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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 halothane on the effective refractory period (ERP) and the ventricular activation were examined in a canine myocardial infarction model, and compared with those of propranolol. Halothane reduced the heart rate and prolonged the ERP in both normal and infarcted zones. A prolongation of ERP with halothane was also observed during atrial pacing at the same rate as in control, but the effect was less than during sinus rhythm. Halothane (1 MAC) further delayed or blocked the delayed activation in the infarcted zones with only slight effects on the activation of the normal zones. Propranolol (0.2 mg/kg) prolonged ERP during sinus rhythm, but it did not affect either the ERP or ventricular activation during atrial pacing. In conclusion, halothane produced a selective depression of the delayed activation and the prolongation of ERP, which may be caused by both direct effects on the myocardium and secondary effects such as a reduction of the heart rate. These effects of halothane may contribute to its antiarrhythmic effects in the myocardial infarction model which have been previously reported.
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PMID:Comparison of the effects of halothane and propranolol on the effective refractory period and the ventricular activation in a canine myocardial infarction model. 128 97

Examination of central hemodynamics in patients in the preperfusion period of radical correction of Fallot's tetrad has demonstrated that after pericardiotomy and the onset of surgical manipulation on the heart there was a depression of circulation both during the use of intravenous total anesthesia on the basis of ketamine and ataralgesia. The depression was more manifest under ataralgesia. The depression of circulation was paralleled by the deepening of initial hypoxemia. Analysis of the efficacy of medicamentous agents with regard to the specific features of intracardiac anatomy of the outlet of the right ventricle, estimated intraoperatively, has established that administration of phenylephrine at a rate of 3 micrograms/kg favoured an increase of partial oxygen pressure and arterial blood saturation with hemoglobin whatever the anatomo-morphological type of stenosis of the outlet of the right ventricle. Propranolol promoted the improvement of arterial blood oxygenation but in the muscular type stenosis of the outlet of the right ventricle. Meanwhile the use of the drugs possessing a beta-adreno-stimulating effect brought about the deepening of hypoxemia.
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PMID:[Approaches to prevention and treatment of arterial hypoxemia in the pre-perfusion period of radical correction of Fallot's tetrad]. 138 54

Paroxysmal supraventricular tachycardia is the most common sustained cardiac arrhythmia in pregnant women. Because nearly 50% of these supraventricular tachyarrhythmias fail to respond to vagal maneuvers, other therapies are used, including electrocardioversion and pharmacologic agents. Propranolol, verapamil, and adenosine have Food and Drug Administration-approved labeling for acute termination of supraventricular tachycardia. Verapamil has been the most commonly used agent in the general population but it has several shortcomings, such as its potential to cause or exacerbate systemic hypotension, congestive heart failure, bradyarrhythmias, and ventricular fibrillation. In addition, verapamil readily crosses the placenta and has been shown to cause fetal bradycardia, heart block, depression of contractility, and hypotension. Adenosine has several advantages over verapamil, including rapid onset, brevity of side effects, theoretical safety, and probable lack of placental transfer. Adenosine ultimately may prove to be the preferred agent for termination of paroxysmal supraventricular tachycardia in the gravid woman.
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PMID:Adenosine in the treatment of maternal paroxysmal supraventricular tachycardia. 149 12

We studied the short-term effects of oral administration of nisoldipine (10 mg) and propranolol (80 mg) alone and in combination in 14 patients with chronic exertional angina pectoris in a double-blind, randomized, cross-over study. The 14 patients (13 men and 1 woman, mean age 56 +/- 7 years) performed symptoms-limited bicycle exercise stress test 3 h after placebo or active substance administration. Maximal work load, exercise duration, and time to 1-mm ST segment depression were significantly increased and ST depression at peak exercise was significantly decreased by drugs alone and in combination. Propranolol and nisoldipine alone improved exercise duration similarly and as well as the combination; however, a different response to the three pharmacologic interventions was found in patients treated with single drugs. The improvement in exercise tolerance was associated with rate-pressure product values at peak exercise, unchanged after nisoldipine and significantly reduced after both propranolol alone and in combination. After placebo, all patients had exercise-induced angina, in 9, 8, and 4 patients after nisoldipine, propranolol, and the combination of the two drugs, respectively. Nisoldipine is effective in the treatment of effort angina and its combination with propranolol may be useful and superior in patients who show poor response to monotherapy.
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PMID:Acute effects of nisoldipine, propranolol, and their combination in patients with chronic stable angina: a double-blind, randomized, cross-over, placebo-controlled study. 169 90

There is circumstantial evidence that increases in prolactin secretion evoked by L-tryptophan infusion involve 5-HT1 receptors, whereas growth hormone responses do not. Propranolol is a beta-adrenoceptor antagonist that also possesses antagonist properties at 5-HT1 receptors. Propranolol (80 mg, PO) failed to attenuate the prolactin response to L-tryptophan infusion (100 mg/kg, IV) in seven volunteers; the role of 5-HT1 receptors in this response remains uncertain. The growth hormone response to tryptophan was enhanced by propranolol, consistent with previous reports of an inhibitory beta-adrenoceptor influence on GH secretion. Excessive beta-adrenoceptor function might explain the blunted growth hormone response to tryptophan in depression.
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PMID:Hormonal response to L-tryptophan infusion: effect of propranolol. 208 37

Long-acting Propranolol (160 mg/day) and Amiodarone (200 mg/day after impregnation) were compared in chronic stable angina pectoris. Forty-three patients with stable angina of effort were included in a randomised double blind trial (19 in the amiodarone and 24 in the propranolol group). The duration of the study was 8 weeks; the placebo phase (2 weeks) was followed by 6 weeks of active treatment. An exercise stress test was performed before and after the treatment period. The number of episodes of angina and the consumption of glyceryl trinitrate decreased significantly (p less than 0.001) in the same proportion with both drugs with respect to the placebo period. The time to the appearance of criteria of positivity of the exercise stress test increased from 6.82 +/- 0.50 mn to 8.35 +/- 0.50 mn with amiodarone, and from 7.15 +/- 0.47 mn to 9.50 +/- 0.52 with the propranolol preparation. This improvement was very significant compared with the placebo phase (p less than 0.001) but the difference between the two drugs was not statistically significant (p = 0.39). The other parameters which were studied (time to onset of angina, total duration of exercise, maximum heart rate, double product, maximum ST depression) changed in a parallel fashion significantly versus placebo. There were no differences between the two treatment groups with the exception of the resting heart rate which decreased more in patients on propranolol (80.94 +/- 3.92 to 62.47 +/- 1.97) than in patients on amiodarone (84.87 +/- 2.63 to 73.41 +/- 2.01; p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anti-angina effect of amiodarone versus delayed-action propranolol. A double-blind randomized study]. 212 69

The relationship between propranolol and depression is a subject of controversy. Numerous case reports suggest that propranolol can cause depression, but two small prospective trials have failed to confirm this. The contemporary psychiatric literature is divided as to whether propranolol can cause depression. This study addresses this issue by re-analyzing side effect data from clinical trials of propranolol as an antihypertensive agent. A literature review was carried out and the data were analyzed using meta-analytic statistical techniques. Propranolol was found to cause depression as a side effect with a statistically greater frequency than the control medications used in these trials. As other side effects of propranolol include fatigue, diminished energy, decreased libido, anorexia and poor concentration, it is suggested that propranolol is a cause of organic mood disorder, depressed type.
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PMID:Propranolol and depression: evidence from the antihypertensive trials. 214 Feb 88

Cancer chemotherapy with anthracyclines, of which doxorubicin (DX2) is the main representative, is limited by cardiomyopathy developing in animals and patients after cumulative dosing. The toxicity is probably related to free radical formation by the anthracycline as well as its metabolites with concomitant O2.- and .OH generation resulting in lipid peroxidation and subsequent membrane damage. An in vitro model is required to investigate the individual contribution of each metabolite to cardiotoxicity. For in vivo studies, the species of choice is the mouse because it lacks the DX-induced nephrotic syndrome seen for instance in rats and rabbits. Thus, isolated mouse heart muscle was chosen as an in vitro model. To characterize the model, we used l-isoprenaline/dl-propranolol and metacholine/atropine to measure the beta-adrenergic and the muscarinic responses of (spontaneously beating) right and (paced) left atrium. Dose response curves (n greater than or equal to 4) were highly reproducible: pD2,iso = 8.0 +/- 0.3 (left) and 8.5 +/- 0.4 (right); pD2,met = 6.7 +/- 0.1 (left) and 6.2 +/- 0.3 (right). Propranolol as well as atropine behaved as competitive antagonists, with pA2-values of 8.4 +/- 0.2/8.5 +/- 0.2 (l/r) and 9.1 +/- 0.1/9.1 +/- 0.2 (l/r), respectively. These values corresponded to those obtained with other organ preparations. We tested the effect of DX in two ways: a) by measuring the direct inotropic and chronotropic effect during 60 minutes of incubation with 10-100 microM DX in the organ bath, and b) by determining the remaining beta-adrenergic response to l-isoprenaline after the incubation period. Both variables turned out to be equally affected. For paced left atria an IC50 (causing 50% depression of contractile force) of 35 microM was determined. Right atria stopped beating at concentrations above 50 microM, thus hampering IC50 determination. The results indicate that anthracyclines exert an effect not related to receptor integrity, but directly to the functionality of heart muscle. To check whether radical stress can be involved in the observed negative inotropic effect, incubations with xanthine/xanthine oxidase (to produce reactive oxygen species) were performed. A pronounced negative effect on mouse atrial contraction was indeed observed. However, initially a positive inotropic effect accompanied by an increased resting tension were seen. It can be concluded that mouse atrium can be used as a model to compare anthracyclines and their metabolites with regard to their acute cardiotoxic effects.
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PMID:Isolated mouse atrium as a model to study anthracycline cardiotoxicity: the role of the beta-adrenoceptor system and reactive oxygen species. 216 63

This was a prospective, randomized, double-blind, placebo-controlled trial to establish whether beta blockers or calcium-channel blockers limit exercise capacity and training responses in men with mild hypertension. Circuit weight and aerobic training was used to assess the effects of drugs on cardiovascular fitness and muscle strength. Fifty-two sedentary men, ages 25-59 yr, with a diastolic blood pressure of 90-105 mm Hg off drugs, without significant ST depression during maximal stress testing, received diltiazem, propranolol, or placebo. Maximal oxygen uptake (VO2max) and exercise duration during treadmill testing, as well as one-repetition maximal strength, were assessed on eight weight machines after a single-blind placebo baseline, after 2 wk of drug run-in, and after 10 wk of exercise training. Total daily doses were 240 mg for propranolol and 360 mg for diltiazem. Propranolol decreased VO2max after drug run-in (P less than 0.05). Exercise training increased VO2max (P less than 0.05) in the diltiazem and placebo groups. After training VO2max in the propranolol group increased (P less than 0.05) from run-in but not beyond baseline levels. Thus, the reduction of VO2max consequent to propranolol therapy limited the overall benefits of training. Exercise duration did not change with run-in and increased (P less than 0.05) with training by 22%, 19%, and 10% for the diltiazem, placebo, and propranolol groups, respectively. Strength after run-in was unchanged, and exercise training increased strength (P less than 0.0001) on all weight machines in all groups. The results show an advantage of diltiazem to propranolol, particularly among physically active patients engaged in aerobic exercise who require antihypertensive therapy.
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PMID:Effects of diltiazem or propranolol during exercise training of hypertensive men. 235 13

The effect of adrenaline (Ad) on muscarinic transmission was examined in B neurones of bullfrog sympathetic ganglia by using intracellular and voltage-clamp recording methods. Bath-application of Ad (5-500 microM) caused a depression of the slow excitatory postsynaptic potential (EPSP) elicited by repetitive stimulations of preganglionic nerve fibres in the presence of curare (30 microM). Ad also depressed the 'muscarinic' ACh potential induced by ionophoretic application of ACh directly to curarized sympathetic neurones in a concentration-dependent manner. Isoprenaline mimicked the effect of Ad in producing the inhibition of the 'muscarinic' ACh potential. Propranolol antagonized the inhibitory action of Ad. Dibutyryl adenosine 3',5'-monophosphate had no significant effect on the 'muscarinic' ACh potential. Under voltage-clamp conditions, Ad caused an inward current associated with inhibition of the M-current (Brown and Adams 1980). Ad depressed the amplitude of slow postsynaptic currents produced by applications of ACh and muscarinic. At a concentration of 100 microM, Ad produced a 68 +/- 8% (n = 12) depression of the amplitude of the muscarinic ACh current. The inhibition of muscarinic transmission induced by Ad is due to a direct suppression of the muscarinic current at the postsynaptic membrane in bullfrog sympathetic ganglia.
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PMID:Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia. 254 82


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