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Biomedical subjects

W F Lubbe

Publications and source records attributed to W F Lubbe.

At least 19 recordsLinked to original sources
PubMed1979

Catecholamine-mediated arrhythmias in acute myocardial infarction. Experimental evidence and role of beta-adrenoceptor blockade.

Ventricular fibrillation is a major mechanism of sudden death. The cellular link between catecholamine activity and the development of serious ventricular arrhythmias may be in the formation of cyclic adenosine monophosphate (cAMP). Cyclic AMP and agents promoting cAMP accumulation allow development of slow responses which, especially in the presence of regional ischaemia, could develop into ventricular fibrillation. The role of beta-antagonist agents in the therapy of acute myocardial infarction is analysed in relation to the hypothesis linking cAMP and ventricular fibrillation. Reasons for the limited effectiveness of anti-arrhythmic therapy with beta-antagonist agents are given.

Adrenergic beta-Antagonists↗
PubMed1979

Oesophageal ulceration due to slow-release potassium in the presence of left atrial enlargement.

Ulceration of the oesophagus was suspected clinically and confirmed radiologically in a patient with an enlarged left atrium while on treatment with slow release potassium chloride. Its discontinuation resulted in resolution of symptoms. This potentially serious complication of treatment should be considered in patients with enlargement of the left atrium who develop dysphagia. It is avoided by using soluble forms of potassium chloride replacement.

Aged↗
PubMed1979

Protective action of amiodarone against ventricular fibrillation in the isolated perfused rat heart.

The pretreatment of rats with amiodarone for 2 minutes to 3 weeks before the excision of their hearts caused a dose-related decrease in heart rate and an increase in the ventricular fibrillation threshold both before and after coronary arterial ligation. Similarly, amiodarone decreased the incidence of ventricular premature extrasystoles, ventricular tachycardia and fibrillation during the period of regional ischemia after coronary arterial ligation and also after reperfusion of the ischemic myocardium. There was no evidence of a metabolic protective effect on ischemic myocardium because tissue high energy phosphate content decreased to a similar extent in ischemic myocardium from control and amiodarone-treated rats. Instead, the protective effect of amiodarone against fibrillation was accompanied by attenuation of the increase in tissue cyclic adenosine monophosphate in ischemic myocardium after coronary arterial ligation. It is proposed that amiodarone exerts a potent antifibrillatory effect by decreasing tissue cyclic adenosine monophosphate in ischemic myocardium.

Amiodarone↗
PubMed1978

Cyclic A.M.P. and arrhythmias revisited.

Further evidence is presented for a hypothesis linking cyclic adenosine 3', 5' monophosphate (cyclic A.M.P.) and arrhythmias: in the isolated rat heart, changes in tissue cyclic A.M.P. are accompanied by changes in the ventricular-fibrillation threshold; and in the pig, large infarcts are associated with raised tissue cyclic A.M.P. and ventricular fibrillation, whereas small infarcts are not. Data showing that changes in the metabolism of potassium, glucose, fatty acids, and lactate can influence the action-potential duration are incorporated into a revised hypothesis which allows for multifactorial arrhythmogenic mechanisms in the early stages of acute myocardial infarction.

Action Potentials↗
PubMed1978

Multiple serous effusions complicating pre-eclampsia. A case report.

A patient with multiple serous effusions and the nephrotic syndrome complicating the middle trimester of pregnancy is described. Rapid resolution of the effusions after delivery and exclusion of other causes of serous effusions and nephrosis make pre-eclamptic toxaemia the most likely cause. Anasarca can be a feature of this disease and there are a few reports of patients in whom clinical ascites has occurred. Our patient was exceptional in that pleural and synovial effusions into the knee joints were also present.

Adult↗
PubMed1978

Clinical usefulness of the beta-adrenergic antagonists.

The pharmacology of the beta-adrenergic antagonists, particularly their role as competitive antagonists at the receptor site, is discussed. The clinical use of these agents is listed and a detailed outline of their use in angina pectoris, hypertension and conditions associated with increased sympathetic activity is provided. The relative contraindications to the use of beta-adrenergic antagonists are summarized and the pharmacology of those drug interactions involving these agents is discussed. A thorough understanding of the pharmacology and therapeutics of these agents, which interfere with physiological function, is mandatory prior to their clinical use.

Adrenergic beta-Agonists↗
PubMed1978

Q fever endocarditis: a report of 2 cases.

Two patients with Q fever endocarditis are described. Both patients demonstrated some of the characteristic features of Q fever endocarditis, i.e. the long course of the disease before diagnosis, persistently negative blood cultures, resistance to conventional antibiotic therapy and a dramatic response to tetracycline therapy. Complications included arteriovenous thrombo-embolism and hepatic enlargement, and 1 patient developed an immune complex form of glomerulonephritis. The possibility of Q fever endocarditis should be considered in all patients with infective endocarditis in whom blood cultures are negative and who fail to respond to conventional antibiotic therapy.

Adult↗
PubMed1978

Labetalol in hypertensive patients with angina pectoris: beneficial effect of combined alpha- and beta-adrenoreceptor blockade.

1. Eight hypertensive patients with angina pectoris had placebo added to their existing medications for 8 weeks, then incremental doses of active labetalol with simultaneous stepwise reduction in other medicines until blood pressure was satisfactorily controlled; after that only labetalol and thiazide (8 weeks) and finally labetalol-placebo together with previous beta-adrenoreceptor antagonists and thiazide for 4 weeks were administered. 2. During the labetalol plus thiazide period resting blood pressures and measurements obtained during isotonic exercise, isometric exercise and the cold pressor test were significantly lower than during the initial placebo addition period. Angina scores were significantly reduced during this period. 3. During the final treatment with placebo, beta-adrenoreceptor antagonist and thiazide, blood pressures remained reduced, but angina was significantly worse. 4. Labetalol which antagonizes both alpha- and beta-adrenoreceptors produced better relief of angina pectoris than beta-adrenoreceptor antagonists during improvement in blood pressure in hypertensive patients.

Adrenergic alpha-Antagonists↗
PubMed1978

Ventricular arrhythmias associated with coronary artery occlusion and reperfusion in the isolated perfused rat heart: a model for assessment of antifibrillatory action of antiarrhythmic agents.

The isolated Langendorff-perfused rat heart, subjected to coronary artery occlusion and reperfusion consistently developed ventricular arrhythmias. The incidence of hearts with ventricular premature extrasystoles, ventricular tachycardia, and fibrillatioon ventricular fibrillation could be abolished in the presence of an extracellular potassium concentration of 12 mmol-litre--1, whereas with 4.5 mmol-litre--1 all hearts developed all the ventricular arrhythmias including fibrillation. This predictable occurrence of ventricular arrhythmias was used to assess the antiarrhythmic effect of lignocaine with particular reference to its effect on the spontaneously occurring reperfusion ventricular fibrillation. Lignocaine decreased the incidence of all ventricular arrhythmias both during ischaemia and on reperfusion in a concentration-related fashion.

Animals↗
PubMed1978

The role of cyclic adenosine monophosphate in adrenergic effects on ventricular vulnerability to fibrillation in the isolated perfused rat heart.

The relation between myocardial tissue cyclic AMP (cAMP) and the vulnerability to ventricular fibrillation was assessed in the isolated perfused rat heart by measurement of ventricular fibrillation threshold (VFT) and vulnerable period duration (VP). Exogenous dibutyryl cyclic AMP (DBcAMP) reduced VFT and increased VP by a concentration-related action whereas exogenous cAMP did not. Theophylline (1.0 mmol/liter) increased the tissue content of cAMP by 58% (P < 0.001) and caused a leftward shift in the concentration-response curve to DBcAMP. An effect of cAMP on VFT and VP could be shown in the presence of phosphodiesterase inhibition by theophylline. beta-1-Adrenergic receptor blockade with atenolol did not alter the concentration-response curve for VFT when DBcAMP was administered. Epinephrine (100 nmol/liter to 1 mumol/liter) also increased vulnerability to VF; this effect was accompanied by a concentration-related increase in tissue cAMP, but inconsistent changes in tissue ATP, phosphocreatine and potassium. The concentration-response curve of VFT to epinephrine was shifted leftward by theophylline and rightward by atenolol. The increases in vulnerability to fibrillation in the isolated perfused rat heart, in response to DBcAMP, theophylline or epinephrine, could be related more closely to changes of tissue cAMP than to effects on tissue high energy phosphates or potassium. The effect of epinephrine and theophylline on vulnerability to ventricular fibrillation is mediated via alterations in the intracellular level of cAMP in the isolated perfused rat heart.

Adenosine Triphosphate↗
PubMed1977

Prazosin in the therapy of uncontrolled hypertension.

Prazosin (Minipress; Pfizer), a new antihypertensive agent, was investigated in 24 outpatients with uncontrolled hypertension. In 12 patients a single-blind placebo-controlled trial was conducted and in 12 patients an open trial with treatment for a minimum of 16 weeks. Three patients developed postural hypotension and were withdrawn from the trial. Fifteen patients responded to treatment with prazosin and normotensive levels were reached in 9. Ten patients had renal impairment at the start of the study; renal function remained static in 9 and serum urea and creatinine values increased in 1. Prazosin maintains renal function well in severely hypertensive patients and has a relatively low incidence of side-effects, related mainly to postural hypotension which develops unpredictably in some patients. In addition to its extensively documented beneficial effect in mild and moderate forms of hypertension, prazosin is of use in the therapy of patients with severe and uncontrolled hypertension.

Adult↗
PubMed1976

Antihypertensive therapy with timolol and alpha-methyldopa. A double-blind trial in patients with moderately severe hypertension.

After 24 moderately severe hypertensive patients had been treated for 4 weeks with a placebo for timolol, alpha-methyldopa was added and titrated until control of the blood pressure or a total daily dose of 2 500 mg was achieved. At the 9th week, the dose of alpha-methyldopa was halved and either timolol or its placebo was titrated in double-blind fashion. Titration over a period of 4 weeks was followed by a further 5 weeks of stabilisation. In 22 patients whose responses were accepted for analysis, alpha-methyldopa caused a significant lowering of blood pressure, with a greater reduction in the upright posture and a reduction in pulse rate. The addition of timolol caused a highly significant further reduction in pulse rate and a significant reduction in blood pressure in 8 of 10 patients. Apart from a statistically significant increase in serum urea and creatinine with, however, retention of normal renal function, no other side-effects were attributable to timolol.

Adrenergic beta-Antagonists↗
PubMed1976

Cyclic adenosine monophosphate, ventricular fibrillation, and antiarrhythmic drugs.

It is proposed that the development of ventricular fibrillation in the context of ischaemic heart-disease and myocardial infarction can be related to accumulation of cyclic adenosine 3',5' monophosphate (A.M.P.) in the ischaemic zone. The known electrophysiological and metabolic actions of cyclic A.M.P. are consonant with the hypothesis, which also provides a framework for the better understanding of the action of antiarrhythmic drugs.

Adrenergic beta-Antagonists↗