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S Heptinstall

Publications and source records attributed to S Heptinstall.

At least 127 records · Page 7Linked to original sources
PubMed1983

Effects of dazoxiben and low-dose aspirin on platelet behaviour in man.

1 We have studied the effects on platelet behaviour of ingestion of the thromboxane synthetase inhibitor dazoxiben (UK 37248), by healthy subjects, and compared the results with the effects of a low dose of aspirin (a cyclo-oxygenase inhibitor), and of a combination of dazoxiben and a low dose of aspirin. 2 Dazoxiben ingestion prevented the release reaction induced by sodium arachidonate (NaAA) in platelet-rich plasma (PRP) from some individuals ("responders") but not in PRP from others ("non-responders"). In vitro testing of PRP from the same subjects, incubated with 10(-4)M dazoxiben, correlated with the effect of dazoxiben ingestion on NaAA-induced release. Platelets from "non-responders" tended to undergo a more extensive release reaction than platelets from "responders" even in the absence of any drug although there was some overlap between the results in the two groups. Platelets from "non-responders" required significantly lower concentrations of NaAA to induce release reaction than platelets from "responders". Platelets from "responders" and "non-responders" did not differ in the amount of malondialdehyde (MDA) produced or in the effectiveness with which dazoxiben ingestion inhibited MDA production. 3 Low dose aspirin had comparable effects on NaAA-induced release to dazoxiben, but in contrast to dazoxiben, the effectiveness of low-dose aspirin in inhibiting NaAA induced release reaction was related to its effectiveness in inhibiting MDA generation. 4 Neither dazoxiben nor low-dose aspirin significantly affected the release reaction induced by adenosine diphosphate (ADP), although both drugs significantly inhibited adrenaline-induced release. 5 A combination of dazoxiben and low dose aspirin had a greater effect on platelet behaviour in response to NaAA, ADP, and adrenaline than either drug alone.

Adenosine Diphosphate↗
PubMed1983

Monoamine oxidase activity in diabetes.

Monoamine oxidase (MAO) activities were measured in platelets from insulin-dependent and non-insulin-dependent diabetic subjects and in platelets from nondiabetic controls. Circulating levels of glycosylated hemoglobin (HbA1) were determined simultaneously. Mean MAO activities were not significantly different in any of these groups. MAO activity did not relate to the age of the individual, but mean values for females were higher than mean values for males in healthy controls and in insulin-dependent diabetics. In this study mean HbA1 levels were higher in female than in male diabetics. There was no relationship between MAO activity and HbA, level when results for males and females were analyzed separately.

Adolescent↗
PubMed1982

Platelet aggregation in whole blood determined using the Ultra-Flo 100 Platelet Counter.

The Ultra-Flo 100 Whole Blood Platelet Counter has proved a useful tool for measuring platelet aggregation in whole blood, the extent of aggregation being deduced from the number of single platelets that remain. The technique has allowed us to show that platelets aggregate spontaneously in citrated blood and in heparinized blood but not in whole blood collected into EDTA. The aggregation occurs during storage but its rate is enhanced by stirring and it occurs more readily when the whole blood has been exposed to plastic rather than glass. It occurs much more readily in whole blood from some individuals than from others and the process may involve adenosine diphosphate (ADP). The rate of aggregation in whole blood is enhanced by several aggregating agents including collagen, ADP and sodium arachidonate which are more usually studied in platelet-rich plasma.

Adenosine Diphosphate↗
PubMed1982

A regimen for low-dose aspirin?

The effects of different regimens of 40 mg aspirin on platelet thromboxane A2 synthesis and vascular prostacyclin synthesis were determined in patients who were undergoing elective surgery for removal of varicose veins. Aspirin 40 mg taken at intervals of 48 hours consistently reduced platelet thromboxane A2 synthesis to a level at which it failed to support platelet aggregation and the associated release reaction. This effect lasted for at least 36 hours. In contrast, aspirin 40 mg every 72 hours did not have the same consistent effect. Both dose regimens led to a reduction in vascular prostacyclin synthesis 12 hours after the last dose, but 36 or 72 hours after the last dose prostacyclin synthesis was not reduced; thus the inhibition of prostacyclin synthesis was short lived. If the balance between platelet thromboxane A2 and vascular prostacyclin synthesis is important in thrombosis 40 mg aspirin every 48 hours may have the maximum antithrombotic effect.

Adult↗
PubMed1981

Differential inhibition by low-dose aspirin of human venous prostacyclin synthesis and platelet thromboxane synthesis.

The capacity of venous tissue for prostacyclin synthesis was determined in 68 patients undergoing surgery for removal of varicose veins. A single dose of aspirin (81 mg or 300 mg) taken 14 h preoperatively strongly inhibited its synthesis, and the effect of 300 mg was still evident 48 h after ingestion. A single dose of 40 mg aspirin taken 14 h preoperatively had no effect on prostacyclin synthesis. The capacity of blood platelets to synthesise thromboxane (measured as malondialdehyde) was determined in volunteers before and at various times after ingestion of 300 mg or 40 mg aspirin. Both doses had an inhibitory effect that lasted for at least 96 h. The length of time for which the amount of thromboxane synthesised was insufficient to support platelet aggregation and the platelet release reaction depended on both the donor and the dose of aspirin. If prostacyclin and thromboxane are important in the pathogenesis of thrombosis, then doses of aspirin much lower than those used previously should be tested. The long-lasting effect of 300 mg aspirin on both venous tissue and platelets indicates that this dose is unlikely to produce a favourable prostacyclin/thromboxane balance.

Aspirin↗
PubMed1980

Platelet-release reaction in myocardial infarction.

A study was made of the platelet-release reaction in heparinised platelet-rich plasma taken from 26 patients, of whom 22 had sustained a definite and four a possible myocardial infarction, and from 54 age-matched controls. No significant differences in reaction were observed between the two groups. Signficant differences were seen, however, between eight patients who died within a year after infarction and the controls (P less than 0.01) and the remaining 18 patients who survived (P = 0.02). These differences were abolished when sodium citrate was included in the experimental procedure. Poor prognosis was thus related to an increased platelet-release reaction after infarction.

Adenosine Diphosphate↗
PubMed1980

The abilities of human blood platelets to bind extracellular calcium and to be aggregated by adenosine diphosphate are related.

A technique is described for preparing platelets rich plasma containing a very low level of extracellular calcium. Using this Ca-depleted PRP it has been possible to demonstrate that extraplatelet calcium is in equilibrium with a small amount of calcium that is bound to the platelet surface. When Ca-depleted PRP is incubated at 37 degrees C the platelets lose their ability to bind calcium. At the same time they lose their ability to aggregate. It is likely that the binding of calcium to the platelet surface is a prerequisite for ADP-induced aggregation.

Adenosine Diphosphate↗
PubMed1980

Platelet behaviour and vascular disease.

Studies of platelets from individuals who have experienced a thrombotic event have not yet conclusively demonstrated an active role for platelets in thrombosis. Platelet hyperactivity after myocardial infarction may relate to poor prognosis but further studies are required. Arachidonate metabolism may differ in platelets from different individuals and studies in vascular disease are warranted.

Adenosine Diphosphate↗
PubMed1979

The effects of citrate and extracellular calcium ions on the platelet release reaction induced by adenosine diphosphate and collagen.

The ADP-induced release of 3H-serotonin from human platelets in heparinized platelets rich plasma is markedly stimulated by the addition of sodium citrate. The aggregation and release that is induced by collagen is less affected by citrate. Data is presented that supports the view that the effects of citrate on both ADP- and collagen-induced release are largely via alteration of the concentration of ionized calcium in plasma. Collagen can induce release of 3H-serotonin via extracellular calcium-independent and -dependent mechanisms. The possibility that the calcium-dependent mechanism is aggregation-dependent and that the calcium is required for platelet aggregation rather than directly involved in the release reaction is discussed.

Adenosine Diphosphate↗
PubMed1979

A comparison of the abilities of acetylsalicylic acid, flurbiprofen and indomethacin to inhibit the release reaction and prostaglandin synthesis in human blood platelets.

1 A quantitative comparison has been made of the abilities of acetylsalicylic acid, flurbiprofen and indomethacin to inhibit the adenosine diphosphate (ADP)-induced platelet release reaction and to inhibit the synthesis of prostaglandins from arachidonic acid. 2 Experiments were carried out on human platelets that had been incubated with the agents in vitro and on platelets obtained from volunteers who had ingested standard doses of the drugs. 3 The results obtained for acetylsalicylic acid show that there is a close relation between the release reaction and the synthesis of prostaglandins in platelets. 4 Flurbiprofen and indomethacin appear to inhibit the release reaction rather more effectively than they inhibit the synthesis of prostaglandins. It is possible that these agents inhibit the release reaction by another mechanism.

Aspirin↗
PubMed1977

Adenosine diphosphate induced platelet aggregation and release reaction in heparinized platelet rich plasma and the influence of added citrate.

Platelets in heparinized platelet-rich plasma (PRP) from 54 volunteers were examined for their ability to aggregate and to release tritiated 5-hydroxy tryptamine (3H-5HT) in response to adenosine diphosphate (ADP). Release of 3H-5HT was considerable in 26 of the preparations. When release was high, lower concentrations of ADP were required to induce irreversible aggregation. Second phase aggregation reflected extensive release reaction. Citrate always augmented the release induced by ADP.

Adenosine Diphosphate↗