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Biomedical subjects

W F Lubbe

Publications and source records attributed to W F Lubbe.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1976

Cyclic AMP as a determinant of vulnerability to ventricular fibrillation in the isolated rat heart.

Ventricular fibrillation threshold and vulnerable period were measured in the isolated perfused rat heart to assess the influence of dibutyryl cyclic AMP on ventricular vulnerability. Doses of dibutyryl cyclic AMP of 0.6-1.6 mumol/min caused an increase in coronary flow but had no effect on vulnerability, whereas doses of 2.6-4.2 mumol/min resulted in an increase in coronary flow, a decrease in VF threshold, and an increase in the width of the vulnerable period. These experiments support the concept of a local myocardial action of catecholamines, mediated by cyclic AMP, whereby vulnerability to ventricular fibrillation is increased.

Animals↗
PubMed1975

Ventricular fibrillation threshold and vulnerable period in the isolated perfused rat heart.

Ventricular fibrillation threshold (VFT) measurements were obtained in the isolated perfused rat heart. Detailed morphology of the vulnerable period (VP) could be described by stimulating repeatedly at increasing levels of stimulus energy. Addition of lignocaine to the system caused an elevation of VGT, but also led to a delay of the VP to the end of the QT interval. The implications of these findings for the understanding of VFT measurements are discussed.

Animals↗
PubMed1975

Effect of substrate on enzyme release after coronary artery ligation in isolated rat heart.

In the present work, we tested the hypothesis that the development of myocardial infarction in the isolated perfused working rat hearts could be influenced by the nature of the substrate reaching the infarction zone. We measured cardiac output and rates of release of lactate dehydrogenase (LDH) after coronary artery ligation in hearts perfused with different substrates: glucose; palmitate, oleate, linoleate bound to albumin; palmitate-albumin plus glucose and/or insulin. Cardiac ouptut after ligation was lowest with palmitate and highest with glucose. LDH release was 5-10 times greater with FFA than with glucose, but was significantly reduced by the addition of glucose or insulin to the palmitate-albumin solution. Our results argue for an important role for substrate effects on the metabolic outocme of experimental myocardial infarction.

Albumins↗