventricular pressure. Elastic stiffness was not changed, but the slope of the line relating viscous stiffness to pressure was significantly increased during ischemic depression, indicating that a change in viscosity was primarily responsible for the increase in total ventricular stiffness.
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PMID:Influence of acute myocardial depression on left ventricular stiffness and its elastic and viscous components. 115 Aug 70

Propranolol (100mug) ivc together with phentolamine (60 mug) decreased spontaneous locomotor activity and weakened post-nialamide locomotor activity in rat. When applied separately in the above doses, neither of the two compounds had this action. Depression of amphetamine-induced locomotor activity was observed after propranolol (250 mug) together with phetolamine (60 mug). Phentolamine alone, had hypothermic action but when applied together with propranolol, it increased after 4 hrs body temperature. The tested compounds prolonged hexobarbital-induced sleeping time but did not affect noradrenaline or dopamine levels in rat's brain.
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PMID:The central action of intraventricularly (ivc) administered propranolol and phentolamine in rat. 116 21

Propranolol therapy has been implicated as a cause of myocardial depression and increased morbidity and mortality in patients undergoing coronary artery surgery. The authors reviewed 169 consecutive patients undergoing cardiac surgery, of whom 143 had been taking propranolol, with regard to preoperative administration of propranolol and intraoperative or postoperative complications. Patients taking propranolol until 24 hours before surgery showed no increased incidence of hypotension or bradycardia before cardiopulmonary bypass. Hypotension after bypass was no more common in patients off propranolol 12 to 48 hours than in patients who either discontinued the drug over 48 hours before operation or had never taken the drug. Myocardial contractility as measured by systolic time intervals was normal 24 to 48 hours after stopping propranolol therapy. Five patients had preoperative myocardial infarctions within 48 hours of discontinuing the drug. The operative mortality rate was 4 percent in patients taking propranolol within 48 hours of surgery and 6 percent in all other patients. Seven risk factors, other than propranolol, were identified in those patients requiring inotropic support. The authors conclude that propranolol can be given safely within 24 to 48 hours of coronary artery surgery provided the patient is a satisfactory candidate for myocardial revascularization.
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PMID:Propranolol and cardiac surgery: a problem for the anesthesiologist? 123 44

There is as yet no adequate animal mode for human myocardial ischemia. The commonly utilized technique of coronary arterial ligation in large animals may induce regional ischemia but introduces variables that make it difficult to compare studies in different laboratories. A model of global ischemia in an isolated perfused rat heart that offers a rapid, inexpensive means for producing graded, controlled, stable state and reproducible ischemia is described. The technique has been utilized with success to study the hemodynamic and metabolic effects of ischemia and to evaluate pharmacologic interventions designed to protect the ischemic myocardium. Propranolol has been shown to improve bioenergetics and reduce anaerobic glycolysis by a depression of the hemodynamic response of ischemic myocardium. Methylprednisolone appears to exert its primary effect by direct coronary vasodilation, increasing resting or control flow and providing an enhanced reserve when ischemia is imposed. Mannitol improves cardiac performance by reducing the increased myocardial cell water content induced by hypoxia or anoxia.
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PMID:Metabolic evaluation of agents designed to protect the ischemic myocardium and to reduce infarct size. 125 90

The data from this study document that dobutamine is a powerful inotropic agent in anesthetized dogs with acute myocardial ischemia and in awake, unsedated ones with chronic myocardial infarction. Dobutamine significantly increases heart rate at relatively small doses in anesthetized dogs with acute myocardial ischemia but considerably larger amounts of dobutamine are required to significantly increase heart rate in awake, unsedated dogs with myocardial infarction. Dobutamine also significantly increases regional myocardial blood flow to all areas of the heart at 20mug/kg/min in both anesthetized dogs with acute myocardial ischemia and awake, unsedated ones with myocardial infarction. However, in anesthetized dogs 20mug/kg/min of dobutamine significantly increases epicardial ST-segment elevation during acute myocardial ischemia. Propranolol prevents the inotropic and chronotropic effects of dobutamine in both anesthetized and awake, unsedated dogs. This study suggests that during experimental acute myocardial ischemia dobutamine given at doses that significantly increase heart rate and contractility may increase the extent of myocardial damage. The data also suggest that this agent should be of value in the setting of severe myocardial depression without associated severe coronary artery disease to increase cardiac contractility at doses that do not markedly alter heart rate. The hemodynamic and coronary blood flow effects of dobutamine in patients with and without severe coronary artery disease should be evaluated.
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PMID:Influence of dobutamine on regional myocardial blood flow and ventricular performance during acute and chronic myocardial ischemia in dogs. 126 Sep 86

The effects of the beta adrenergic stimulant drug, "Nylidrin", and the beta adrenergic blocking agent, "Propranolol", on human basal gastric acid secretion were studied in 20 healthy volunteer subjects and 10 chronic D.U. cases. Nylidrin increased gastric acid secretion and volume. All effects of nylidrin were blocked by prior administration of beta adrenergic inhibitor propranolol. Propranolol diminished both acid secretion and volume in both normal and D.U. cases. The presence of beta adrenergic receptors in the human stomach was suggested. The effects of beta adrenergic blocking agent propranolol on gastric secretion, stimulated with histamine, were studied in 10 normal subjects and 10 cases of chronic duodenal ulcer patients. Pretreatment with propranolol produced a signigicant depression of the 90 minute acid response to histamine in both volume and acidity in normals and duodenal ulcer cases. It is concluded that propranolol has an antisecretory effect, not only on basal gastric secretion but also on histamine stimulated secretion in man. Reserpine stimulated gastric acid secretion and volume in normals but showed no similar effect in D.U. cases. After pretreatment with propranolol it reduces the gastric acid secretion and volume in normals and D.U. cases.
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PMID:Beta-adrenergic receptors and the effect of beta-adrenergic blocking agent propranolol on histamine and reserpine stimulated gastric acid secretion in man: normals and duodenal ulcer cases. 126 68


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