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J J Walker

Publications and source records attributed to J J Walker.

At least 145 records · Page 8Linked to original sources
PubMed1985

A comparative study of the effects of adrenoceptor antagonists on platelet aggregation and thromboxane generation.

Platelet aggregation and thromboxane A2 have been implicated in the pathogenesis of several forms of vascular disease. The aim of this study was to determine the effect of a wide range of adrenoceptor antagonists on platelet aggregation, and thromboxane A2 production, from normal human platelet rich plasma in vitro. Labetalol, pindolol and propranolol inhibited platelet aggregation to collagen in a dose dependent manner. Increasing the concentration of collagen "shifted" the dose response curve to the right. These 3 drugs also significantly inhibited thromboxane A2 generation in response to collagen but not to arachidonic acid. This effect was independent of any inhibitory effect of these drugs on platelet aggregation, and occurred at a drug concentration close to that obtained in vivo. Atenolol, metoprolol, prazosin and timolol were similarly assessed but had no effect on either platelet aggregation or thromboxane A2 generation. This ability of labetalol, pindolol, and propranolol to inhibit platelet aggregation and thromboxane generation, may be of clinical benefit in view of the increasing evidence implicating thromboxane A2 in the pathogenesis of vascular disease.

Adrenergic beta-Antagonists↗
PubMed1985

Inhibition of thromboxane and prostacyclin production in whole blood by adrenoceptor antagonists.

There is increasing evidence implicating thromboxane A2 (TxA2) in vascular disease. Adrenergic blocking agents have been used with success in the secondary prevention of myocardial infarction. The aim of this study was to determine whether adrenergic blocking agents had any effect on the production of TxA2 and prostacyclin (PGI2) from whole blood in vitro. Fresh whole blood without anticoagulant was placed in glass tubes containing either drug or vehicle, the latter acting as control, and allowed to clot at 37 degrees C for 30 minutes. The serum PGI2 metabolites (PGI2M) and TxB2 (the stable hydration product of TxA2) were determined by radioimmunoassay. Labetalol, pindolol and propranolol all inhibited both PGI2M and TxB2 production in a dose dependent manner, while atenolol had no effect. Labetalol was the most potent significantly inhibiting TxB2 production at a drug concentration compatible with that found in-vivo. This inhibitory effect on TxB2 production may be of benefit in the treatment of vascular disease.

Adrenergic alpha-Antagonists↗
PubMed1985

Immunoreactive prostacyclin and thromboxane metabolites in normal pregnancy and the puerperium.

Prostacyclin and thromboxane have been implicated in the pathophysiology of several disorders of pregnancy, but there is little information on concentrations of these prostaglandins in normal pregnancy. The aim of our study was to determine the range of values throughout normal pregnancy and the puerperium and to compare this with concentrations in normal non-pregnant women. Measurement was by radioimmunoassay of prostacyclin and thromboxane metabolites. We observed a significant difference in prostacyclin metabolites in the first trimester, (mean 19.9, SEM 0.96 pg/ml) compared with the normal non-pregnant group (mean 15.9, SEM 0.68 pg/ml). There were no significant differences between values in the normal non-pregnant group and those in the second and third trimester or postnatally. The increase in prostacyclin in the first trimester may be associated with placentation and physiological vasodilation, and insensitivity to angiotensin II seen in early pregnancy. We noted a significant reduction in thromboxane metabolites in the second (mean 133, SEM 14.9 pg/ml) and third (mean 123, SEM 10.7 pg/ml) trimesters and the puerperium (mean 119, SEM 6.3 pg/ml) compared with the values in the normal non-pregnant group (mean 142, SEM 4.9 pg/ml). This may be due to increased platelet stability or decreased thromboxane synthesis.

Epoprostenol↗
PubMed1984

Blood rheology in pre-eclampsia and intrauterine growth retardation: effects of blood pressure reduction with labetalol.

Blood viscosity ( Contraves L S 30) and its determinants were measured in 23 patients with mild/moderate pre-eclampsia, 10 patients with intrauterine growth retardation and 22 control subjects, matched for age and gestation. Both abnormal groups had a significantly increased blood viscosity at high shear rate (94 s-1) associated with increased haematocrit. Fibrinogen levels were also increased, but there were no significant differences between groups in plasma viscosity, low shear viscosity (0.94 s-1) or red cell deformability, measured by a low-shear washed cell system of filtration through 5-micron pore diameter Nuclepore filters. In the pre-eclamptic group, measurements were repeated after 1-2 weeks in nine patients treated with labetalol (a combined alpha and beta adrenergic blocker) and in 10 patients treated with bed rest. Labetalol reduced blood pressure but no change in rheology was seen in either group. Control of blood pressure by labetalol does not adversely affect rheology, in contrast to diuretics which are known to cause haemoconcentration and increased blood viscosity.

Adult↗
PubMed1982

Herbal medicine.

Explore the source record for details and available documents.

Animals↗
PubMed1975

Indomethacin--aspirin interaction: a clinical appraisal.

Plasma profiles of indomethacin after a 50-mg oral dose were constructed in six healthy volunteers before and after a week of aspirin treatment. Aspirin did not interfere with indomethacin plasma levels. To examine the clinical effect of concurrent indomethacin and aspirin treatment 20 patients with seropositive rheumatoid arthritis were given indomethacin 100 mg/day, aspirin soluble 4 g/day, and the two drugs taken together in random order. Analysis of the clinical indices of inflammation--articular index and mean pain score--and of the efficacy of each treatment showed no significant differences between the three treatment groups. With the proliferation in the number of anti-rheumatic drugs available, the case for giving two or more nonsteroidal anti-inflammatory drugs concurrently remains unproved.

Arthritis, Rheumatoid↗
PubMed1975

Phenylbutazone: a clinico-pharmacological study in rheumatoid arthritis.

A clinical trial of phenylbutazone in high dose (300 mg daily) and low dose (50 mg daily) is presented. 2. By analysis of the data by different methods, significant differences in clinical efficacy were shown between the two therapeutic regimes. 3. A relationship between the clinical effect and plasma level of phenylbutazone was demonstrated. 4. Some problems in the interpretation of plasma level-clinical effect correlates are discussed.

Arthritis, Rheumatoid↗