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Biomedical subjects

M J Kendall

Publications and source records attributed to M J Kendall.

At least 19 recordsLinked to original sources
PubMed1995

Beta-blockers and sudden cardiac death.

OBJECTIVES: To 1) consider the problem of sudden death from heart disease and the role of beta-blockers and other agents in preventing sudden death and 2) review perceived problems with beta-blocker therapy, such as effects on blood lipids, complications in diabetes, and adverse effects on heart failure and quality of life. DATA SOURCES: MEDLINE and EMBASE searches done from July 1994 on, and recognized texts. STUDY SELECTION: More than 400 original and review articles were evaluated, of which the most relevant were selected. DATA EXTRACTION: Data were extracted and reviewed by two authors. Accuracy was confirmed, when necessary, by the other authors. DATA SYNTHESIS: Of all of the therapies currently available for the prevention of sudden cardiac death, none is more established or more effective than beta-blockers. Indeed, the evidence that beta-blockers have a cardioprotective effect is compelling. They probably reduce the rate of atheroma formation; they reduce the risk for ventricular fibrillation in animal models of myocardial ischemia; they appear to reduce cardiac mortality in primary prevention trials; and they reduce mortality, particularly from sudden death, in patients who have had infarction. Moreover, withholding beta-blockers because of problems perceived to be associated with them is usually not warranted and may frequently prevent their use in those who will benefit most from them. CONCLUSION: Clinicians should reappraise the evidence for the significant effect of beta-blockers on morbidity and mortality, and they should recognize the importance of initiating and maintaining beta-blocker therapy when the less well-informed might suggest otherwise.

Adrenergic beta-Antagonists↗
PubMed1995

Exercise metabolism during 1 hour of treadmill walking while taking high and low doses of propranolol, metoprolol, or placebo.

Aerobic exercise and beta-blocking drugs are regularly prescribed as treatment for hypertension and as a prophylactic for patients at risk from coronary heart disease and for those recovering from an infarct. Some beta blockers, particularly non-beta 1-selective drugs, may make exercise more difficult, possibly by interfering with substrate metabolism during exercise. This study examined the effects of low and high doses of a beta 1-selective blocker, metoprolol, and a non-selective beta blocker, propranolol, on exercise metabolism. The study involved 20 healthy subjects (10 men, 10 women) who walked on a treadmill at 50% of their maximal oxygen uptake for 1 h on five occasions, separated by 7 days. On each of the five occasions they received one of the following treatments, given in random order: placebo, metoprolol 50 mg, metoprolol 100 mg, propranolol 40 mg, or propranolol 80 mg, all taken twice daily. Fat oxidation, expressed as a percentage of total energy expenditure, was significantly lower than with placebo for all of the active treatments except metoprolol 50 mg (placebo: 42.7 +/- 11.6%; metoprolol 50 mg: 38.7 +/- 14.1%, p = NS; metoprolol 100 mg: 36.3 +/- 13.7%, p = 0.05; propranolol 40 mg: 31.2 +/- 9.3%, p = 0.01; propranolol 80 mg: 29.5 +/- 10.9%, p = 0.01); and significantly lower with propranolol than with metoprolol (propranolol 40 mg: p = 0.0036; propranolol 80 mg: p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Nitrate tolerance.

Explore the source record for details and available documents.

Administration, Cutaneous↗
PubMed1995

Effects of captopril and enalapril on renal function in elderly patients with chronic heart failure.

OBJECTIVE: To compare the effects on renal function of captopril and enalapril in elderly patients with chronic heart failure. DESIGN: A multi-centre double-blind parallel-group comparison of the two angiotensin-converting enzyme (ACE) inhibitors, captopril (12.5 mg bid) and enalapril (2.5 mg bid). SUBJECTS: 80 elderly patients with chronic heart failure (41 in the captopril group, 39 in the enalapril group). MAIN OUTCOME MEASURES: The blood pressure and pulse rate response to the first dose of ACE inhibitor was assessed in all patients. Glomerular filtration rate (GFR) was measured radioisotopically by 99mTcDTPA or 51CrEDTA clearance after three and six months of each treatment. Subgroups were assessed for effective renal plasma flow (33 patients), exercise tolerance (25 patients) and by a symptom-oriented questionnaire (45 patients). RESULTS: No serious adverse effect on GFR was noticed. There was no significant difference between the two treatments in the mean baseline GFR or in changes from baseline at three and six months (captopril mean baseline GFR 49.6 ml min-1 1.76 m-2, enalapril 54.7 ml min-1 1.76 m-2; mean change (95% confidence interval) at three months captopril 12 ml min-1 (+3.0, +21.0), enalapril -2 ml min-1 (-13.0; +9.0); mean change at six months, captopril 3.7 ml min-1 (-6.7; +14.2), enalapril -6.0 ml min-1 (-21.0; +9.4). Significantly more patients given captopril had an improvement in GFR during the study period (26/31 compared with 20/31 enalapril-treated patients at three months, p = 0.0096, and 23/30 compared with 15/27 at six months, p = 0.021). There were no significant changes in effective renal plasma flow. Three patients treated with enalapril developed symptomatic hypotension within three days of starting treatment. Quality of life questionnaires revealed more gastrointestinal symptoms in the enalapril group (p = 0.039). CONCLUSIONS: Captopril seems marginally preferable to enalapril in the treatment of chronic heart failure in elderly patients.

Aged↗
PubMed1994

Lack of effect of H2-receptor antagonists on the pharmacokinetics of alcohol consumed after food at lunchtime.

The possibility of a pharmacokinetic interaction between H2-receptor antagonists and alcohol consumed at lunchtime, was investigated in 24 healthy non-alcoholic male subjects, each receiving ranitidine 150 mg four times daily, cimetidine 400 mg four times daily, famotidine 20 mg four times daily and placebo in an open, four-way cross-over study. The subjects consumed 50 g alcohol after a standard lunch on the eighth day of dosing with study medication. Blood samples taken during the 6 h after alcohol consumption were analysed for alcohol concentrations by gas liquid chromatography using head space analysis. None of the H2-receptor antagonists had any statistically significant effects on any of the pharmacokinetic parameters for alcohol. Mean Cmax (95% CI) results for ranitidine were 547 (516, 580), cimetidine 531 (501, 563), famotidine 563 (530, 598) and placebo 529 (499, 561) mg l-1.

Adult↗
PubMed1994

Exercise metabolism in healthy volunteers taking atenolol, high and low doses of metoprolol CR/Z0K, and placebo.

1. Exercise and beta-adrenoceptor blockade have important roles in the prevention and treatment of cardiovascular disease, but fatigue and a reduced capacity to exercise are commonly reported side effects of beta-adrenoceptor blockers. The reduced capacity to exercise may be partly caused by a reduction in fat metabolism. 2. We investigated the effects of atenolol 50 mg, metoprolol CR/Z0K 50 mg, metoprolol CR/Z0K 100 mg and placebo, on heart rate, energy expenditure, fat oxidation, plasma free fatty acids, glycerol, glucose, lactate, ammonia and perceived exertion during 2 h of treadmill walking at 40% of maximal oxygen uptake in 20 healthy volunteers. 3. Compared with placebo (38.0%), total fat oxidation was significantly lower on atenolol 50 mg (30.1%) and metoprolol CR/Z0K 100 mg (31.0%), but not on metoprolol CR/Z0K 50 mg (33.7%). Reductions in fat oxidation correlated well (r2 = 0.970) with reductions in exercising heart rate, and probably reflected the degree of beta 1-adrenoceptor blockade. Maximum plasma ammonia concentration was reached after 45 min of exercise on atenolol, 60 min on metoprolol CR/Z0K 100, and 75 min on metoprolol CR/Z0K 50, and was higher than placebo on all active drug treatments. 4. The greater reduction in fat oxidation with atenolol may be a reflection of a peak in plasma concentration, which is avoided with a controlled release preparation.

Adipose Tissue↗
PubMed1994

Evidence for downregulation of hypothalamic 5-hydroxytryptamine receptor function in endurance-trained athletes.

Serum prolactin (PRL) was used as a hormone marker of serotoninergic function following oral administration of an acute dose of a serotoninergic agonist. Five male endurance-trained athletes (ET) and five healthy non-endurance-trained controls (NT) were studied. The peak PRL concentration was lower (P = 0.031) for the ET athletes (486 +/- 208 mU l-1; mean +/- S.D.) than for the NT controls (1000 +/- 385 mU l-1); the total release of PRL was also lower (P = 0.042) for the ET subjects. The lower neuroendocrine response to a serotoninergic agonist in the endurance-trained athletes suggests a downregulation of central serotoninergic receptor function in response to endurance training in man.

Adult↗
PubMed1994

Corticosteroids: do they damage the cardiovascular system?

Since their introduction for the treatment of rheumatoid arthritis, corticosteroids have become widely used as effective agents in the control of inflammatory diseases. Although there have been undoubted benefits upon mortality in diseases such as systemic lupus erythematosus, many patients survive only to suffer a high incidence of premature atherosclerosis. There is also evidence of increased rates of vascular mortality in other corticosteroid-treated diseases, such as rheumatoid arthritis, reversible airways obstruction and transplant recipients. Possible mechanisms of damage include elevated blood pressure, impaired glucose tolerance, dyslipidaemia, and imbalances in thrombosis and fibrinolysis. This paper reviews the clinical evidence supporting the contention that there is an excess cardiovascular mortality in steroid-treated patients and the underlying mechanisms, and points to further areas of research.

Adrenal Cortex Hormones↗
PubMed1994

A risk-benefit assessment of celiprolol in the treatment of cardiovascular disease.

Celiprolol is a third-generation beta-adrenoceptor blocker with selective beta 1-antagonist, partial beta 2-agonist and mild alpha 2-antagonist actions. It seems to be as effective as other beta-blockers in the treatment of hypertension and angina pectoris. beta-Blockers have many cardioprotective effects and have been shown to reduce the morbidity and mortality from coronary artery disease in a number of trials. However, there is no good clinical evidence that celiprolol itself has specific cardioprotective properties other than those attributable to this class of drugs. Because of its pharmacological profile, celiprolol is less likely to cause bradycardia, deterioration in cardiac function and other adverse effects mainly caused by beta 2-blockade. Unlike most other beta-blockers, celiprolol has no adverse effects on plasma lipids. It seems to be well tolerated in diabetic patients and patients with renal dysfunction.

Adrenergic beta-Antagonists↗
PubMed1993

The treatment of elderly hypertensive patients.

Treatment of hypertension in the elderly has hitherto been considered to be potentially dangerous. Three recent studies have clearly shown that in selected elderly hypertensives, blood pressure reduction very effectively reduces cardiovascular complications without causing unacceptable adverse effects. The impact on non-fatal stroke was most striking although a reduction in coronary events was also achieved. Thiazide diuretics were used in all three trials, and beta-blockers were used in two. Thiazide diuretics had a major beneficial effect. In this review the applicability of these results to the whole unselected population of elderly hypertensives is considered, and the choice of therapy in different subgroups of patients discussed.

Adrenergic beta-Antagonists↗
PubMed1993

Sudden cardiac death and the potential role of beta-adrenoceptor-blocking drugs.

Sudden cardiac death is a major health problem in the industrially developed countries. The risk of sudden cardiac death may be reduced by early detection of coronary heart disease, elimination of the risk factors, treatment of the ischaemia in patients known to have coronary heart disease and suppression of ventricular arrhythmias. Of all the therapeutic measures currently available to reduce the risk of sudden cardiac death, beta-adrenoceptor-blocking drugs (beta blockers) appear to be the most effective. In this paper their actions are reviewed and evidence for their efficacy is presented.

Adrenergic beta-Antagonists↗
PubMed1992

Co-administration of misoprostol or ranitidine with indomethacin: effects on pharmacokinetics, abdominal symptoms and bowel habit.

This three-way randomized crossover study in 18 healthy male volunteers compared the pharmacokinetics of 50 mg indomethacin b.d. during concomitant twice daily dosing with 400 micrograms misoprostol, 150 mg ranitidine or placebo. Plasma indomethacin concentrations were determined by HPLC assay of samples collected over 12 h after the first dose, and over 14 h after the last dose on Day 8 of each dosing period. A daily diary of bowel habits, and the occurrence and severity of abdominal symptoms, was kept by each subject throughout the study. Statistical comparisons were made by analysis of variance. In the presence of misoprostol there was a 13% decrease in the area under the plasma concentration-time curve of indomethacin over one dosing interval on Day 1 (P less than 0.01), and at steady state there was a 24% decrease in the maximum plasma concentration (P less than 0.02). The pharmacokinetics of indomethacin were not affected by co-administration of ranitidine. Accumulation of indomethacin after repeated oral dosing was not significantly altered by the co-administration of either misoprostol or ranitidine. The frequency and severity of abdominal symptoms was significantly increased (P less than 0.01) during misoprostol dosing, compared with either ranitidine or placebo plus indomethacin. When the dosing phase (Days 1-8) was compared with the washout phase (Days 9-15) in each period, misoprostol, but not ranitidine or placebo, plus indomethacin resulted in an increase (P less than 0.001) in abdominal symptom severity, frequency of bowel motions and a decrease in faecal consistency.

Abdominal Pain↗
PubMed1992

Hypertension, coronary artery disease and insulin resistance--linked disorders with an impact on treatment.

Coronary artery disease is a very common disorder for which hypertension is a well-recognized risk factor. However many trials of antihypertensive therapy have failed to demonstrate a reduction in the incidence of coronary events. One explanation is that hypertension is a disorder associated with hyperinsulinaemia, obesity and non-insulin dependent diabetes. Furthermore certain antihypertensive drugs, notably thiazide diuretics, increase the hyperinsulinaemia and thereby increase one of the other coronary risk factors. In this review the links between hypertension and hyperinsulinaemia are explored and the mechanisms whereby an increased plasma insulin can lead to the more rapid development of coronary artery disease are explained. These observations may influence the choice of drugs used to treat hypertension.

Arteriosclerosis↗