Activation of platelet cyclooxygenase by red cells in vitro.
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Biomedical subjects
Publications and source records attributed to L Iuliano.
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Thrombin-induced platelet malondialdehyde (MDA) formation and plasma malondialdehyde-like material (MDA-LM) were evaluated in 12 healthy subjects before and after 1 and 7 days from aspirin (1 g) ingestion. 24 hr after aspirin administration, platelet MDA was almost abolished while MDA-LM showed a 23% decrease. Platelet MDA and plasma MDA-LM returned to baseline values 7 days after aspirin ingestion. These data suggest that platelet cyclooxygenase pathway affects only in part plasma MDA-LM. The evaluation of plasma MDA-LM before and after aspirin could be useful for evaluating in vivo platelet cyclooxygenase activation.
The study was carried out in order to evaluate if Ticlopidine induces lipid metabolism changes. Twenty seven healthy subjects were studied, 14 with placebo and 13 with Ticlopidine treatment (500 mg/day), for 30 days. Total cholesterol, HDL cholesterol, triglycerides, apolipoproteins A and B were evaluated before and after treatment. No significant changes of the blood lipid parameters were observed.
A simple and rapid spectrophotometric method for evaluating platelet superoxide dismutase is reported. Platelets prepared avoiding erythrocyte and leucocyte contamination were lysated and tested in a Tris-cacodylic buffer containing pyrogallol. Platelet superoxide dismutase was calculated by evaluating the degree of the pyrogallol autoxidation inhibition induced by platelet lysate. Possible interferences of hydrogen peroxide, peroxidases and reducing substances were excluded. Platelet superoxide dismutase content was studied in 38 healthy subjects and was 19.1 +/- 4.1 U/10(8) platelets or 35 +/- 7.8 U/mg protein.
The behaviour of plasma malondialdehyde-like material (MDA-LM) was evaluated in 13 healthy subjects by a single-blind study that consisted of placebo (30 days), vitamin E treatment (300 mg/day) (30 days) and placebo (30 days). The study demonstrated that MDA-LM did not change during placebo treatment while it significantly decreased after vitamin E administration.
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Apolipoproteins A-I, A-II and B were evaluated in 18 chronic active hepatitis and 27 liver cirrhotic patients. The latter were also divided into compensated and decompensated subgroups. Significantly low values of apolipoproteins A-II and B were seen in chronic active hepatitis and liver cirrhotic patients, while apolipoprotein A-I was decreased in liver cirrhotic patients only. Chronic active hepatitis had higher apolipoprotein values than liver cirrhosis and in the latter one decompensated subgroup showed lower apolipoprotein levels than the compensated one. Apolipoproteins A-I, A-II and B correlated also well with prothrombin activity (Normotest) in liver cirrhotic patients, especially the apolipoprotein A-II values. This study suggests that serum values of apolipoproteins are affected by the type of liver damage and that their decrease could be partly due to impaired liver synthesis.
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This study investigates the influence of dipyridamole on platelet aggregation as evaluated by a single agonist or a pair of agonists in human platelet rich plasma and whole blood. Dipyridamole up to 30 microM was not found to influence the platelet aggregation of platelet rich plasma or whole blood; aspirin (100 microM), on the contrary, did inhibit platelet aggregation. The inhibition of platelet aggregation by aspirin could be reversed by using high concentrations of agonists or pairs of agonists. In this model dipyridamole inhibited platelet aggregation in both platelet rich plasma and whole blood in a dose-dependent fashion. Thromboxane A2 was less than 10% of controls in aspirin-treated PRP stimulated with low or high concentrations of collagen or with a pair of agonists. This study suggests that dipyridamole has direct antiplatelet activity in platelet rich plasma and whole blood when the cyclooxygenase pathway is blocked by aspirin.
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