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At least 757 records · Page 42Linked to original sources
PubMed1978

Effect of dobutamine, a new cardioselective sympathomimetic drug, on myocardial oxygen balance in conscious dogs.

The effects of (+/-)-4-(2-[3-(p-hydroxyphenyl)-1-methylpropyl]-amino)-ethyl-pyrocatechol hydrochloride (dobutamine) on myocardial O2 balance were investigated in healthy conscious dogs with experimental AV-block. Dobutamine, injected as a bolus of 3, 6, 10 micrograms/kg, increased myocardial contractility, coronary flow, coronary venous O2 saturation and aortic pressure, while initially decreasing SA-node rate. Following ganglionic blockade the effects of dobutamine on myocardial contractility were unchanged while those on coronary flow and coronary venous O2 saturation were reduced by 30%. Aortic pressure and heart rate showed a dose dependent, long-lasting increase. The effects of dobutamine on heart rate and myocardial contractility could be abolished by beta 1-adrenoceptor blockade with practolol (2 mg/kg) while the effects on coronary flow and myocardial O2 extraction were reduced by 40% after practolol. Following beta 1 + 2 adrenoceptor blockade with propranolol, dobutamine increased aortic pressure and coronary flow while coronary resistance and myocardial oxygen extraction were unaffected.

Animals↗
PubMed1977

Effects of atropine, isoprenaline, neostigmine and practocol on cardiac arrhythmias induced by potassium in anesthetized dogs.

Either atropine, isoprenaline, neostigmine or practolol was given intravenously in therapeutic doses to dogs anesthetized with pentobarbitone sodium. Cardiac arrhythmias were induced by potassium chloride intravenously as a bolus injection in a dose of 0.3 mmol/kg. The standard electrocardiographic lead II was recorded continuously. pH, Po2 and Pco2 were checked from arterial blood samples before and after the injection. The isoprenaline treated dogs showed the smallest amount of arrhythmias and all the dogs survived. More severe arrhythmias were seen in the neostigmine and practolol treated dogs and the most severe occurrences were encountered in the atropine treated dogs.

Animals↗
PubMed1984

Alpha-adrenoceptor stimulation enhances automaticity in barium-treated cardiac Purkinje fibers.

We used intracellular microelectrodes to study the effect of alpha-adrenoceptor stimulation on automaticity of sheep cardiac Purkinje fibers exposed to low (10(-5) - 4 X 10(-5) M) barium concentrations. Concentrations of norepinephrine (NE) (3 X 10(-8) - 3 X 10(-7) M), which did not induce spontaneous activity in the absence of barium, consistently induced or enhanced it (if already present) in the presence of barium. Similar results were obtained in the presence of practolol (10(-6) M), which in 13 out of 17 experiments did not counteract the effect of NE. However, phentolamine (3 X 10(-7) M) caused a slowing or blocking of the spontaneous activity induced by NE in barium-treated preparations either in the presence or in the absence of practolol. We conclude that alpha-adrenergic responsiveness is enhanced in barium-treated Purkinje fibers and that under these experimental conditions, alpha-adrenoceptor stimulation may influence automaticity. The possible mechanisms underlying such effects are discussed.

Action Potentials↗
PubMed1981

Role of released catecholamines in the vascular response to injected angiotensin II in the dog.

The contribution of released epinephrine and norepinephrine to the pressor response induced by i.v. injected angiotensin II was assessed in pentobarbital-anesthetized dogs. Control pressor dose-response curves for i.v. angiotensin II were obtained in dogs pretreated with hexamethonium, atropine and practolol. Hexamethonium and atropine minimized the cardiovascular reflex responses elicited by the pressor action of angiotensin II which would preclude interpretation of the results. Practolol was administered to antagonize indirect cardiac stimulation selectively through sympathoadrenal activation by angiotensin II. Three additional pressor dose-response curves for angiotensin II were obtained in each dog. The second dose-response curve was obtained after the administration of phentolamine and the third dose-response curve was obtained after the subsequent administration of sotalol. The final dose-response curve was obtained after partial recovery of the pressor responsiveness to norepinephrine and epinephrine from phentolamine blockade. The pressor responses for angiotensin II after phentolamine and sotalol (curve 3) were significantly smaller than those in the control dose-response curve (curve 1). No significant differences in the pressor responses to angiotensin II were noted after phentolamine when compared with those obtained after phentolamine plus sotalol (curve 2 vs. curve 3). The angiotensin II pressor responses after partial recovery from phentolamine (curve 4) did not differ significantly from those obtained in the control dose-response curve. These results of released catecholamines mediated through alpha adrenergic receptors in the pressor response to angiotensin II.

Adrenal Medulla↗
PubMedDate not supplied

A mechanism of action of phenylephrine on heart.

Phenylephrine exerted a positive chronotropic and inotropic effect on isolated, spontaneously beating, atria of reserpinised rabbits. Addition of phenoxybenzamine and phentolamine resulted in a depression of control contractile amplitude. Practolol, however, was devoid of this effect. The positive inotropic response to phenylephrine was significantly antagonised by all the three blockers used, while positive chronotropic response was annulled by phentolamine and practolol, but not with phenoxybenzamine. It is, therefore, suggested that phenylephrine exerts its cardiostimulant effects through mediation of both alpha and beta-1 adrenoceptors. A probable mechanism of action could be, that phenylephrine acts on some specific chemical group, shared by alpha and beta1 receptors. This specific group is probably blocked by both alpha and betaceptor antagonists separately, so phenylephrine becomes ineffective in presence of these antagonists.

Animals↗
PubMedDate not supplied

Protective effects of different beta-blocking agents against electroshock lethality in mice.

The protective effect of phenytoin against an electroshock lethal dose (ELD), was compared with that of three different beta-blocking agents. These compounds were propranolol with quinidine-like activity (QLA) but no intrinsic sympathomimetic activity (ISA), practolol with ISA but no QLA and metoprolol with no ISA but some QLA. Phenytoin (15 mg/kg) and propranolol (70 mg/kg) protected all the animals. Metoprolol was only effective at higher concentrations (130 mg/kg). Practolol afforded some degree of protection at low doses (20 mg/kg) but at higher doses its ISA can be deleterious by decreasing the ELD threshold. These results suggest that QLA is more important than beta-blocking activity for protection against electroshock lethality.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Influence of beta-adrenoceptor antagonists on spontaneous rate and on force of contraction of isolated rabbit atria.

The influence of beta-adrenoceptor antagonists on the spontaneous rate and on force of contraction of the myocardium was studied independently on spontaneously beating right and electrically driven isolated left atria of rabbit. On spontaneous rate, practolol had sympathomimetic effect only, N-isopropylmethoxamine (IMA), had both sympathomimetic as well as depressant effects, whereas alprenolol, procinolol, bunolol and H 35/25 had depressant effects only in higher concentrations. The order of potency was procinolol greater than bunolol greater than alprenolol greater than H 35/25 greater than and IMA. On the contractions of isolated left atria, all beta-adrenoceptor antagonists produced concentration-dependent depressant effect. In relation to procinolol, these agents were 5-125 times less potent for depressing the contractions of left atria by 15% and the order of beta-potency was procinolol greater than alprenolol greater than bunolol = H 35/25 greater than IMA greater than and practolol. The present results indicate that the depressant effects of beta-adrenoceptor antagonists on spontaneous rate of right atria and on contraction of isolated left atria are not related to each other.

Adrenergic beta-Antagonists↗
PubMed1984

Effect of some beta adrenergic blocking agents and phenytoin on potentiation of quinidine antiarrhythmic activity in the mouse.

Quinidine coadministered with propranolol produces antiarrhythmic potentiation. The mechanism is uncertain although some in vitro electrophysiologic studies have suggested that it may be due to propranolol-induced cardiac beta receptor blockade. Other effects of propranolol, however, including a decrease in cardiac sympathetic nerve activity as well as some direct cardiac membrane effects might also contribute. The possible contributions of these effects were studied indirectly by coadministering quinidine with several compounds (d-propranolol, l-propranolol, d-practolol, practolol, pronethalol, and phenytoin) which have varying effects on these parameters. Antiarrhythmic activity was determined as protection against chloroform-induced ventricular arrhythmias and beta blockade as inhibition of isoproterenol-induced tachycardia. Only d- and l-propranolol and phenytoin potentiated quinidine. The d-isomer was only approximately 1/8th as potent as the l-isomer for inhibiting isoproterenol tachycardia, and the lowest dose of the d-isomer coadministered with quinidine produced antiarrhythmic potentiation but little if any inhibition of isoproterenol tachycardia. The results suggest that cardiac beta blockade alone does not adequately explain the potentiation of quinidine by propranolol in the mouse. Perhaps a decrease in cardiac sympathetic nerve activity and the direct membrane effects as occur with d-, l-, and d,l-propranolol and phenytoin may also contribute to the potentiation.

Animals↗
PubMed1984

[Drug eruptions caused by beta-blockers].

Adverse skin reactions due to betablocking agents are less frequent and severe since the 1974 "practolol syndrome". Psoriasiform, eczematous and lichenoid eruptions are the common manifestations with low-titres of auto-antibodies. The exact pathogenesis of these cutaneous reactions is unknown but an immunopharmacological mechanism is the probable cause in the majority of cases. The eruption may appear many months after the initiation of treatment and, in the case of practolol, was followed by sclerosis of the internal organs. Therefore, these cutaneous reactions must be recognised as a signal of possible high toxicity when observed with a high incidence in new betablocking agents.

Adrenergic beta-Antagonists↗
PubMed1976

Propranolol in the treatment of angina: a review.

The use of beta-adrenergic blocking drugs in angina pectoris was one of the original indications for these drugs suggested by Black. An anti-anginal effect was demonstrated with the first beta-adrenergic blocking drug, pronethalol, that was used clinically. This benefit in angina was confirmed in the early trials with propranolol in 1964-65. Although some definite anti-anginal effect can be demonstrated with low fixed dosage, evidence suggested that those trials which used a higher and a variable dose displayed a greater anti-anginal action of the drug. After a two dose trial (Gillam and Prichard, 1966,) demonstrated a dose dependent anti-anginal effect, a log-dose response study demonstrated a progressive reduction in angina attacks as dosage was increased (Prichard and Gillam, 1971). While a highly significant effect was found with an average dose of 52 mg a day a progressive reduction in angina attacks was found with logarithmic increases in dosage up to an average of 417 mg a day. Dosage in this trial was adjusted to produce a supine heart rate of 55-60 beats/minute provided this was not prevented by side effects. As the dosage of 417 mg a day was still on the straight line part of the dose response curve and therefore suboptimal, we not adjust dosage to produce a standing heart rate of 55-60. Fully meaningful comparative trials require that optimum dose of the drugs being compared are used. A variable dose comparative trial comparing propranolol and practolol, showed propranolol was the more effective agent. More recently a variable dose comparative trial of sotalol and propranolol indicated propranolol had greater anti-anginal action although sotalol, unlike practolol, was more effective than low dose propranolol. The use of beta-blocking agents in angina pectoris is relatively safe provided that the contraindications of asthma and cardiac insufficiency are observed and that treatment is commenced at a low dosage. The most dramatic change in the sympathetic environment of the heart takes place when treatment with a beta-blocking drug is commenced. The greatest danger of precipitating heart failure is therefore at the beginning of treatment even with a small starting dose. Once treatment has begun even an increase of 25% per dose represents a small pharmacological increment as there is no great change in the sympathetic drive to the heart. The larger dosage of beta-blocking drugs required for optimum treatment of angina may be gradually approached, but it has been my experience that heart failure is not likely to be precipitated at larger doses, provided they are not used initially. In other than mild angina pectoris the average optimum dosage of propranolol is 500-800 mg a day, similar, or perhaps more than the average dose in hypertension.

Alprenolol↗
PubMedDate not supplied

Spontaneous synthesis of acetylcholine in the rat brain after beta adrenergic receptor blockade.

Spontaneous synthesis of acetylcholine in the rat brain after beta adrenergic receptor blockade. Acta Physiol. Pol., 1977, 28 (1): 31-38. The purpose of this work was to determine the effects of propranolol, oxprenolol and practolol on acetylcholine synthesis in the cerebral cortex and brain stem of rats in vitro and in vivo. Propranolol and oxprenolol inhibited acetylcholine synthesis in slices of cerebral cortex and brain stem in vitro but not in vivo. Practolol reduced the synthesis of acetylcholine in cortical neurons but was without effect on acetylcholine synthesis in brain stem neurons. The authors suppose that the inhibition of acetylcholine synthesis in vitro by the beta-adrenergic blocking agents used in this experiment was due to disturbances either in glycolysis or in the transport of sodium, potassium and calcium ions across cell membranes.

Acetylcholine↗
PubMed1976

The antihypertensive action of several beta-adrenoreceptor-blocking drugs.

The antihypertensive and pulse-slowing effects of racemic propranolol, oxprenolol, pindolol, practolol and d-propranolol were assessed in 54 hypertensive patients. Drug dosage was selected to be proportionate to beta-adrenoreceptor-blocking potency; d-propranolol dosage equalled approximately that of racemic propranolol. D-propranolol had onlyslight antihypertensive effect; the four other drugs were found to have a considerable and approximately equal antihypertensive effect. The degree of slowing of heart rate varied with the different drugs, being greatest with racemic propanolol. The effect on pulse rate did not correlate with the effect on blood pressure for most of the drugs. The falls in blood pressure induced by racemic propanolol were strongly correlated with those induced by each of the other drugs. The small falls in blood pressured induced by d-propranolol correlated also with those induced by practolol (which had no membrane activity) and are presumably due to its weak beta-adrenoreceptor-blocking action. The beta-adrenoreceptor-blocking action per se is responsible for the antihypertensive action of these drugs.

Adrenergic beta-Antagonists↗
PubMed1977

Effect of cardioselective beta-blockade by metoprolol on the phasic myocardial blood content and epi/endocardial ratio.

Using I131-albumin labelling of plasma and a special biopsy cutting device, the blood content of the subendocardium and subepicardium was determined in guinea pig hearts. Measurements were done both in untreated animals and after intravenous administration of metoprolol, a new cardioselective beta-blocking compound. The data were compared with results obtained with propranolol and practolol. Metoprolol decreased the blood content less than propranolol. Practolol in a small dose even increased the blood content in the subendocardium in end-systole. The heart rate decreased by about the same magnitude after all the compounds tested, suggesting that the cardioselectivity of metoprolol was the likely explanation for its differing response from propranolol.

Animals↗
PubMed1976

Influence of "Polarizing" infusions on anthiarrhythmic effects of beta-blockers.

The antiarrhythmic effect of practolol (0.30 mg/kg) was studied in 25 patients pretreated with infusion of glucose-insulin (GI) solution. GI solution showed an antiarrhythmic effect either after or before the beta-blocker with pH in normal range or compensated metabolic acidosis. GI infusion produced a metabolic acidosis and an arrhythmogenic effect in some cases. Practolol had no antiarrhythmic effect in patients with VPB and GI infusion raised metabolic acidosis.

Acidosis↗
PubMed1987

Dobutamine: positive inotropy by nonselective adrenoceptor agonism in isolated guinea pig and human myocardium.

Positive inotropic responses to dobutamine have been examined using isolated myocardium from guinea pigs und humans. The potency (EC50) of dobutamine was 1.5 X 10(-6) mol/l on guinea pig papillary muscles, 1.8 X 10(-6) mol/l on guinea pig left atria and 2.5 X 10(-6) mol/l on human papillary muscle strips. In guinea pig cardiac muscles, Schild plots for the beta 1-selective antagonist, 1-practolol, using dobutamine as agonist, had slopes of less than unity. This suggested the involvement of other receptors in the inotropic response to dobutamine. The beta 2-selective antagonist, ICI 118,551, but not the alpha 1-selective antagonist, prazosin, attenuated the dobutamine response in guinea pig papillary muscles. Both ICI 118,551 and prazosin shifted the dobutamine concentration-response curve in guinea pig left atria. The positive inotropic response to dobutamine in human papillary muscles was antagonised by l-practolol and ICI 118,551 but not by prazosin. The maximal inotropic response to dobutamine was 90% that of calcium measured in the same guinea pig papillary muscles but only 37% that of calcium in human papillary muscle strips. This reduced maximal effect of dobutamine in human myocardium is probably a disease-induced change but species variations cannot be excluded.

Animals↗
PubMed1986

The modulation of head-twitch behaviour by drugs acting on beta-adrenoceptors: evidence for the involvement of both beta 1- and beta 2-adrenoceptors.

Drugs selective for either the beta 1- or beta 2-adrenoceptor have been investigated for their effects on the head-twitch behaviour induced by L-5-hydroxytryptophan (L-5-HTP) in mice. All four agonists, dobutamine and prenalterol (beta 1-), and salbutamol and procaterol (beta 2-), potentiated the effect of L-5-HTP although they were ineffective in inducing the head-twitch when administered alone. The corresponding antagonists, practolol and metoprolol (beta 1-) and butoxamine and ICI 118,551 (beta 2-), were without effect on the L-5-HTP head-twitch. The antagonists each significantly reduced the effect of the corresponding agonists but, while butoxamine and ICI 118,551 were inactive against dobutamine and prenalterol potentiation, both practolol and metoprolol reduced the effect of salbutamol and procaterol. Thus it is argued that dobutamine and prenalterol potentiation is due to an action at beta 1-adrenoceptors, while at least a component of the potentiating effect of salbutamol and procaterol is exerted through beta 2-adrenoceptors. The lack of effect of the antagonists alone is discussed.

5-Hydroxytryptophan↗
PubMed1985

Antihypertensive therapy with a single daily dose of acebutolol in essential hypertension, response and ophthalmological assessment in the Japanese.

Twenty patients with essential hypertension were given 400 mg acebutolol once daily for 24 weeks. In order to study if side effects resembling the "Practolol syndrome" developed, ocular effects were sought and antinuclear antibody (ANA) in blood was assessed before and after treatment. ANA was negative both before and after the study in 17 patients; in one patient ANA was positive, but the titre (1:10) was low and did not change during the study. Acebutolol produced no undesirable effects on cornea, conjunctiva or lens. During acebutolol treatment, tear secretion was reduced but tear lysozyme concentration was not significantly altered. Overall, acebutolol had no undesirable action similar to the practolol-induced syndrome, nor did it cause such common clinical ocular symptoms such as dry or gritty eyes.

Acebutolol↗
PubMed1982

Clinical pharmacology of adrenergic-adrenoreceptor-blocking drugs.

The development of beta-adrenoreceptor-blocking drugs provided an important group of agents to treat the cardiovascular disorders hypertension, angina pectoris, and cardiac arrhythmias and to manage patients with thyrotoxicosis. For clinical purposes, these drugs can be divided into two groups, that is, those with intrinsic sympathomimetic activity (ISA) and those without (non-ISA). The non-ISA drugs include propranolol, which is noncardiac selective: labetalol, which is noncardiac selective with alpha blockade: and and metoprolol and atenolol, which are cardiac selective. The drugs with ISA include pindolol, oxprenolol, and alprenolol which are noncardiac selective, and practolol which is cardiac selective. These drugs resemble isoprenaline in chemical structure, but their interaction with the beta-adrenoreceptors causes no response or only a slight response if the drug has ISA. By occupying the receptors, they block excitation by noradrenaline released from the sympathetic nerves and by adrenaline from the adrenal medulla. Drugs with ISA appear to depress cardiac activity and to interfere with bronchodilator drive less than do non-ISA drugs. Beta-blocking drugs differ considerably in their bioavailability because of differences in the rate and extent of metabolism in the first past through the liver after absorption from the gut. The therapeutic dose range varies widely for those with low bioavailability but is more predictable for those with high bioavailability. The drugs also differ in plasma protein binding and in their receptor affinities. In addition to their usual adverse effects, which include exacerbation of cardiac failure, bronchospasm, sleep disturbances, and Raynaud's phenomenon, concern has arisen about possible ocular and mucocutaneous side effects with beta-blocking drugs. This is a recognized problem with practolol, and it is not certain whether it occurs with other beta-blocking drugs. A double-blind study reported here of 110 matched patients, 36 of whom were on pindolol for more than 2 years, did not reveal any evidence of oculomucocutaneous problems related to drug treatment.

Adrenergic beta-Antagonists↗