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)

The effects of three concentrations of halothane or ketamine were investigated on isolated rabbit hearts, which were perfused with hydralazine, clonidine, propranolol or methyldopa. In hearts not subjected to the influence of an anaesthetic, clonidine was the only drug stimulating myocardial function. In those perfused with halothane or ketamine alone, both anaesthetics exerted a negative chronotropic and inotropic action in a dose-related manner. Ketamine markedly increased the coronary flow. Clonidine distinctly reduced the myocardial depression caused by halothane or ketamine. Hydralazine had no marked effects with either of these anaesthetics, except that it sensitized the hearts to the arrhythmic action of a high concentration of halothane. Propranolol, when combined with halothane, aggravated myocardial depression and decreased coronary flow. With ketamine, propranolol caused no other harmful interactions, apart from inhibiting the increase in coronary flow caused by this anaesthetic. Methyldopa intensified the myocardial depression induced by halothane, but tended to diminish that caused by ketamine. The results suggest that clonidine has a stimulatory cardiac action when combined with either of these anaesthetics. Disadvantageous interactions may exist between methyldopa or propranolol and halothane.
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PMID:The combined effects of antihypertensive drugs and anaesthetics (halothane and ketamine) on the isolated heart. 72 70

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.
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PMID:Adrenergic activity and gastric secretion. 77 88

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.
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PMID:Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal. 77 91

Propranolol is known to decrease ischaemic damage in developing myocardial infarction. Besides acting on mechanical parameters which help determine the balance of oxygen supply and oxygen demand in the ischaemic tissue, propranolol decreases the myocardial uptake of free fatty acids and increases that of glucose. It is suggested that propranolol may favourably alter developing myocardial infarction in dogs by altering the supply of substrates reaching the ischaemic zone. However, propranolol also decreases enzyme release from isolated rat hearts with coronary ligation at a relative constant arterial free fatty acid concentration. Propranolol causes more marked depression of mechanical function and of heart rate in hearts perfused with free fatty acids than with glucose. It is suggested that the glucose-promoting and anti-lipolytic actions of propranool might be important not only in decreasing infarct size but also in helping to prevent undesirable side effects in hearts with experimental myocardial infarction.
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PMID:Propranolol and experimental myocardial infarction: substrate effects. 78 52

Since 1964, of 725 patients presenting with anxiety syndromes, 513 were treated with propranolol for periods of several days to over 10 years, some intermittently, others virtually without interruption. Of these, 237 had previously received or were receiving psychotropic drugs, mostly benzodiazepines and/or phenothiazines, which had proved ineffective or deleterious. Dosage was adjusted to achieve an optimum clinical response and a relatively high degree of beta-blockade, as judged by the virtual abolition of orthostatic and hyperventilatory tachycardia. As a rule, 80-320 mg daily sufficed, but increments up to 1200 mg were temporarily required to control bizarre or unusually intense symptoms. With few exceptions, the somatic and psychic symptoms were relieved or moderated and overall functional capacity was restored. Depression, evident in 50% of the patients, usually lifted, but persisted in one-third as a lone symptom responsive to antidepressants. Propranolol requirements usually diminished and lasting remissions were not infrequent. The effects of propranolol contrasted sharply with those experienced by the patients receiving tranquillizers. Single-blind placebo trials involving 76 cases endorsed the specificity of the response to beta-blockade. This long term study reveals that effective control of the somatic and psychic symptoms of anxiety can be achieved with propranolol in appropriate dosage.
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PMID:Propranolol in the treatment of anxiety. 78 57

The effect of metoprolol on pulmonary function was compared with that of propranolol and placebo in twelve patients with chronic obstructive lung disease. Propranolol caused a significant reduction in FEV1 compared with metoprolol and placebo. Metoprolol gave a slight reduction compared with placebo. FVC was not significantly influenced by metoprolol, but propranolol caused a significant depression compared both with metoprolol and placebo. The isoprenaline-mediated increase in FEV1 and FVC was not significantly altered after metoprolol compared with placebo. After propranolol the isoprenaline-mediated increases in FEV1 and FVC were 40 and 24% lower respectively than after metoprolol and placebo. Unwanted effects and pulmonary symptoms were at an acceptable level in all cases except in two patients who had to be given i.v. theophyllamine therapy during propranolol treatment. It is concluded that metoprolol exhibits a selective beta1-blocking action and thus may be given to patients with chronic obstructive lung disease provided that adequate beta2-stimulator treatment is given concomitantly.
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PMID:Effects of muliple doses of metoprolol and propranolol on ventilatory function in patients with chronic obstructive lung disease. 79 May 61

To clarify the influence of propranolol-and particularly its heart-rate effects-on myocardial ischemia, coronary hemodynamics and metabolism were studied in 15 patients utilizing a protocol to control heart rate. Ten patients had significant coronary narrowing (CAD) and 5 were normal. Systemic pressure, coronary sinus blood flow (CSBF), left ventricular oxygen utilization (LVVO2), ST Segment depression, and myocardial lactate extraction were measured before and after propranolol (10 mg IV), at rest, during pacing-induced tachycardia stress. Propranolol-related reduction in CSBF and LVVO2 at rest was reversed when heart rate was controlled in both patient groups. Propranolol failed to alter heart-rate threshold, tension-time index (TTI), CSBF, or LVVO2 at angina in the CAD patients. Likewise, ischemic-type ST depression, decreases in lactate extraction, and coronary resistance were unchanged compared to values observed during tachycardia stress before propranolol. In normal coronary patients, propranolol also produced no significant change in LVVO2 or coronary resistance when its heart rate effects were controlled. These data imply that a major coronary and metabolic influence of propranolol relates to changes occurring secondary to its influence on heart rate. Furthermore, this agent's anti-ischemic effect is not prominent during tachycardia stress suggesting that this stress test may be clinically useful in patients taking propranolol.
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PMID:Effects of propranolol on coronary hemodynamic and metabolic responses to tachycardia stress in patients with and without coronary disease. 83 33

The effects of coronary occlusion and of subsequent propranolol administration were examined in 18 conscious dogs. Overall left ventricular (LV) function was assessed by measurements of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work", i.e., pressure-length loops in normal, moderately, and severely ischemic zones. Regional intra-myocardial electrograms were measured from the same sites along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones with graded flow reduction and graded elevation of the ST segment. Propranolol depressed overall LV function, function in the normal zone (work fell by 17+/-4%), and in the majority of moderately ischemic segments (work fell by 7+/-3%). In severely ischemic segments the extent of paradoxical motion and post-systolic shortening was reduced by propranolol. After propranolol regional myocardial blood flow fell in the normal zone (11+/-2%) and rose in the moderately (15+/-4%) and severely (63+/-10%) ischemic zones. Thus, in the conscious dog with regional myocardial ischemia, propranolol induces a redistribution of myocardial blood flow, with flow falling in normal zones and rising in moderately and severely ischemic zones. The improvement in perfusion of ischemic tissue was associated with slight but significant depression of shortening, velocity, and work in the moderately ischemic zones and of paradoxical bulging and post-systolic shortening in the severely ischemic zone.
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PMID:Effects of propranolol on regional myocardial function, electrograms, and blood flow in conscious dogs with myocardial ischemia. 87 96

Electrophysiologic modifications produced by intravenous administration of 0.1 mg/Kg Oxprenolol were studied in 16 subjects with estimated normal impulse formation and conduction. Significant effects were sinus bradycardia, mild increase of sino-atrial conduction time, depression of intranodal conduction and prolongation of A-V node refractory periods. Sinus node recovery time and atrial refractory periods were unchanged. Infranodal conduction and the refractory periods of the His-Purkinje system, as well as of the bundle branches, were unchanged. These effects are compared with those observed after intravenous Propranolol and Prindolol.
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PMID:Electrophysiologic properties of intravenous oxprenolol in man. 88 7

1. The positive chronotropic and inotropic actions of dopamine and noradrenaline have been compared in anaesthetized dogs and isolated guinea-pig atria. 2. Inotropic activity was measured with a strain-gauge arch in vagotomized dogs or estimated from max (dp/dt) in dogs with denervated hearts. 3. The effects of propranolol and haloperidol on the concentration-response curves to both amines were studied in isolated atria. 4. In anaesthetized vagotomized dogs noradrenaline was more potent than dopamine but dopamine appeared to have a selective inotropic action, less apparent with noradrenaline. In denervated hearts, doses of noradrenaline and dopamine which caused similar increases in max (dp/dt) also caused similar increases in heart rate. 5. In isolated atrial preparations, concentrations of dopamine and noradrenaline which produced similar increases in force of contraction also had similar chronotropic effects. 6. Propranolol produced a shift to the right of the concentration-response curves to both dopamine and noradrenaline but the antagonism of noradrenaline was quantitatively greater. Haloperidol had not effct in concentrations below those found to cause general tissue depression. 7. It is concluded that neither dopamine nor noradrenaline show any real difference in their relative inotropic and chronotropic activities in the absence of autonomic innervation.
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PMID:A comparison of the cardiac actions of dopamine and noradrenaline in anaesthetized dogs and guinea-pig atria. 88 5


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