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Biomedical subjects

P Parise

Publications and source records attributed to P Parise.

At least 37 records · Page 2Linked to original sources
PubMed1992

Failure to demonstrate beneficial effect of prostacyclin (PGI2) infusion on red blood cell deformability in patients with peripheral vascular disease: a possible role of the leukocytes.

The effect of prostacyclin (PGI2) on red blood cell deformability is still controversial. The authors have evaluated some hemorrheologic parameters during PGI2 infusion to patients with severe obstructive peripheral arterial disease not suitable for surgery and not responsive to other medical treatments. PGI2 infusion resulted in a positive clinical effect in 12 of 16 patients, who experienced a significant improvement of their rest pain lasting from two days to more than seven months. Hematocrit, platelet count, and fibrinogen were not modified during PGI2 infusion whereas leukocyte count rose significantly. The evaluation of red blood cell filterability (VRBC) (volume of RBC filtered in one minute) by a whole blood filtration technique showed no significant changes during PGI2 treatment. However, since whole blood filterability is negatively correlated to leukocyte count, a specific regression line was elaborated to remove the potential negative influence of the increased leukocyte counts. VRBC values adjusted to a standard leukocyte number significantly increased during PGI2 treatment.

Adult↗
PubMed1992

Bolus thrombolysis in venous thromboembolism.

Thrombolytic therapy is rarely used in venous thromboembolism because of the fear of hemorrhagic complications. Preliminary clinical experiences with recombinant tissue-type plasminogen activator (rt-PA) in patients with deep vein thrombosis have shown that even this fibrin-specific plasminogen activator causes an unacceptable rate of hemorrhagic complications. Theoretical considerations and the available experimental and clinical data suggest that infusion of rt-PA over a short period of time would result in a more favorable risk-benefit ratio. Shortening the period of rt-PA infusion results in higher peak plasma levels, thus allowing a higher concentration of the plasminogen activator on the surface and inside the occluding thrombus. In addition, a bolus infusion can prevent or minimize the interaction between rt-PA and the hemostatic system, reducing the likelihood of a systemic lytic state, of a platelet function defect, and, possibly, of bleeding side effects. In venous thromboembolism animal models, the efficacy of bolus rt-PA can be further increased by the adjunctive administration of an effective antithrombotic treatment. This is because the accretion of new fibrin on the thrombi counteracts the lysis of preformed fibrin and influences negatively the final thrombus size. Effective adjunctive antithrombotic treatment includes either high doses of heparin, producing an unclottable activated partial thromboplastin time (aPTT), or doses of recombinant hirudin, doubling the aPTT. When used as an alternative to rt-PA, bolus doses of a hybrid plasminogen activator with prolonged half-life efficiently reduce thrombus size by lysing preformed and newly formed fibrin. Preliminary clinical experience in patients with pulmonary embolism seems to confirm that rt-PA infused as a bolus is at least as effective as, and probably more effective than, rt-PA infused over a longer period.

Animals↗
PubMed1991

Thrombus resistance to lysis and reocclusion after thrombolysis: the role of platelets.

Thrombolytic therapy reduces the mortality rate in patients with acute myocardial infarction. However, thrombolytic agents, which are primarily directed toward the lysis of fibrin, fail to achieve reperfusion in at least 20% of patients and an early reocclusion occurs in up to 25% of cases. The role of platelets in both thrombus resistance to lysis and early reocclusion is demonstrated by experimental and clinical observations. Platelets and the fibrinolytic system interact in numerous ways. Platelet activation can potentiate or inhibit the fibrinolytic process. The activation of the fibrinolytic system has been found to induce either an activation or an inhibition of platelet function. In animal models it has been shown that platelet-rich thrombi are resistant to lysis, and that platelets and fibrin still accumulate on lysing thrombi during effective thrombolysis. One of the most attractive strategies to optimize thrombolytic therapy is adjunctive treatment with pharmacological agents which inhibit platelet function.

Animals↗
PubMed1991

Generation of arachidonic acid metabolites from stimulated whole blood in patients with chronic myeloproliferative disorders.

We have evaluated the arachidonic acid (AA) metabolism in patients with myeloproliferative disorders (MPD). In essential thrombocythemia (ET), the generation of thromboxane B2 was found significantly reduced and inversely correlated with platelet count. Polycythemia vera (PV) patients showed an increased formation of this metabolite of AA. Prostaglandin E2 and 6-keto-PGF1 alpha generation were markedly reduced in patients with chronic myelogenous leukemia. Our study confirms that the arachidonate metabolism is frequently deranged in patients with MPD. The opposite changes in thromboxane formation in ET and PV could be one of the factors responsible for the different incidences of thrombotic and hemorrhagic complications in these diseases.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[Picotamide does not interfere with the anticoagulant activity of warfarin in patients wearing heart valve prostheses].

Picotamide, a new antiplatelet drug which has only slight effects on bleeding time, could be useful, in combination with oral anticoagulants, for the prevention of thromboembolic complications in patients with heart valve prostheses. We have evaluated in a randomized, controlled, double-blind, cross-over study, the effect of picotamide on the anticoagulant activity of warfarin. Administration of 300 mg t.i.d. for 10 days to 10 patients with aortic or mitral valve prostheses did not modify significantly either the level of anticoagulation or the mean daily dosage of warfarin. We observed a trend towards a reduction of plasma levels of beta-thromboglobulin. In conclusion the results of this study show that picotamide does not interfere with the anticoagulant activity of warfarin.

Aged↗
PubMed1990

"In vitro" and "ex vivo" effects of picotamide, a combined thromboxane A2-synthase inhibitor and -receptor antagonist, on human platelets.

Picotamide (G 137), a new non prostanoid inhibitor of in vitro arachidonic acid induced platelet aggregation, has been further characterized in in vitro and ex vivo studies. When whole blood was activated with collagen in the presence of picotamide 5 x 10(-4) M, thromboxane B2 production was decreased, and 6-keto-PGF1 alpha generation was significantly increased, suggesting a reorientation of platelet endoperoxide metabolism following blockade of thromboxane synthetase. Picotamide also inhibited platelet aggregation and clot retraction induced by the endoperoxide analogue U46619 in human platelets, indicating thromboxane A2-receptor antagonism, possibly of competitive nature. A single oral dose of picotamide 1 g in 24 healthy volunteers produced a significant inhibition of collagen, arachidonic acid and U46619-induced platelet aggregation. Serum levels of thromboxane B2 were also reduced. Chronic administration of picotamide 1.2 g/d to patients with vascular disease resulted in a prompt and persistent fall in their increased plasma levels of beta-thromboglobulin. The results indicate that picotamide is a combined thromboxane B2-synthetase inhibitor and thromboxane A2-receptor antagonist in human platelets, and that it may prove useful as an antithrombotic agent.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Effects of dipyridamole on the hypoxemic pulmonary hypertension of patients with chronic obstructive pulmonary disease.

Based on the hypothesis that blood platelets contribute to the pathogenesis of hypoxemic pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD), the effect of a prolonged treatment with dipyridamole, a platelet-inhibiting drug, on hypoxemic pulmonary hypertension was evaluated in a double-blind cross-over study. Eight patients with COPD, pulmonary hypertension [mean systolic pressure 52.2 +/- (SD) 9.7 mm Hg; mean diastolic pressure 25.8 +/- (SD) 6.8 mm Hg] and shortened platelet regeneration time [mean 5.2 +/- (SD) 1.2 days] received, in a cross-over random sequence, the following two 3-month treatments: (a) dipyridamole 100 mg and acetylcysteine 100 mg every 6 h; (b) acetylcysteine, 100 mg every 6 h. Dipyridamole significantly prolonged the platelet regeneration time [mean 6.5 +/- (SD) 1.0 days; p less than 0.05]. There was no significant effect on diastolic pulmonary pressure. However, systolic pressure was significantly (p less than 0.05) lower after dipyridamole [46.8 +/- (SD) 16 mm Hg] than after placebo [56.1 +/- (SD) 14 mm Hg]. These results suggest that dipyridamole can slow the progression of hypoxemic pulmonary hypertension in patients with COPD.

Aged↗
PubMed1987

In vitro and ex vivo effects of indobufen on red blood cell deformability.

We have studied the effect of indobufen, a cyclo-oxygenase blocking agent which has proved useful in patients with obstructive vascular disease, on red blood cell (RBC) filterability in vitro and in a pilot study ex vivo. The addition of indobufen in vitro to blood samples from 10 healthy volunteers did not significantly modify RBC deformability. We evaluated the ex vivo effect of indobufen (200 mg bd) in 14 patients with obstructive vascular disease. A significant improvement in RBC deformability was noted on the 5th, 14th, and 28th days of treatment, 2 h after the morning dose. Acetylsalicylic acid given to 6 similar patients had no effect suggesting that the positive haemorheological effect of indobufen is probably not linked to its cyclooxygenase blocking effect.

Aspirin↗
PubMed1986

Cephalosporin-induced hypoprothrombinemia: is the N-methylthiotetrazole side chain the culprit?

The reported high incidence of vitamin-K-reversible hypoprothrombinemia associated with the new beta-lactamase-stable cephalosporins prompted us to evaluate the effect on hemostasis of three cephalosporins (cefamandole, ceftriaxone, and ceftazidime) in 30 patients with serious infections. Cefamandole and ceftriaxone, both containing a sulfhydryl group, induced a significant and similar prolongation of prothrombin time and decrease in factor VII activity. Ceftazidime, in contrast, had no effect on these two parameters.

Azoles↗
PubMed1985

Platelet activation in psoriasis.

Recent epidemiological studies have suggested that psoriasis represents a risk factor for thrombotic vascular diseases. In order to evaluate the possible role of hemostatic changes in the development of thrombotic episodes in psoriasis, some parameters of the hemostatic "balance" were investigated in 22 male psoriatic patients and compared to those of 22 male control subjects. Incidence of known risk factors for vascular diseases (diabetes, hypertension, smoking, dyslipidemia) was comparable in the two study groups. There were no statistically significant differences in platelet count, circulating platelet aggregates, platelet production of malondialdehyde (MDA), total plasma antithrombin and fibrinolytic activities. In patients with psoriasis the incidence of spontaneous platelet hyperaggregability and plasma levels of beta-thromboglobulin were significantly higher than in control subjects. Platelet regeneration time, measured as MDA recovery after aspirin ingestion, was significantly shorter in psoriatic patients. These data suggest that an in vivo platelet activation occurs in patients with psoriasis and could contribute to the development of thrombotic complications. The release of mitogenic and inflammatory substances by activated platelets may play a role in the histogenesis of psoriatic lesions.

Adolescent↗
PubMed1983

[Optimization of a method for determining platelet malondialdehyde production].

The platelet MDA production assay is widely used for studying platelet function and turnover. However, as original Stuart's method has low sensitivity, it is not accurate when MDA concentrations are very low. The effects of anticoagulants, incubation periods and clearing procedures were studied in an attempt to overcome this limitation and improve the sensitivity of this method. The results demonstrated that higher PCA and thrombin concentrations and a final addition of concentrated KOH increase the sensitivity of the method by almost eight fold. The higher transparency of the solutions, which is obtained through the sieving effect achieved by insoluble potassium perchlorate cold precipitation, is mainly responsible for the improvement.

Blood Platelets↗
PubMed1983

Platelet malondialdehyde production kinetics after cyclooxygenase block. A study performed with a modified high sensitivity assay.

A modification of the original thiobarbituric acid (TBA) method for malondialdehyde (MDA) assay is described. The improvement is essentially based on the clearing effect of KClO4 that makes measurements more simple and sensitive. MDA values obtained in normal subjects were almost eightfold higher than those obtainable with Stuart's original assay method, so that after cyclooxygenase block it was possible to assess platelet regeneration time even in thrombocytopenic patients with at least 60,000 platelets/microliter and MDA production early after aspirin intake. To challenge this modification, platelet regeneration time was studied in normal subjects as well as in thrombocytopenic patients, either hypoplastic or idiopathic, and in hypoxemic patients with increased platelet consumption. The initial disappearance kinetics of platelet MDA and thromboxane B2 production after aspirin suggests that TBA-reactive material is synthesized through the lipoxygenase pathway. The reversible block determined by acetylsalicylic acid and salicylate on hydroperoxi-eicosatetraenoic acid peroxidase can be responsible for the initial increase of this TBA-reactive material.

Adult↗
PubMed1982

Persistent spontaneous heparinaemia in systemic mastocytosis.

A case of systemic mastocytosis with lymphatic, digestive, nervous and bone involvement and with persistent heparinaemia is described. The true heparin nature of the circulating anticoagulant was proved by the conventional titrimetric method with protamine sulphate and by the new specific amidolytic assay of its Xa-inhibiting properties. This human circulating heparin displayed a low specific activity as expressed by its activity/weight ratio.

Blood Coagulation↗
PubMed1982

Inhibition of spontaneous platelet aggregation and adhesion by indobufen (K 3920). A randomized, double-blind crossover study on platelet, coagulation and fibrinolysis function tests.

In a randomized double-blind crossover study in 12 patients with atherosclerotic disease, the effect of 2 dosages (100 and 200 mg twice daily) of indobufen, a new synthetic inhibition of platelet aggregation, on some platelet functions, coagulation and fibrinolysis tests was investigated. Regardless of the dosage used, indobufen was shown to induce a prompt normalization of the enhanced platelet aggregation of these patients. The effect lasted for the entire period of drug administration and in 50% of patients a normal platelet aggregation was maintained until the fourth day after discontinuation of the drug. Indobufen was also able to reduce platelet adhesiveness and to lengthen bleeding time, especially when the higher dosage was used.

Aged↗