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PubMed1977

Practolol peritonitis. A study of 16 cases and a survey of small bowel function in patients taking beta adrenergic blockers.

Sixteen patients with practolol peritonitis are described. Dense peritoneal thickening and adhesions caused small bowel stasis and obstruction with characteristic radiology and histology. The disease was best treated by surgery though complications were frequent and three of 16 patients died. Ocular and skin involvement were common. Fifty four asymptomatic patients who had taken a beta adrenoceptor blocking drug for more than 12 months were studied. Seven were found to have radiological abnormalities of the small bowel. These changes were associated with propranolol, oxprenolol and practolol therapy. It is not known whether they are related to practolol peritonitis.

Aged↗
PubMed1977

[Sclerosing peritonitis and practolol (author's transl)].

Skin manifestations, eye complications, a nephrotic syndrome, appearance of lupus erythematosus cells and antinuclear antibodies, sometimes combined with a systemic side effects of the beta adrenergic blocker Practolol. Another side effect is though to be sclerosing peritonitis. The latter is identical with the idiopathic fibroplastic peritonitis, described at the turn of this fibroplastic peritonitis, described at the turn of this century by German authors. Our own observation of a case of sclerosing peritonitis is compared with the literature. There is strong evidence for a causal relationship between longstanding Practolol-therapy and sclerosing peritonitis. Practolol was withdrawn from the market in 1975.

Aged↗
PubMed1976

[Reaction of peripheral veins and arteries following administration of beta-active agents. Studies on isoproterenol, propranolol, and practolol].

The local effect on veins and arteries of isoprenaline, propranolol and practolol was investigated in the human after intra-arterial application at the forearm. The injection of isoprenaline was followed by a dilatation of the arteries and veins. This effect was inhibited by propranolol, but not by practolol. The results demonstrate, that the peripheral vasoactive beta-stimulatory effect is mediated by so-called beta2-receptors, which were not influenced by a selective beta1-blocking agent like practolol. The results were discussed in respect to their clinical relevance.

Adult↗
PubMed1971

Distribution kinetics and intestinal absorption of practolol in the rat.

1. After intravenous injection of practolol the blood concentration-time curve is fitted by a bi-exponential function. A two compartment open system model is therefore a minimal requirement in order to describe adequately the distribution of the drug in the body.2. The parameters of the two compartment model for practolol were determined. The mean values for the ;fast disposition' half life and the ;slow disposition' half life were 0.5 min and 13.3 min, respectively.3. The rate constants of distribution and elimination were similar in different animals. The volume of the central compartment was related to the weight of the animal.4. The absorption of practolol from an intestinal site was measured by its appearance in the blood. The rate constant for this process was estimated to be 0.03 min(-1).

Acetanilides↗
PubMed1972

A comparison of the haemodynamic effects of propranolol, 4-hydroxypropranolol and practolol in anaesthetized dogs.

1. The haemodynamic effects of propranolol, practolol and 4-hydroxypropranolol have been compared in anaesthetized dogs both at free heart rates and at heart rates fixed by electrical pacing. All three drugs produced a fall in heart rate at the lowest dose of 0.09 mg/kg.2. Practolol caused less change in dP/dt, cardiac output and blood pressure than did propranolol. 4-Hydroxypropranolol had intermediate effects. Since the changes in dP/dt caused by these three drugs were still present when the heart rate was fixed by pacing, it is concluded that these were independent of changes in heart rate.3. The fact that practolol and 4-hydroxypropranolol cause less change in haemodynamic function than propranolol may be associated with the intrinsic sympathomimetic activity possessed by the first two of these drugs.

Adrenergic beta-Antagonists↗
PubMed1969

Mechanism of action of beta-adrenergic receptor blocking agents in angina pectoris: comparison of action of propranolol with dexpropranolol and practolol.

The effect on exercise tolerance of racemic propranolol has been assessed in eight angina pectoris patients and compared with that of dexpropranolol (the dextro isomer of propranolol), practolol (I.C.I. 50172), and saline. Dexpropranolol has the same local anaesthetic action as propranolol with negligible beta-adrenergic receptor blocking activity, while practolol is a cardio-selective beta-adrenergic blocking agent which does not have local anaesthetic activity.Saline and dexpropranolol had no significant effect on exercise time; racemic propranolol and practolol improved exercise tolerance in six subjects, the response to the two drugs being very similar in individual patients. It was concluded that the beneficial effect of propranolol in angina pectoris results from its action as a beta-adrenergic receptor blocking agent and is not due to its local anaesthetic, or quinidine-like, activity.

Acetanilides↗
PubMed2005

A ranked presentation of the MHRA/CSM (Medicines & Health Care Regulatory Agency/Committee on Safety of Medicines) Drug Analysis Print (DAP) data on practolol.

PURPOSE: To display a ranked presentation of the data given in the Drug Analysis Prints (DAPs) provided by the MHRA/CSM so that the monitoring clinician may be readily alerted to the most important findings. The practolol DAP is taken as an example of the presentation. METHOD: The data for the ranked system organ classes, the ranked deaths and the ranked reaction reports within each system organ class are considered separately. RESULTS: It has been found that there are advantages in considering the system-organ classes, the deaths and the reports of the individual reactions separately and then, within these groupings, providing the mathematically ranked data. The results for practolol, withdrawn due to the associated oculomucocutaneous syndrome, are given as a single worked example. CONCLUSIONS: Presentations of the ranked data arising from spontaneous adverse drug reactions reporting may have useful advantages.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Practolol inhibition of some salbutamol-induced metabolic and hormonal responses.

The effect of practolol (a selective beta1-adrenergic receptor blocking agent) on increased blood insulin, sugar, lactate and FFA and decreased blood phosphorus and potassium induced by salbutamol (a primarily beta2-adrenergic stimulant) was studied in 6 normal volunteers. Practolol abolished the rise of lactate and glucose, suggesting that changes in these parameters due to salbutamol are mediated by beta1-receptors. The rise of insulin and the fall of potassium were only partially inhibited, and the possible involvement of the beta2-receptors as well in these 2 cases cannot be ruled out. The decrease of phosphorus and the FFA rise were not affected and thus appear to be primarily dependent on beta2-receptors.

Adult↗
PubMed1985

Immediate central hemodynamic effects of five different beta-adrenoceptor-blocking agents, acebutolol, atenolol, pindolol, practolol, and propranolol, in patients with ischemic heart disease.

The hemodynamic effects of acebutolol were studied in six patients with ischemic heart disease. The changes in heart rate, cardiac output, and arterial blood pressure were determined after intravenous administration of six increasing doses of acebutolol to a cumulative dose of 0.64 mg/kg. After the sixth dose of acebutolol, cardiac output and heart rate were reduced 15% and 8%, respectively. Pulmonary artery pressure was increased by 4 mm Hg. Arterial blood pressure was not changed significantly. The effects of graded doses of acebutolol on heart rate and cardiac output were compared with earlier obtained results after atenolol (0.19 mg/kg), pindolol (0.025 mg/kg), practolol (0.64 mg/kg), and propranolol (0.19 mg/kg). The effects of increasing doses of acebutolol and practolol were very similar and significantly different from the effects of the other three drugs in spite having been administered at equipotent doses. The hemodynamic effects of acebutolol support the hypothesis that the hemodynamic response to beta-adrenoceptor antagonist drugs at rest is determined primarily by the degree of intrinsic sympathomimetic activity, whereas beta-1 selectivity does not modify the central hemodynamic response.

Acebutolol↗
PubMed1984

Effect of propranolol, practolol and atenolol on human platelet thromboxane formation and plasma levels of prostaglandins 6-keto-F1 alpha and E2.

The effects of three different beta-adrenergic blocking drugs, propranolol, practolol and atenolol on platelet thromboxane production and the release of prostacyclin and prostaglandin E2 into the circulation were investigated in healthy volunteers. The beta-adrenergic antagonists were administered intravenously at equipotent doses. The serum TxB2 levels after whole blood clotting and the arterial and venous plasma concentrations of 6-keto-PGF1 alpha and PGE2 were measured before and during a 60 min period after the administration of the drugs, using radioimmunoassay. Practolol and atenolol elicited a significant decrease in platelet thromboxane formation but remained without effect on plasma 6-keto-PGF1 alpha and PGE2 levels. In contrast, propranolol did not influence serum TxB2 concentrations but induced a significant increase in plasma content of 6-keto-PGF1 alpha and PGE2. The results indicate that beta-adrenergic antagonists alter the balance between the proaggregatory, vasoconstricting and antiaggregatory, vasodilating prostanoids in the human cardiovascular system. Although the direction of the action of these drugs seems to differ depending on the selectivity of the beta-adrenoceptor blocking properties the net effect of this action should be beneficial.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Reoxygenation dysrhythmias in the isolated guinea-pig heart: sensitivity to prazosin, atenolol and practolol.

Isolated guinea-pig hearts were perfused aerobically for 60 min, then made anoxic for 30 min and finally reoxygenated for 30 min. The effects of prazosin, atenolol and practolol on contractility, coronary pressure, ECG and LDH release were examined. Prazosin and atenolol were able to reduce significantly the incidence of ventricular fibrillation and LDH release. The same two drugs increased the recovery of normal electrical activity after 30 min of reoxygenation. Practolol, on the other hand, was ineffective in reducing the incidence of ventricular arrhythmias and LDH release.

Animals↗
PubMed1977

Respiratory disease associated with practolol therapy.

Six patients who had surgical treatment for sclerosing peritonitis caused by practolol now have a respiratory disorder characterised by dyspnoea, extensive fibrotic pleural thickening, and lesions in the lung parenchyma. Respiratory disease appears to be a further feature of the practolol syndrome.

Aged↗
PubMed1977

Practolol and deafness.

Practolol ('Eraldin') is a beta-blocking agent whose prolonged use may result in the appearance of untoward side-effects, notably ocular symptoms, skin rashes and deafness. We report ten cases of deafness due, or thought to be due, to practolol; and in all except three of the cases (8,9 and 10), the deafness became manifest many months after the appearance of lesions in the skin and eyes. Progression of any hearing loss caused by this drug seems to be arrested by its withdrawal. Otologists are urged to report any suspicious cases to the Committee on Safety of Medicines, Finsbury Square House, 33/37A Finsbury Square, London EC2A IPP.

Aged↗
PubMed2006

Testing times: the emergence of the practolol disaster and its challenge to British drug regulation in the modern period.

This article analyses how practolol, the first British drug disaster of the modern, post-thalidomide regulatory period, related to the pharmaceutical industry, the medical profession and government regulation of patients' health. Drawing on comparison with the USA, it argues that, contrary to public expectation and perception, the aftermath of thalidomide did not give rise to strident British drug control, imposing the highest possible safety standards on the pharmaceutical industry. Rather, there existed a culture of reluctant regulation that was characterised by continued optimism about, and trust in the purported benefits of new drugs among manufacturers and regulators in the United Kingdom, together with commitment to the protection of the industry and its institutional support for the medical profession. In particular, British regulators were willing to allow new drugs on to the market, fully aware of uncertainty about their safety, but unwilling to be pro-active in issuing warning letters about risks and requiring 'certainty' before acting to withdraw a product. Even after the practolol disaster, the British system was unable to reform itself to construct more rigorous and pro-active monitoring of drug risks. This was because of conflicts with industry interests.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Comparative effects of propranolol, pindolol, and practolol after excision of the sinoatrial node in dogs.

We studied the effects of intravenous injections of three beta-adrenoceptor antagonists on cardiac automaticity in conscious dogs after sinoatrial node (SAN) excision. Injections were repeated for 60 days postoperatively. In controls, mean corrected sinoatrial node recovery time (CSNRT) was 535 +/- 24 ms. One milligram per kilogram of dl-propranolol did not modify heart rate but raised CSNRT (p less than 0.01). One-half milligram per kilogram of dl-pindolol raised heart rate (p less than 0.05) and reduced CSNRT (p less than 0.05). Ten milligrams per kilogram of dl-practolol were needed to significantly reduce heart rate and raise CSNRT (p less than 0.01). In dogs after SAN excision, 0.1 mg/kg and 0.5 mg/kg of dl-propranolol lowered heart rate on days 3, 30, 43, and 60. Corrected recovery time (CRT) at a cumulative dose of 0.5 mg/kg rose to 9015 +/- 1028 ms on day 3 and to 3064 +/- 810 ms on day 30 (p less than 0.001). dl-Pindolol stabilized the rhythm. With 0.1 mg/kg, heart rate and CRT were not modified significantly on days 9 and 46. dl-Practolol at cumulative doses of 1 and 5 mg/kg lowered heart rate significantly on days 7 and 46. On day 12, the same doses did not modify heart rate but raised CRT (p less than 0.05). This suggests that of the beta-adrenoceptor antagonists studied here pindolol may be preferable in treatment of certain supraventricular arrhythmias.

Adrenergic beta-Antagonists↗
PubMed1976

Practolol in acute myocardial infarction.

A double blind trial of practolol in coronary heart disease has been conducted for 2 years. In 298 patients with acute myocardial infarction there was no reduction in overall mortality. In a group with initial heart rate over 100 per minute mortality was significantly lowered up to 1 year. Of 484 patients with coronary heart disease treatment for 2 years did not produce a significant reduction in infarction or sudden death. Beta-adrenergic blocking drugs have been shown to reduce left ventricular work and to have an antiarrhythmic action. On these grounds they would seem theoretically to have a place in the management of acute myocardial infarction. Practolol is a cardio-selective beta-blocking agent with an intrinsic sympathomimetic action, but devoid of local anaesthetic effect. It has been found effective in post infarction arrhythmias (1). In early infarction it reduces the area of necrosis as measured by surface ST segment mapping (2).

Acute Disease↗
PubMed1981

Speed of onset of pharmacodynamic activity of propranolol, practolol, oxprenolol and metoprolol after intravenous infection in man.

1 The speed of onset of the pharmacodynamic activity of intravenous propranolol, practolol, oxprenolol and metoprolol was determined, using attenuation of isoprenaline-induced tachycardia as the end-point, in 16 patients with clinically coronary heart disease. 2 Antagonism was evident within 15 s of injection into the central circulation of all four drugs. The time to maximum attenuation of isoprenaline tachycardia was significantly more rapid with propranolol and oxprenolol than with practolol and metoprolol.

Adrenergic beta-Antagonists↗