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At least 919 records · Page 51Linked to original sources
PubMed1974

Failure of beta-adrenergic receptor blockade to prevent arrhythmias induced by sympathetic nerve stimulation.

Cardiac arrhythmias produced by electrical stimulation of the ventrolateral cardiac sympathetic nerve in dogs were not blocked by the combined administration of propranolol and practolol in amounts that completely blocked cardiac beta-adrenergic receptors. Blockade of cardiac alpha-adrenergic receptors, as well as cardiac cholinergic receptors, also had no influence on the arrhythmias. These results suggest that the adrenergic neuroeffector junction is fundamentally different from any hitherto described, differing perhaps in the neurotransmitter involved or in the nature of the receptor.

Adrenergic alpha-Antagonists↗
PubMed1975

Selective inhibition of cholera toxin- and catecholamine-stimulated lipolysis by blocking agents.

Vibrio cholerae enterotoxin stimulates lipolysis in rat epididymal fat cell suspensions. Like hormones this toxin increases adenylate cyclase activity, raising levels of cyclic adenosine 3',5'-monophosphate (cAMP), which activates a cellular lipase. Using specific blocking agents, we studied the responses to the adrenergic lipolytic hormones epinephrine, norepinephrine, and isoproterenol, and to cholera toxin. All stimulators were used at 100 x threshold dose. Propranolol (34 muM), a beta blocking agent, inhibited epinephrine stimulation (P less than 0.001) but not that of toxin (P greater than 0.2). Choleragenoid (25 mug/ml), a natural toxoid of cholera toxin, blocked stimulation by toxin (P less than 0.001) but not that of the adrenergic agents (P greater than 0.2). A beta blocker, practolol (3 mM), inhibited stimulation by the catecholamines tested (P less than 0.005) but not that of toxin (P greater than 0.05). Higher concentrations of propranolol (340 muM) and the alpha blocking agents phenoxybenzamine (3 mM) and phentolamine (1.6 mM) inhibited all agonists (P less than 0.001). The response to theophylline was inhibited by all blockers (P less than 0.05) except propranolol at the lower concentration (34 muM). A combined beta and alpha blockade using propranolol and epinephrine together did not inhibit toxin-mediated lipolysis. It appears that stimulation by cholera toxin is independent of beta adrenergic receptors. A major inhibition of theophylline-mediated lipolysis by alpha blocking drugs indicated a nonspecific effect of these agents at the concentrations used. The uninhibited response to toxin in the presence of propranolol and epinephrine suggests a lack of relationship of the toxin receptor to either alpha or beta receptors.

Adenylyl Cyclases↗
PubMed1976

Abnormal lymphocyte function is secondary to drug-induced autoimmunity.

Abnormal lymphocyte function has been frequently reported in patients with connective tissue diseases but its significance has been uncertain. Sequential studies of lymphocyte function were carried out in patients receiving the beta-adrenergic blocking drug practolol (Eraldin) both before and during the development of autoimmune complications. No evidence was obtained that abnormal lymphocyte function presaged the onset of autoimmunity, and when these tests did show deficient responses these could be correlated with disease activity in general.

Adult↗
PubMed1982

Beta adrenergic receptors in pigmented ciliary processes.

Beta adrenergic receptors from membrane fragments of pigmented sheep eyes were studied and characterised by ligand binding techniques after the removal of melanin. In a representative experiment the beta max (total number of beta receptors) was 394.9 fmol/mg protein. The receptor affinity (Ka) was 440 pM. The potency series of drugs to displace 125I-HYP from the receptors was timolol = (-) propranolol greater than (+) propranolol greater than salbutamol greater than practolol. beta 1 Receptors were not detected in the ciliary processes. beta 2 Receptors were the prominent adrenergic receptors present. The theory as to how beta blockers work in glaucoma, their site of action, and the potential role of beta 2 blockers for use in intraocular pressure control is discussed.

Albuterol↗
PubMed1983

Slow-release artificial tear inserts in the treatment of dry eyes resulting from the oculomucocutaneous syndrome.

Patients with dry eyes resulting from the practolol syndrome present a therapeutic challenge. Very frequent instillation of preservative-free drops are the only therapy in most cases. Using an entirely new agent--a hydrophilic polymer in insert form--we have provided in this open study an alternative therapy which shows some subjective and objective advantages. Few patients experienced problems, and none left the study because of failure of retention of the insert. Some patients preferred the cooling, soothing effects of frequent drops. The problems in mounting a clinical trial of this sort are discussed.

Aged↗
PubMed1975

Effect of new beta-adrenergic blocking agent, Atenolol (Tenormin), on pain frequency, trinitrin consumption, and exercise ability.

In 11 patients with severe angina pectoris a new beta-blocking drug, atenolol (Tenormin; I.C.I.66082), was found in a double-blind randomized trial to reduce significantly the frequency of anginal attacks (P less than 0-001) and the amount of trinitrin consumed (P less than 0-03) in comparison with practolol and placebo. There was no significant improvement in the patients' ability to exercise on the bicycle ergometer.

Administration, Oral↗
PubMed1975

Effect of chronic beta-adrenergic receptor blockade in congestive cardiomyopathy.

Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, and echocardiogram showed improved ventricular function in all cases. The present study indicates that adrenergic beta-blocking agents can improve heart function in at lease some patients with congestive cardiomyopathy. Furthermore, it is suggested that increased catecholamine activity may be an important factor for the development of this disease, as has been shown in animal experiments.

Adult↗
PubMed1975

Surdocardiac syndrome of Jervell and Lange-Nielsen, with prolonged QT interval present at birth, and severe anaemia and syncopal attacks in childhood.

A case of the surdocardiac syndrome of Jervell and Lange-Nielsen, with prolonged QT interval in the electrocardiogram at birth, is described. The affected girl presented 3 1/2 years later with severe iron deficiency anaemia, despite apparently adequate nutrition. At the age of 4 1/2 years she had a sudden attack of unconsciousness. Treatment with the beta-adrenoceptor blocker practolol was started and 3 years after initiation of this treatment she has been free from syncopal attacks. The QT interval remains prolonged. Her brother also had severe iron deficiency anaemia and had several attacks of unconsciousness before he died suddenly at the age of 3 1/2 years.

1-Propanol↗
PubMed1975

Beta blockade in lithium tremor.

Practolol, propranolol, and placebo have been tested on an objective test of lithium induced tremor. Both beta-blocking agents produced significantly more tremor than the placebo. It is argued that lithium induced tremor is closer to essential than to physiological tremor.

Affective Symptoms↗
PubMed1978

Mediation of isoproterenol-induced thirst in rats by beta2-adrenergic receptors.

Isoproterenol-induced thirst in rats has been attributed to the activation of beta-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into beta1 and beta2 types, experiments were performed using several beta-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The beta1- and beta2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 microgram/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little beta-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 microgram/kg). Practolol (125 mg/kg), a beta1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective beta2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 microgram/kg), a beta2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that beta2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Albuterol↗
PubMed1979

The effect of propranolol and dimethylpropranolol on cardiac conduction.

Isolated dog hearts perfused with blood from a donor dogand driven at two heart rates were used to compare the effects of propranolol with those of its quaternary ammonium derivative on atrial, atrioventricular (AV) nodal, and His-Purkinje conduction. Propranolol slowed only AV-nodal conduction, increasing the minimal conduction time and the effect of prematurity, without affecting fatigue. Practolol did not have this effect. Dimethylpropranolol had similar but not identical effects on the AV node, but also slowed atrial and ventricular conduction. In contrast with the quaternary derivative of lidocaine, dimethylpropranolol's effect on atrial and ventricular conduction was not dependent on the heart rate. The effect of dimethylpropranolol on ventricular conduction was observed at doses lower than those reported by others to be antiarrhythmic.

Animals↗
PubMed1982

Characterization of the beta receptor responsible for enhanced histamine release from bovine leukocytes.

The present study was undertaken to determine the beta-receptor subtype responsible for the enhanced anaphylactic histamine release from bovine leukocytes produced by isoprenaline. The selective beta 1 antagonist practolol competitively inhibited the enhancement of histamine release produced by isoprenaline. The selective beta 2 agonists salbutamol and terbutaline produce no significant effect on antigen-induced histamine release. This indicates that the receptor responsible for enhancement of histamine release from bovine granulocytes is of the beta 1 subtype. The question is raised as to whether this is a normal physiological response or an abnormal condition produced by the sensitization procedure.

Albuterol↗
PubMed1978

Protein kinase regulation of cardiac phosphorylase activity and contractility.

The relationship between cAMP-dependent protein kinase activity and epinephrine-produced activation of phosphorylase and increase in contractility was investigated in the intact working rat heart. Epinephrine was administered as a bolus into the superior vena cava of open-chest preparations and the hearts were rapidly frozen. cAMP increased within 5 s and returned to control within 20-30 s. Protein kinase and phosphorylase kinase activity ratios increased transiently with the same time course as that for cAMP. The phosphorylase activity ratio and the rate of left ventricular pressure development increased maximally within 15 s and returned to control in 30-60 s. Continuous infusion of epinephrine caused a sustained elevation of the protein kinase. Free catalytic protein kinase activity increased proportionately with the dose of epinephrine. The beta-adrenergic blocking agent, practolol, had no effect on the basal levels of the five parameters studied, but did prevent the epinephrine-produced increases. The results suggest that the time course of cAMP-dependent protein kinase activation is appropriate if this enzyme is to play a role in the catecholamine-induced increase in both glycogenolysis and contractility in the in vivo heart.

Animals↗
PubMed1978

Mechanism of cardiac output response to hypertonic sodium chloride infusion in dogs.

Hypertonic sodium chloride and tris(hydroxymethyl)amino-methane (Tris) hydrochloride (0.3 mmol/kg.min) were infused intravenously into chloralose-anesthetized dogs over a 20-min period. Cardiac output, maximum left ventricular dP/dt, and (dP/dt)/P increased by 55, 33, and 23%, respectively, during NaCl infusion, but Tris HCl infusion had no effects. NaCl infusion did not change heart rate or left ventricular end-diastolic pressure. Mean systemic and pulmonry arterial blood pressures increased, whereas total peripheral and pulmonary vascular resistances decreased. Responsiveness of cardiac beta-adrenergic receptors, as determined by serial intravenous injections of epinephrine, was not affected by NaCl infusion. Plasma catecholamine concentration, however, increased during NaCl infusion. In addition, the increases in cardiac output, maximum left ventricular dP/dt and (dP/dt)/P were abolished by prior treatment with practolol, a cardioselective beta-adrenergic receptor blocking agent. These results suggest that the hemodynamic effects of NaCl infusion were caused, at least in part, by the inotropic action of catecholamines.

Animals↗
PubMed1990

Beta-receptor subtypes in the canine coronary circulation.

The principal difficulty in determining the subtype of coronary vascular beta-receptors in vivo is to avoid the local metabolic coronary vasodilation that occurs secondary to activation of myocardial beta-receptors. Therefore, a nonbeating cardiac preparation without chronotropic or inotropic effects is needed. In this study, the coronary circulation was perfused at constant pressure in closed-chest chloralose-anesthetized dogs. The increase in coronary blood flow due to intracoronary injections of the combined beta 1- and beta 2-agonist isoproterenol was determined during prolonged asystoles after the cessation of cardiac pacing in atrioventricular heart-blocked animals. Both beta 1-selective (practolol and L 650,744) and beta 2-selective (ICI 118,551) antagonists blocked isoproterenol-induced coronary vasodilation. In contrast, isoproterenol vasodilation in the femoral circulation was blocked by beta 2- but not by beta 1-selective antagonists. In conclusion, both beta 1- and beta 2-receptors in coronary resistance vessels are stimulated by isoproterenol to produce vasodilation during prolonged asystoles, when cardiac chronotropic and inotropic effects are absent.

Adrenergic beta-Antagonists↗
PubMed1975

Inotropic responses to digoxin during hypoxia and autonomic blockade.

Inotropic responses to digoxin (0.08 mg/kg) were studied in dogs and compared with responses during hypoxemia and autonomic blockade. Changes in left ventricular contractility (VC) were assessed by constructing function curves relating left ventricular (dP/dt)max and stroke volume to end-diastolic pressure. Augmentation of VC was observed 20 min after digoxin infusion and continued to increase until termination of the experiment after 60 min. In animals subjected to autonomic blockade with practolol, TEAC, and atropine, the increases in VC after digoxin were substantially greater. Equally large increases occurred in blocked dogs during sustained hypoxia (Pao2 = 28 mmHg). However, in animals without blockade there was a progressive fall in VC during hypoxia despite digoxin infusion, although less than in those not given digoxin. Serum digoxin levels were measured by radioimmunoassay and did not differ significantly in blocked compared to unblocked dogs or in hypoxic compared to nonhypoxic animals. These findings indicate that digoxin protects the heart from the decrease in myocardial contractility which occurs during extended hypoxia. This protective effect is more pronounced in animals deprived of autonomic function, possibly reflecting the elimination of reflex sympathetic withdrawal ordinarily induced by digitalis.

Adrenergic beta-Antagonists↗
PubMed1975

Pressure-flow and volume-flow relationships of the systemic circulation of the dog.

Mean systemic pressure-flow (Ps-Q) and volume-flow (V-Q) relationships of the systemic vascular bed were determined in two groups of dogs anesthetized with sodium pentobarbital (group I) and with methoxyflurane (group II). All blood returning to the heart (Q) was removed from the right atrial appendage and passed through a Starling resistor, a pump, a flowmeter , and then returned directly into the pulmonary artery. Ps was estimated from plateau values of right atrial pressure obtained during stop-flow procedures. Both the Ps-Q and V-Q relationships were nonlinear. This nonlinearity may be attributed to a redistribution of blood flow between systemic vascular compartments of unequal time constants. With group II, the Ps-Q and V-Q curves were shifted markedly to the right along the Ps and V axes, respectively. Evidence is presented which suggests that this shift was due to an effective back pressure other than right atrial pressure produced by a hepatic waterfall. The beta-adrenergic antagonist practolol increased the effective back pressure and augmented the shift in the Ps-Q and V-Q curves.

Abdomen↗
PubMed1976

Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.

The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.

Animals↗