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PubMed1976

Histamine hypersensitivity in mice induced by Bordetella pertussis or pharmacologic beta adrenergic blockade. Effects of adrenergic, cholinergic, and other drugs.

The effects of prostaglandin E1, E2, F2alpha (PGE2 PGF2alpha), isoproterenol, epinephrine, norepinephrine, salbutamol, practolol, atropine, aminophylline, and corticosterone on the hypersensitivity to anaphylaxis, histamine, and serotonin in Bordetella pertussis-treated mice and propranolol-treated mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected with pertussis vaccine intravenously 4 days before challenge with antigen, histamine, or serotonin. Alternatively, instead of pertussis vaccine, propranolol was injected intraperitoneally 45 min before histamine challenge. Test drugs were administered intraperitoneally 15 min before challenge. PGE1 and PGE2 at a narrow range of between 10 and 100 mug and epinephrine at 100 mug protected both pertussis- and propranolol-treated mice. Isoproterenol (25 mug) and aminophilline (800 mug) protected beta-blocked mice, but did not protect pertussis-treated mice even with very high doses (1,000 and 3,2000 mug, respectively), although salbutamol (500 mug) did. PGF2alpha, norepinephrine, and atropine were not protective at all. Practolol, a beta 1-blocker, given intraperitoneally 30 min before histamine neither sensitized normal mice nor changed the effect of isoproterenol or salbutamol in pertussis-treated mice. Corticosterone 10 mg/kg reduced the number of deaths from histamine in beta-blocked mice, but not in pertussis-treated mice. The protective effect is discussed in connection with probable effects of the drugs on intracellular cyclic adenosine monophosphate (cAMP) levels.

Adrenergic beta-Antagonists↗
PubMed1983

Beta-adrenoceptor blocking drugs: adverse reactions and drug interactions.

Beta adrenoceptor blocking drugs are relatively well tolerated and adverse reactions to them are not common. The ones that do occur are reviewed in this paper under the following headings: Short term adverse reactions, drug interactions, long term adverse reactions, risks in pregnancy and hazards of abrupt withdrawal. Predictable short term effects may be caused either by the actions of these drugs on the beta 1- or beta 2-receptors. The beta 1 adverse effects are hypotension, bradycardia and cardiac failure; these are best avoided by not giving beta-adrenoceptor blocking drugs to susceptible patients with cardiac disease. The beta 2 adverse effects on the bronchi, the peripheral arteries and various metabolic functions may be reduced to some extent by using a relatively cardioselective drug. Unpredictable short term effects such as fatigue, sexual dysfunction and gastrointestinal symptoms may occur but are not common problems with this group of drugs. Similarly, serious drug interactions are infrequent. Under the heading of long term adverse effects the practolol problem and the risk of causing malignant disorders have been considered. There is no evidence that any of the currently available drugs will cause either a practolol syndrome or malignant disease in man. However, the need for careful appraisal by drug regulatory bodies and continued vigilance by all prescribers of beta-adrenoceptor blocking drugs remains. The possible adverse effects of treatment during pregnancy are also considered. It now appears that beta-adrenoceptor drugs can be used safely in pregnancy but since neonatal bradycardia and hypoglycemia may occur, care should be taken to look for these complications. A serious deterioration may occur when beta-adrenoceptor drugs, given to patients with significant ischemic heart disease, are suddenly stopped. This is a rare occurrence but prescribers should be aware of it.

Adrenergic beta-Antagonists↗
PubMed1986

A two-parameter flow cytometry protocol for the detection and characterization of the clastogenic, cytostatic and cytotoxic activities of chemicals.

Cultured, freshly-isolated rat fibroblasts were exposed in vitro to vincristine sulphate (VC), amethopterin (AM), bleomycin (BL), benomyl (BE) and practolol (PR). Cells treated for 5 h were subjected 24 h later to a two-parameter (DNA/protein) flow cytometry analysis. The fluorochromes used were sulphorhodamin 101 and DAPI. From DNA and protein histograms, alterations in cell-cycle kinetics, variations in the amount of DNA in individual G1-phase cells and the enhancement of or increased variation in the protein content of the exposed cells were determined. Each of the 5 chemicals induced a specific dose-dependent pattern of changes in the DNA and protein histograms. DNA dispersion was enhanced with VC, AM, BL and BE but not with PR. The cell cycle was blocked in the G2 phase with VC, at early S phase with amethopterin and, depending on the dose, at the G1 or G2 phase with bleomycin or at the S phase or G2 phase with benomyl. Practolol inhibited cells slightly in the S phase at the highest exposure level. Protein analysis allows cytotoxic activity (loss of proteins) or induced unbalanced growth (protein accumulation) of test compounds to be recognized. The results obtained imply that the proposed two-parameter DNA/protein analysis by flow cytometry is a suitable method for prospective testing of chemicals for their induction of structural or numerical chromosome aberrations. Simultaneously, a broad range of cytotoxic, cytostatic and cell-cycle perturbing activities of the test agents can be recognized.

Animals↗
PubMed1987

Carotid sinus reflexes in rats given small doses of lead.

The effect of low level lead poisoning on the carotid sinus reflex in rats was studied. The reflex was evoked by carotid artery clamping, in control and lead-poisoned animals. Wistar rats were given lead acetate trihydrate (50 mg/kg) via stomach tube once weekly for 5 weeks; control animals were given equimolar amounts of sodium acetate. Both groups were fed a regular animal food diet. At the end of the 6th week, and under urethane anesthesia, mean arterial blood pressure and heart rate were continuously recorded for both groups, before and after clamping, and after unclamping the left common carotid artery. In other experiments, some animals were pre-treated with dopamine, 0.040 mg/kg; practolol, 3 mg/kg; propranolol, 0.1 mg/kg; or atropine, 0.1 mg/kg. In animals not given drugs, lead produced a less pronounced rise in mean arterial blood pressure after clamping, and a more pronounced decrease in heart rate after unclamping, compared to control animals. Some drugs altered this response pattern. Atropine led to a more pronounced tachycardia in the lead-poisoned rats, whereas practolol led to a more pronounced bradycardia in the lead-poisoned rats. Propranolol pretreatment led to a less pronounced decrease in heart rate for lead-poisoned rats, again as compared to the controls. Atropine and beta-adrenergic receptor blocking agents produced similar carotid sinus reflex responses in control and lead-poisoned animals.

Animals↗
PubMed2005

Modeling the electrophoretic mobility of beta-blockers in capillary electrophoresis using artificial neural networks.

Artificial neural networks were used for modeling the mobility of five beta-blockers (i.e., labetalol atenolol, practolol, timolol and propranolol) in running buffer with ternary solvent background electrolyte systems containing 80 mM acetate buffer dissolved in water, methanol, ethanol and their ternary mixtures. The volume fractions of two solvents (f(2), f(3)) and cologarithm of electrophoretic mobilities in pure solvents (i.e., -Lnmu(1), -Lnmu(2) and -Lnmu(3)) were used as inputs and cologarithm of the mobility in mixed solvents was the output of the networks. The number of neurons in hidden layer, learning rate, momentum and the number of epochs were optimized, in which two neurons in hidden layer, 0.2, 0.9 and 20000 were found the optimized values for learning rate, momentum and number of epochs, respectively. Mean percentage deviations (MPD) between calculated and experimental mobilities were computed as an accuracy criterion. To assess the correlative ability of the model, all data points in each set were used as training set and the mobilities were back-calculated by the trained networks, in which the overall MPD (OMPD)+/- standard deviation (SD) for correlative study was 3.1+/- 2.3. To evaluate the prediction capability of the proposed ANN model, the network was trained using 15 data points for each analyte and the remaining data points were predicted. The obtained OMPD (+/-SD) for this analysis was 3.6+/-3.0. To further investigate on the applicability of ANN, a generalized network was trained with 10 data points from each beta-blocker and then the network was employed to predict the mobilities of the analytes in ternary solvent electrolyte systems. The MPDs for predicted mobilities were 3.6%, 3.6%, 3.9%, 3.7% and 2.9% respectively for labetalol, atenolol, practolol, timolol and propranolol.

Adrenergic beta-Antagonists↗
PubMed1979

Effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker in awake dogs.

The effect of the autonomic blockade on the automaticity of the A-V junctional pacemaker was evaluated in 15 awake dogs with experimentally induced A-V junctional rhythm. The duration of asystole after overdrive (D.A.O.) in these dogs was prolonged significantly in accordance with increase in the drive rate, and the mean +/- SD of the D.A.O. reached 4.7 +/- 1.1 seconds (N = 15) after overdrive at 2.5 times the spontaneous heart rate. After administration of atropine (0.4 mg/kg; i.v.) to eight dogs, the mean +/- SD of the D.A.O. at the same rate decreased from 4.5 +/- 0.9 to 3.4 +/- 1.2 seconds. After administration of practolol (0.5 mg/kg; i.v.) to the seven other dogs, the mean +/- SD of the D.A.O. at the same rate increased remarkably from 4.9 +/- 1.3 to 9.4 +/- 3.0 seconds. Intravenous injection of practolol (0.5 mg/kg) had no effect upon the D.A.O. in the five dogs with sinus rhythm. Thus, it is suggested that (1) the sympathetic nerve might play a more important role in regulating the automaticity of the A-V junctional pacemaker than the vagus and (2) it physiologically might take over 5.0 seconds for the A-V junctional pacemaker to initiate an escape beat during longstanding sinus arrest, if a marked dysfunction of the A-V junctional pacemaker occurs due to a decrease in tension of the sympathetic nerve.

Animals↗
PubMed1978

Synthesis and biologic distribution of radioiodinated beta-adrenergic antagonists.

Iodinated analogues 2, 7, and 8 were prepared from propranolol, practolol, and acebutolol in 30--50% yields. Radioisotopic exchange between carrier-free Na125I and the molten iodinated beta-adrenergic antagonist yielded the corresponding 125I-labeled product. The biodistribution in rats, determined at 15 and 60 min postinjection, indicated that the radioiodinated analogues of the cardioselective drugs practolol and acebutolol localized to a greater degree in the liver and heart than the analogue of propranolol. Conversely, [125I]iodopropranolol (2) was concentrated to a greater extent in the lungs than [125I]iodopractolol (7) or [125I]iodoacebutolol (8). Therefore, 123I- or 131I-labeled cardioselective beta-adrenergic antagonists, such as 7 or 8, may prove useful as radiodiagnostic agents for the external imaging of the myocardium.

Acebutolol↗
PubMed2002

Calculation of electrophoretic mobility in mixed solvent buffers in capillary zone electrophoresis using a mixture response surface method.

The electrophoretic mobilities of three beta-blocker drugs, practolol, timolol and propranolol, have been measured in electrolyte systems with mixed binary and ternary water-methanol-ethanol solvents with acetic acid/sodium acetate as buffer using capillary electrophoresis. The highest mobilities for the analytes studied have been observed in pure aqueous, the lowest values in ethanolic buffers. The measured electrophoretic mobilities have been used to evaluate the accuracy of a mathematical model based on a mixture response surface method that expresses the mobility as a function of the solvent composition. Mean percentage error (MPE) has been computed considering experimental and calculated mobilities as an accuracy criterion. The obtained MPE for practolol, timolol and propranolol in the binary mixtures are between 0.9 and 2.6%, in the ternary water-methanol-ethanol solvent system the MPE was about 2.7%. The MPE values resulting from the proposed equation lie within the experimental relative standard deviation values and can be considered as an acceptable error.

Adrenergic beta-Antagonists↗
PubMed1982

Intravenous beta-blockade in coronary heart disease: is cardioselectivity or intrinsic sympathomimetic activity hemodynamically useful?

Beta-blocking drugs are increasingly prescribed in coronary heart disease, but controversy surrounds the hemodynamic relevance of their ancillary pharmacologic properties--cardioselectivity and intrinsic sympathomimetic activity. We therefore compared the effects of four intravenous beta-adrenoreceptor antagonists with different ancillary properties on left ventricular function in 24 patients with coronary heart disease. All four drugs depressed the relation between left ventricular filling pressure and cardiac output at rest and during exercise. However, practolol and oxprenolol, which have intrinsic sympathomimetic activity, induced significantly less depression of left ventricular function than either propranolol or metoprolol, which do not have this activity. Cardioselectivity, a property of both practolol and metoprolol, had no discernible hemodynamic advantage. Beta-blocking drugs that have intrinsic sympathomimetic activity appear to be more effective in maintaining cardiac function than drugs without this property, when given intravenously to patients with coronary heart disease.

Adrenergic beta-Antagonists↗
PubMed1980

Effect of selective beta-adrenergic blockade and stimulation on regional myocardial blood flow following acute coronary artery occlusion in the awake dog.

This study was designed to evaluate the effects of alterations of beta-receptor activity on intercoronary collateral blood flow after acute coronary artery occlusion in the awake dog. Blood flow following acute circumflex coronary occlusion was measured during: 1) control conditions; 2) selective beta1-blockade with practolol; 3) combined beta1 and beta2 blockade with propranolol; and 4) selective beta2 stimulation. Neither practolol nor propranolol significantly altered the volume or distribution of blood flow into the normally perfused or ischaemicmyocardial areas, while beta2 stimulation increased blood flow to the normally perfused myocardium from 1.13 +/- 0.12 to 1.28 +/- 1.10 cm3 .min-1 .g-1 (P <0.05). This increase in flow, which was directed preferentially to the subepicardium, was mediated by a significant decrease in coronary vascular resistance. In contrast to the effect on normally perfused myocardiu, beta2 stimulation resulted in a 47 +/- 12% decrease in collateral flow into the central ischaemic zone (P <0.05), which was mediated by a combination of decreased arterial pressure and increased collateral vascular resistance during beta2-agonist administration. Thus, although beta2 stimulation produced a modest increase in blood flow to normally perfused myocardium, in the setting of acute myocardial ischaemia, beta2 stimulation resulted in a significant decrease in intercoronary collateral flow.

Adrenergic beta-Agonists↗
PubMed1983

The B-aminopropionitrile-fed turkey: a model for detecting potential drug action on arterial tissue.

Broad-breasted white male turkeys develop hypertension, tachycardia and aortic arteriosclerosis spontaneously by approximately 5 weeks of age. When fed B-aminopropionitrile (BAPN), aortic tensile strengths are lowered, and a high percentage of the turkeys die from aortic dissecting aneurysms. There are essentially no deaths from aneurysms when either dl-propranolol or reserpine is fed in concert with BAPN; practolol and soltalol partially protect the BAPN-fed turkey from lethal aneurysms while hydralazine and phenelzine sulphate potentiate mortality from aneurysms. Dl-propranolol decreases and reserpine increases dP/dtmax and both drugs lower arterial pressure and heart rate when fed with BAPN. Such diets also decrease the ultrastructural disarray of collagenous and elastic fibres in the media of the abdominal aorta that occurs from the feeding of BAPN and thereby raise aortic tensile strength. Sotalol and practolol when fed to BAPN-fed turkeys lower blood pressure and dP/dtmax, but neither drug affects aortic tensile strength and both counteract the deleterious effect of BAPN on the ultrastructure of collagenous and elastic fibres to a minor degree. Phenelzine sulphate does not affect arterial pressure while hydralazine reduces arterial pressure; both drugs decrease aortic tensile strength and increase the ultrastructural disruption of aortic elastin and collagen in the BAPN turkey. The results suggest that dl-propranolol, reserpine, phenelzine sulphate, and hydralazine have an action on aortic tissue and indicate the usefulness of the BAPN-fed turkey as a model for identifying potential drug effects on aortic elastin and collagen.

Aminopropionitrile↗
PubMedDate not supplied

Exercise-induced increase in plasma arachidonic acid and thromboxane B2 in healthy men: effect of beta-adrenergic blockade.

We examined the effects of beta-blockade with the nonselective antagonist propranolol, the cardioselective antagonist atenolol, and the cardioselective antagonist with partial agonist activity, practolol, on the levels of free arachidonic acid (AA), thromboxane B2 (TxB2), prostaglandin (PG) E2, and 6-keto-PGF1 alpha in plasma, and TxB2 production by platelets during clotting in six normal subjects during submaximal dynamic exercise. The drugs were given intravenously in equipotent increasing doses before the exercise test. Exercise induced a clear increase in AA, TxB2, and 6-keto-PGF1 alpha in plasma. During the first 60 min of exercise all three beta-blockers decreased the plasma levels of AA and TxB2. Propranolol (0.19 mg/kg) was slightly more effective than atenolol (0.19 mg/kg) or practolol (0.64 mg/kg); however, at exhaustion, propranolol was markedly more effective than the other two blockers. Plasma 6-keto-PGF1 alpha and PGE2 levels were less affected by beta-blockade during exercise, and no significant effect was seen on TxB2 formation by platelets. The plasma 6-keto-PGF1 alpha/TxB2 ratio was markedly higher after propranolol treatment than after treatment with the other two blockers during the exercise period. These results suggest that the capability of a nonselective blocker to inhibit both beta 1- and beta 2-adrenergic receptors may be of advantage because of the more effective inhibition of thromboxane formation than with a cardioselective blocker, especially when the sympathetic tone is markedly increased.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Beta blockers after myocardial infarction--aspects on study design based on current knowledge.

The beta-blocker trials published so far may be subdivided into three different categories: 1) retrospective, 2) prospective non-conclusive, 3) prospective conclusive studies. The retrospective studies suffer the weaknesses of the retrospective method and may only be used as supportive evidence. There have so far been four prospective studies producing positive results, three with alprenolol and one with practolol. The studies presented support the concept that practolol and alprenolol reduce the long-term mortality due to sudden death from ischemic heart disease after myocardial infarction. All the studies have been criticized on various grounds and a list of unanswered remaining issues may be made. Acute and long-term effects of betablockade need not be the same. Our knowledge about the necessary doses and plasma levels is incomplete. All the studies published so far cover a maximum period of two years. If the study observation periods were prolonged it is likely that at some time the relative benefit becomes less. Ideal treatment should be reserved for those patients likely to derive significant benefit from it. At the present time identification of such patients is not sufficiently precise. Whether or not the beta-blockers have an antiarrhythmic effect, for instance demonstrated on chronic PVC's, this information is of little value in interpreting the proper mechanism of the beta-blockers in acute ischemia and lethal arrhythmias. In order to contribute new knowledge future studies should involve sufficiently large numbers of representative groups of patients, a stratified study design and a beta-blocker with ancillary properties different from alprenolol.

Adrenergic beta-Antagonists↗
PubMed1978

Characterization of beta-adrenoceptor subtype mediating the metabolic actions of salbutamol.

1. The following four intravenous treatments were administered in a balanced, randomized, Latin square design to four healthy volunteers: (1) saline injection (10 min); salbutamol infusion (0.15 microgram kg-1 min-1 for 60 min) (sS), (2) propranolol injection (0.3 mg kg-1 for 10 min); salbutamol infusion (pS), (3) practolol injection (2 mg kg-1 for 10 min); salbutamol infusion (PS) and (4) saline injection; saline infusion (ss). 2. Heart rate was recorded and venous blood taken for estimation of insulin, glucose and potassium before and after each injection (0 and 12-15 min) and at various times during the infusion (30,45,60 and 75 min). 3. The mean, peak % heart rate changes from baseline, control were +65.8%, +23.0%, -10.9% and -12.1%, the mean, peak % glucose changes, +61.0%, +7.1%, +3.6% and +6.9%, and the mean, peak % insulin changes, +298%, +28%, -28% and -43% during the infusions for sS, PS, ss and pS respectively. 4. The mean serum potassium levels before the injections and at the completion of the infusions were 3.98 and 3.08 4.03 and 3.63, 4.07 and 4.15, and 4.03 and 4.13 meq/l for sS, PS, ss and pS respectively. 5. Propanolol completely abolished the cardiac and metabolic responses of salbutamol. 6. Practolol produced only partial cardiac beta-adrenoceptor blockade, but completely inhibited the metabolic actions of salbutamol.

Adult↗
PubMed1979

Quantitative assessment of bronchial beta-adrenoceptor blockade in man.

1. We describe a method for assessing bronchial beta-adrenoceptor blockade quantitatively in man. Specific airway conductance is measured after increasing doses of inhaled salbutamol and the extent to which the dose-response curve is displaced to the right after beta-adrenoceptor blocking drugs is used to assess bronchial beta-adrenoceptor blockade. 2. Salbutamol dose-response curves were plotted for six normal subjects by measuring sGaw 15 min after increasing doses of inhaled salbutamol. Salbutamol produced a 30-70% increase in sGaw. 3. Salbutamol dose response curves were obtained 2 h after oral practolol (100 mg and 200 mg) and oral propranolol (40 mg and 80 mg) on separate days and were displaced to the right. 4. The mean dose ratios for practolol 100 mg and 200 mg were 1.2 and 2.1 and for propranolol 40 mg and 80 mg they were 21 and 61 respectively.

Adrenergic beta-Antagonists↗
PubMed1984

Enhancement of physiological finger tremor by intravenous isoprenaline infusions in man: evaluation of its role in the assessment of beta-adrenoceptor antagonists.

Graded intravenous isoprenaline infusions produce dose-related increases in finger tremor. The dose-response curves constructed with intra-arterial or intravenous isoprenaline behave similarly in the presence of both atenolol 50 mg and propranolol 40 mg. In Five subjects, practolol 120 mg, atenolol 50 mg, propranolol 40 mg and sotalol 200 mg reduced exercise heart rate by 20.2 +/- 2.3, 21.4 +/- 1.8, 17.4 +/- 2.5, 23.9 +/- 3.6% respectively: the differences were not significant. The corresponding dose-ratios for reduction of an isoprenaline tachycardia were 2.8, 2.3, 19.1 and 16.9 respectively. At doses which had comparable effects on an exercise tachycardia, the non-selective beta-adrenoceptor antagonists, propranolol 40 mg and sotalol 200 mg, attenuated the finger response to isoprenaline (dose ratios 33.3 and greater than 25.0 respectively) more than the beta 1-selective adrenoceptor antagonists, practolol 120 mg and atenolol 50 mg (dose ratios 1.0 and 2.3 respectively). In two out of five subjects, dose-response curves could not be constructed with sotalol, either at a dose of 200 or 100 mg. The enhancement of physiological finger tremor by intravenous infusions of isoprenaline may be useful in the investigation of beta 2-adrenoceptors and their antagonists in man.

Adolescent↗
PubMed1984

Cardiac dysrhythmias during outpatient dental anaesthesia with enflurane. The role of "beta blockade".

In a study of 120 unpremedicated outpatients presenting for outpatient dental anaesthesia, the incidence of dysrhythmias was lower with enflurane than had previously been found with halothane (1). The intravenous use of the cardioselective beta adrenergic blocking agents practolol and metoprolol, in a dose of 0.05-0.22 and 0.16-0.17 mg/kg body weight, respectively, proved effective in the treatment of sinus tachycardia in excess of 150 beats/min and/or ventricular dysrhythmias. Although metoprolol, unlike practolol, has no intrinsic sympathetic activity, there were no side-effects related to either beta-blocker in the dosages used during enflurane anaesthesia.

Adolescent↗