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Biomedical subjects

W F Lubbe

Publications and source records attributed to W F Lubbe.

At least 55 records · Page 3Linked to original sources
PubMed1982

Antihypertensive treatment and fetal welfare in essential hypertension in pregnancy: a retrospective survey of experience with various regimes at National Women's Hospital, Auckland, 1970-80.

A series of 184 pregnancies in 161 hypertensive women was classified according to the regimen of antihypertensive treatment used during pregnancy. In 72 pregnancies management was with bed rest alone, attaining a mean gestation of 37.8 +/- 0.4 weeks, a mean birthweight of 2941 +/- 97 g with 38 percent of infants below the 25th percentile. Late deterioration of hypertension with development of proteinuria occurred in 16.6 percent with fetal mortality of 6.9 percent. Antihypertensive therapy involved methyldopa, thiazide diuretics, sympathetic ganglion blockers, hydralazine, beta-adrenergic blockers and the combination of oxprenolol and prazosin. Fetal growth was compared in pregnancies that reached term on the various regimens. Significantly better growth was achieved where debrisoquine plus a thiazide were used (3617 +/- 113 g in six subjects) and oxprenolol/prazosin (3411 +/- 72 g in 14 subjects) compared to 11 comparably hypertensive patients on bed rest alone (2975 +/-87 g). Therapy with the ganglion blocker plus thiazide was complicated by the deterioration of hypertension with proteinuria in 37.2 percent of women; this did not occur in patients receiving oxprenolol/prazosin. Maternal age had no effect on fetal growth, but smoking more than 10 cigarettes per day caused significant growth retardation.

Antihypertensive Agents↗
PubMed1982

Alternatives to beta-blockade in therapy of hypertension with angina pectoris: role of nifedipine or of labetalol.

1 Patients with combined hypertension and angina pectoris may represent a therapeutic dilemma, with the angina being refractory to conventional beta-blockade. 2 The added benefit of peripheral vasodilation in control of blood pressure is documented in the case of nifedipine. 3 Improved blood pressure control by added nifedipine may not be accompanied by decreased severity of angina pectoris, emphasizing the complex causation of the angina in such patients. 4 The clinically proven added alpha-blocking activity of labetalol distinguishes labetalol from other beta-blockers. However, the suggested benefits of the added alpha-activity in patients with hypertension and angina remain to be proven by further trials in patients.

Angina Pectoris↗
PubMed1982

Serum myoglobin, creatine kinase and creatine kinase-MB as mutually supportive indices of myocardial infarction and infarct size.

A comparison was made between the appearance of serum myoglobin and creatine kinase in 22 patients with acute myocardial infarction who were admitted to a coronary-care unit within four hours of onset of chest pain. The MB isoenzyme of creatine kinase was measured in 12 patients. The more rapid appearance and disappearance of myoglobin relative to creatine kinase and creatine kinase-MB was confirmed, as was the correspondence between their respective peak values. A significant correlation was also obtained between the area under the myoglobin time-course and the respective peak levels. Whereas creatine kinase activity declined exponentially from a single peak, myoglobin appeared in multiple episodes inadequately represented by a single peak value and having no clear clinical correlation. The role of myoglobin as a diagnostic aid in myocardial infarction is probably limited to its ability to support creatine kinase and creatine kinase-MB as indices of infarct size.

Creatine Kinase↗
PubMed1981

Combined alpha- and beta-adrenoceptor antagonism with prazosin and oxprenolol in control of severe hypertension in pregnancy.

The combination of prazosin (3-21 mg/day) and oxprenolol (60-360 mg/day) was used to treat 25 pregnant women with severe essential hypertension and 19 women with the hypertension-oedema-proteinuria syndrome. In the group with essential hypertension control of blood pressure was sufficient to avoid addition of hydralazine infusions in all but one patient. No patient developed late proteinuria and exacerbation of hypertension once control was established using this regimen. The birthweights of 58 percent of infants were above the 50th percentile of birthweights for the same ages of gestation in normal pregnancies; two intrauterine deaths occurred. In the hypertension-oedema-proteinuria group, blood pressure control was more difficult to sustain, necessitating additional hydralazine infusions in 11 patients. Pregnancy had to be terminated urgently because of progression of the disorder in 13 patients. There were three intrauterine deaths in this series and one infant was lost eight hours after delivery at 27 weeks following five weeks of antihypertensive therapy.

Acute Disease↗
PubMed1981

Amiodarone in long term management of refractory cardiac tachyarrhythmias.

Amiodarone was used in 30 patients with tachyarrhythmias refractory to treatment with several antiarrhythmic agents. In 18 patients with supraventricular arrhythmias (recurrent atrial tachycardia in seven; atrial fibrillation, recurrent in four and persistent in five; Wolff-Parkinson-White syndrome in two), complete control was obtained in eight and marked improvement in eight patients. Conversion of persistent atrial fibrillation to sinus rhythm was documented in three patients. Congestive heart failure improved markedly in three patients who had persistent atrial fibrillation during amiodarone therapy. In 12 patients with tachycardia of ventricular origin effective control was obtained in nine. The incidence of side effects was low. Amiodarone is effective in maintaining sinus rhythm in many patients with both supraventricular and ventricular tachyarrhythmias when standard antiarrhythmic agents have failed.

Adult↗
PubMed1981

Influence of propranolol isomers and atenolol on myocardial cyclic AMP, high energy phosphates and vulnerability to fibrillation after coronary artery ligation in the isolated rat heart.

The isolated rat heart with ligation of the left coronary artery was used to assess the role of the beta 1- adrenergic receptor-cyclic AMP mechanism in the genesis of vulnerability to ventricular fibrillation in early myocardial ischaemia. Coronary artery ligation was followed after 3 min by a reduction in ventricular fibrillation threshold which reached a minimum at 15 min. This was accompanied by reduction of ATP and phosphocreatine while cyclic AMP was significantly increased in ischaemic myocardium. The dl-, l- and d-isomers of propranolol attenuated the decrease in ventricular fibrillation threshold and the increase in ischaemic myocardial cyclic AMP, without altering the tissue depletion of ATP. Specific beta 1-adrenergic receptor antagonism with atenolol did not prevent either the increase of tissue cyclic AMP or the reduction in ventricular fibrillation threshold and high energy phosphates. These findings suggest that the mechanism whereby vulnerability to fibrillation is increased in very early myocardial ischaemia is linked to changes in cyclic AMP content of ischaemic myocardium and appears independent of depletion of myocardial high energy phosphates.

Adenosine Triphosphate↗
PubMed1980

Psittacosis: a clinical spectrum in New Zealand.

Two patients suffering from psittacosis, of whom one had renal impairment, are described. Both recovered after treatment including the antibiotics, ampicillin and doxycycline. Chlamydia psittacae is endemic among New Zealand birds. The difficulties of diagnosis are discussed.

Ampicillin↗
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↗