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Biomedical subjects

D G Beevers

Publications and source records attributed to D G Beevers.

At least 289 records · Page 16Linked to original sources

The effect of a non-selective lipophilic beta-blocker on the blood pressure and noradrenaline, vasopressin, cortisol and renin release during alcohol withdrawal.

Alcoholics during detoxification have elevated blood pressures which are related to the severity of their withdrawal symptoms. We studied the effect of a non-selective beta-blocker, timolol on symptoms, blood pressure and plasma levels of cortisol (PC), noradrenaline (NA), vasopressin (AVP) and renin activity (PRA) during alcohol withdrawal. Eighteen alcoholics, admitted for detoxification, were randomly allocated to timolol or placebo in a double blind trial. Alcohol withdrawal symptoms did not differ either before or after timolol or placebo but patients receiving timolol required less sedation with chlormethiazole. Systolic blood pressures (SBP) and pulse both fell significantly during detoxification in both groups, the change being greater with timolol. Plasma levels of cortisol, NA, AVP and PRA fell significantly, though only NA and PC correlated with initial SBP. Timolol had no effect on any of the biochemical parameters observed. The pressor response to alcohol withdrawal is reduced by beta-blockade and the height of the blood pressure is related to plasma NA and PC levels. Alcohol withdrawal hypertension is probably due to increased sympathetic activity.

Adult↗

The possible mechanisms of alcohol associated hypertension.

The association between alcohol intake and blood pressure has been known for nearly 70 years. It was postulated that the alcohol blood pressure association was not causal but linked to common factors such as stress, obesity or salt intake. Recently large population studies have shown that the association is independent of these factors. Alcohol dependent persons have a high incidence of hypertension which is a common clinical problem. It is probably due to alcohol withdrawal and is mediated via increased cortisol and catecholamine production. Alcohol has also a direct effect causing arteriolar vasoconstriction. This direct effect may result from an alcohol associated alteration of intracellular Ca in arteriolar smooth muscle leading to supersensitivity to circulating pressor agents.

Arteries↗

Possible role for insulin receptors in the mechanism of thiazide induced glucose tolerance.

The role of cellular insulin receptors in the mechanism of thiazide induced glucose intolerance was studied in 10 non-diabetics and six diet controlled type II diabetics with mild essential hypertension. Glucose tolerance tests (75 g) were performed at the start of the study, after one month of placebo and after one month on bendrofluazide 5 mg daily. Erythrocyte insulin receptor status was measured on each occasion in the fasting state. In non-diabetics, low affinity insulin receptor concentration increased after bendrofluazide but high affinity receptor concentration remained unchanged. In the diabetics, there was no change in either high or low affinity insulin receptor concentration. No change in insulin receptor affinity occurred in either group. In the long term, non-diabetics may maintain normal glucose tolerance on thiazide diuretics by increasing insulin receptor numbers. This adjustment did not occur in diabetic patients which may explain the deterioration in glucose tolerance.

Bendroflumethiazide↗

Strokes and alcohol.

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Alcoholic Intoxication↗

Pregnancy induced hypertension: evidence for increased cell membrane permeability to sodium.

In a cross sectional study of 137 women of childbearing age (16-40) the effects of normal pregnancy, hypertensive pregnancy, and oral contraceptives on red cell electrolyte content and sodium efflux rates were examined and the results compared with values in a control group of normotensive, non-pregnant women. Efflux rate constants were significantly increased in normotensive pregnancy and in women taking oral contraceptives. This was associated with a significant increase in sodium permeability in the contraceptive group. A much larger increase in sodium permeability and efflux rate constant was seen in the hypertensive group. The results permit a hypothesis that the hormonal changes induced by pregnancy and oral contraceptives increase membrane permeability to sodium and stimulate sodium efflux. The rise in blood pressure associated with use of oral contraceptives may have a similar aetiology to that occurring in pregnancy induced hypertension.

Adolescent↗

Comparison of the effects of single doses of atenolol and labetalol on airways obstruction in patients with hypertension and asthma.

1 The effects of atenolol (100 mg), a cardioselective beta-adrenoceptor blocking agent, and labetalol (300 mg), a combined alpha- and non-selective beta-adrenoceptor blocking agent given in single doses were examined in a double-blind placebo controlled study in 11 asthmatic patients with hypertension. Changes in forced expiratory volume in one second (FEV1) were measured. 2 There were no significant differences between the effects of the active drugs, approximately half the patients having higher FEV1 values during each of the two active treatments. When compared with placebo, labetalol significantly reduced the effect of inhaled salbutamol on FEV1. 3 Whilst beta-adrenoceptor blockings drugs cannot be recommended in patients with airways obstruction, should they inadvertantly be given, labetalol like atenolol may be considered relatively safer then pure non-selective beta-adrenoceptor blocking drugs.

Adult↗

Malignant hypertension: cardiac structure and function at presentation and during therapy.

We have studied electrocardiograms, chest radiographs, and digitised apex echocardiograms in 16 patients with malignant hypertension before and after up to six months of antihypertensive treatment and compared them with those of eight patients with severe benign hypertension. Adequate blood pressure reduction was obtained in 14 with resolution of retinopathy, but one patient died and another had poor blood pressure control. Nine had electrocardiographic criteria of left ventricular hypertrophy which did not change with treatment and 10 had lateral ischaemia which resolved in seven. The malignant hypertensives were divided into seven with and nine without a previous hypertensive history. Both groups had normal echocardiographic cavity dimensions, but the former group tended to have hypertrophy (similar to that in benign hypertensives) and the latter did not. After adequate reduction of blood pressure, no change in wall and septal thickness occurred (except in one patient with poor blood pressure control). At entry, malignant hypertensives showed delayed mitral valve opening with significant cavity dimension increase during prolonged isovolumic relaxation, reduced peak rate, and prolonged duration of cavity dimension increase and cavity shape change (inward wall motion) during the upstroke of the apexcardiogram which showed a tall "a" wave. After reduction of blood pressure, though the delay in mitral valve opening persisted, the timing of A2 returned towards normal and the dimension change during the upstroke of the apexcardiogram and the relative height of the "a" wave were reduced but remained significantly different from normal. Some patients without a previous hypertensive history may develop a malignant phase without left ventricular hypertrophy on the electrocardiogram or echocardiogram. They maintain their pump function even with radiological pulmonary oedema, have incoordinate relaxation and contraction, and have abnormal filling. Similar functional abnormalities were found in malignant hypertensives with hypertrophy. Treatment to reduce blood pressure reduces incoordinate contraction, but impaired diastolic function persists as in benign hypertension, suggesting that these abnormalities are the result of altered myocardial properties that may occur without hypertrophy.

Adult↗

Blood pressure in black, white and Asian factory workers in Birmingham.

A screening survey was conducted among factory workers, aged 15-64 years, in Birmingham, England to investigate ethnic differences in blood pressure. One-thousand and forty-nine subjects (784 men, 265 women) were screened, representing 79% of the eligible population. Mean systolic and diastolic blood pressures generally did not differ between men of black West Indian (n = 173), local white (n = 439) or Asian (n = 172) origin, when matched by 10-year age groups. Analysis of covariance using age as the covariate revealed that, overall, Asian men had significantly lower systolic but higher diastolic pressures than the other ethnic groups. The proportion of men arbitrarily defined as hypertensive (greater than or equal to 160 mmHg systolic or greater than or equal to 95 diastolic or blood pressures below this figure whilst receiving antihypertensive therapy) was 26% of West Indians, 22% of whites and 17% of Asians, but these were not significantly different when age was accounted for. Black West Indian women (n = 101) did have higher diastolic pressure than white women (n = 164), but this difference was dependent on body mass index. Overall, systolic pressures in women were not significantly different. These findings differ from those consistently reported from the United States.

Adolescent↗

The Birmingham blood pressure school study.

Four-hundred and twenty-eight school leavers of 3 ethnic groups (white, black and Asian) were screened for blood pressure, resting pulse rate and general anthropometric characteristics. Asian pupils were both shorter and lighter than the other two groups whilst black males were heavier and taller. There was no significant difference in the mean systolic or diastolic blood pressure between the 3 groups, although the black pupils had a stronger family history of hypertension, particularly on the mother's side. These observations differ in some respects from other ethnic blood pressure studies and establish values for the local population.

Adolescent↗