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Biomedical subjects

D S Bloom

Publications and source records attributed to D S Bloom.

15 recordsLinked to original sources
PubMed1995

Adjunctive therapy in epilepsy: a cost-effectiveness comparison of alternative treatment options.

A pharmaco-economic study of the administration of adjunctive therapy in patients with chronic epilepsy is described. A decision-analytic model has been used, which represents the consequences of treatment over a 1-year time period, when one of three drugs is used first. The cost-effectiveness ratio for clobazam, lamotrigine and vigabatrin have been calculated. The expected cost per patient of treatment over the 1-year period was up to 50% higher with vigabatrin and lamotrigine compared with clobazam, with a cost-effectiveness ratio around 40% higher.

Acetates↗
PubMed1985

Captopril as a replacement for multiple therapy in hypertension: a controlled study.

A controlled study was conducted in hypertensive patients to investigate whether captopril can be substituted for the various other antihypertensive drugs (not including diuretics) to reduce side effects and improve the quality of life. Captopril in a twice daily dose of 25-50 mg, was substituted and titrated in 54 patients. Fifty-two patients, matched by age and sex, comprised the control group, and were treated with a variety of agents. During a follow-up of 9 months, 44 of the patients receiving captopril (81%) achieved the goal of supine blood pressure less than 90 mmHg. Captopril was discontinued in two patients due to side effects. Mild proteinuria was observed in two patients. A significant reduction in scores or rates of side effects (numbness, blurred vision, insomnia, vivid dreams, cold extremities, sleepiness, sexual dysfunction and fatigue) and improvement in quality of life (general feeling, mood and concentration) was observed in the study group compared with the control group. Captopril alone in a twice daily dose of 25-50 mg, or in co-treatment with thiazide, provided sustained blood pressure control with minimal side effects and improvement in quality of life compared with the treatment of hypertension with beta-blockers, vasodilators or methyldopa.

Aged↗
PubMed1983

An inhibitor of cerebral uptake of noradrenaline in jaundiced blood plasma.

The permeability of the blood-brain barrier to noradrenaline was estimated in rats with bile duct ligation by intracarotid injection of [14C]-L-noradrenaline, 3H2O, and [113mIn]ethylene diamine tetraacetate (EDTA) under pentobarbitone anaesthesia. Brain uptake of [14C]noradrenaline was expressed as a percentage of that of 3H2O (brain uptake index, BUI) and corrected for the "blood background" by the 113mIn. The BUI of noradrenaline (1.20 +/- 0.19) was not increased in jaundice (0.78 +/- 0.18). The capacity of oxygenated homogenates of rat brain to remove noradrenaline was measured. The presence of jaundiced plasma always caused a substantial suppression of noradrenaline removal. No effect of jaundice on specific radioactive assays for catechol-O-methyl transferase (COMT) or monoamine oxidase (MAO) could be demonstrated.

Animals↗
PubMed1979

The protective action of inosine on isolated arteries in hypoxia.

1 The pressor responses to injected noradrenaline (NA) of isolated perfused femoral or renal arteries of the rabbit were studied.2 Vascular smooth muscle is relatively resistant to hypoxia. A combination of hypoxia and dinitrophenol (DNP) respiratory uncoupling was necessary to abolish the pressor response to NA. Loss of the pressor response was assumed to result from decreased capacity of arteries to form adenosine 5'-triphosphate (ATP). Reperfusion of the hypoxic arteries with oxygenated medium resulted in recovery of the pressor response to NA.3 Inclusion of inosine (10 mM) in the hypoxic perfusion medium increased significantly the rate and extent of post-hypoxic recovery of the pressor response to NA.4 Whereas the presence of inosine in the hypoxic perfusion medium aided post-hypoxic recovery, inosine had no direct action on the pressor dose response to NA. Therefore, the action of inosine was protective as opposed to direct.5 The protective action of inosine did not involve potentiation of NA binding to NA-adrenoceptor sites (the equilibrium coefficient, K(eq) for NA-receptor interaction was unaltered by hypoxia and/or inosine).6 The results are discussed in terms of a presumptive mechanism whereby inosine is believed to act by maintaining intracellular adenine nucleotide concentrations in hypoxia.

Adenine Nucleotides↗
PubMed1978

Potentiation of the cerebrovascular response to intra-arterial 5-hydroxytryptamine.

Infusion of 5-hydroxytryptamine (5HT) into the internal carotid artery of normal baboons was not accompanied by alteration of gray matter cerebral blood flow. In animals pretreated with depot estrogen and progesterone (dosage equivalent to oral contraceptive preparations), infusion of 5HT produced a marked decrease in gray matter blood flow. A similar decrease in flow was obtained when the 5HT was infused with a concentrate of beta-lipoprotein. Steroid substances appear to enhance the cerebrovascular constrictor responses to 5HT. A further series of six experiments has shown that the monoamine oxidase inhibitor tranylcypromine similarly produced constrictor responses to 5HT. It is possible that the steroids, the beta-lipoprotein, and the tranylcypromine produced constrictor responses to 5HT by the same mechanism (inhibition of cerebrovascular monoamine oxidase).

Animals↗
PubMed1976

Effects of hypertensive plasma on the responses of an isolated artery preparation to noradrenaline.

The effect of hypertensive plasma on the responses of an isolated artery preparation to noradrenaline were studied. In addition, because of the association between hypercholesterolaemia and hypertension, the effect of pure cholesterol and low density lipoprotein on the arterial responses to noradrenaline was also investigated. Both hypertensive plasma and low density lipoprotein potentiated the responses of the arterial preparation to noradrenaline.

Animals↗
PubMed1976

Noradrenaline sensitivity of an isolated perfused artery: effects of normal and hypertensive plasma.

1. The noradrenaline sensitivity of the isolated perfused rabbit artery was studied, during perfusion with Krebs solution, normal plasma, hypertensive plasma and a low-density lipoprotein (LDL) extract of normal plasma. 2. There was no difference in noradrenaline sensitivity between arteries perfused with Krebs and normal plasma. 3. Both hypertensive plasma and LDL potentiated the noradrenaline-induced vasoconstriction. 4. This potentiation was associated with increases in both the intrinsic activity of the drug-receptor complex and the drug-receptor affinity. 5. There is a circulating factor in the plasma of hypertensive patients which sensitizes arteries to noradrenaline, and this factor may be LDL.

Animals↗
PubMed1975

Modification of the cerebrovascular response to noradrenaline by bile duct ligation.

The effects of intracarotid infusions of noradrenaline on the cerebral vasculature were studied in seven baboons with bile duct ligation. Infusion of 8 mug and 16 mug/min of noradrenaline resulted in a significant decrease in cerebral blood flow in the jaundiced animals. In normal baboons, these doses produced cerebrovascular dilatation. These results indicate that there is an increased cerebrovascular sensitivity to noradrenaline in the obstructive jaundice which follows bile duct ligation. It is postulated that noradrenaline smooth muscle uptake mechanisms are disturbed allowing a greater concentration of the amine at the receptor sites.

Animals↗
PubMedDate not supplied

Renal blood flow in obstructive jaundice: an experimental study in baboons.

1. The distribution of intrarenal blood flow has been measured using the 133Xe-washout technique in thirteen baboons 2 weeks after ligation of the common bile duct. 2. In comparison with eight sham-operated baboons, there was a signifigant decrease in the percentage distribution of blood to the cortex, although the rate of flow was unchanged. These changes were accompanied by a significantly increased flow rate and percentage distribution of flow through the juxtameduallary circulation. 3. In a further five baboons treated in the same way, various doses of noradrenaline were infused into the renal artery. In these animals there was an enhanced pressor response to noradrenaline, and this effect was completely abolished by an alpha-adrenoreceptor blocking agent (phenoxybenzamine). The beta-adrenoceptor blocking drug (propranolol) had no such effect. 4. This enhanced response was not seen when noradrenaline was infused into three sham-operated baboons. 5. These observations suggest that the alterations in renal perfusion in obstructive jaundice may be due to an increase renovascular sensitivity to circulating catecholamines and an enhanced alpha-adrenoceptor activity.

Animals↗