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Biomedical subjects

S Colli

Publications and source records attributed to S Colli.

At least 73 records · Page 4Linked to original sources
PubMed1984

Pharmacological control of platelet-vessel wall interactions in patients with chronic obstructive airway disease.

In the last few years great interest has been devoted to the role of platelet activation in the haemodynamic and thrombotic complications which frequently occur in patients with chronic obstructive airway disease. Several recent studies have shown, in fact, a number of alterations of platelet function in this pathological condition, such as an increased betathromboglobulin level and higher levels of malondialdehyde after collagen and thrombin platelet stimulation compared to age and sex matched control subjects. Our study indicates that the platelet regeneration time is shortened in patients with chronic obstructive airway disease in respect to that of controls (p less than 0.001). The administration of dipyridamole (425 mg/die) resulted in a significant prolongation of the platelet regeneration time in these patients indicating that the drug was effective in reducing the increased platelet turnover.

Aspirin↗
PubMed1983

Effects of PGI2 on platelet aggregation and adenylate cyclase activity in human type IIa hypercholesterolemia.

The sensitivity to PGI2 of platelets of 20 selected type IIa hypercholesterolemic patients was studied and compared to that of platelets of 14 normocholesterolemic subjects. Type IIa subjects required higher concentrations of PGI2 to inhibit platelet aggregation elicited by 1 microM ADP, 1 microgram/ml collagen and 1.4 microM epinephrine. Adenylate cyclase activity was also measured in washed platelet membranes from the two groups of subjects. Adenylate cyclase activity, both basal and PGI2-stimulated, was not statistically different in the two groups examined. Therefore changes at the level of PGI2 receptors coupled to adenylate cyclase are not likely to be responsible for the different platelet sensitivity to prostacyclin.

Adenylyl Cyclases↗
PubMed1983

Clofibrate and tiadenol treatment in hyperlipoproteinemias. A comparative trial of drugs affecting lipoprotein catabolism and biosynthesis.

Changes in plasma lipoprotein levels and platelet reactivity were evaluated during sequential treatments with clofibrate and tiadenol, two hypolipidemic agents with apparently different mechanisms, in 27 hyperlipoproteinemic patients. The objective of the study was to determine the pattern of plasma lipoprotein variations, induced by a drug mainly affecting lipoprotein catabolism (clofibrate) and by a drug affecting biosynthesis (tiadenol), and to single out-patients specifically responding to either treatment. Both drugs proved significantly active in type IIA and IV hyperlipoproteinemias, not in type IIB. Clofibrate significantly lowered very low density lipoprotein (VLDL) associated cholesterol in all three hyperlipoproteinemia phenotypes, and it also lowered VLDL triglycerides in type IV, while increasing high density lipoprotein (HDL) cholesterol in type IIA patients. Low density lipoprotein (LDL) cholesterol levels were minimally reduced by clofibrate in type IIA (-4%), and increased in types IIB (+ 14.2%) and IV (+ 6.1%) patients. Conversely, tiadenol lowered VLDL cholesterol and triglycerides to a lesser extent, but it did significantly reduce LDL cholesterolemia in type IIA (-17.6%), while increasing HDL cholesterol in type IIB. Statistical evaluation of the results did not permit identification of parameters associated with the response to either drug, although individuals specifically responding to one or the other agent, or to both, were detected in all three phenotypes. The sensitivity to the major platelet aggregating factors, ADP, adrenaline and collagen, was not significantly altered after drug treatments. Evaluation of the hypolipidemic response to agents with different mechanisms may be of help in selecting the best treatment for individual patients.

Adult↗
PubMed1983

Effects of dilazep on human platelets and rat vascular tissue: in vitro studies on platelet aggregation, and arachidonic acid oxidation.

The "in vitro" effects of Dilazep on platelet aggregation and arachidonic acid oxidation in platelets and vessel wall were studied. Dilazep exerted a clearcut inhibitory effect on platelet aggregation induced by several stimuli. In addition, the compound completely suppressed malondialdehyde production by platelets elicited by collagen and thrombin, in a dose-dependent fashion. The evaluation of Dilazep effects on the in vitro release of prostacyclin-like material by rat aortic tissue did not provide any indication about an interference of the drug on the generation of endogenous antiaggregatory material.

Animals↗
PubMed1982

Dipyridamole treatment in chronic obstructive airways disease: effect on platelet regeneration time.

The platelet regeneration time (PRT) determined in a group of hypoxaemic patients with chronic obstructive airways disease (COAD), before and after treatment with dipyridamole 150 mg tid, was compared with a group of control subjects. The PRT was computed by a modified non-radioisotope technique and was expressed as t1/2 in days. The patient group showed a significantly shortened PRT as compared to controls of the same age and sex (2.10 +/- 0.16 vs 3.65 +/- 0.26 days; p less than 0.001). One month of dipyridamole administration resulted in prolongation of the PRT in COAD patients (2.10 +/- 0.16 days pre-treatment vs 2.75 +/- 0.20 post-treatment; p less than 0.01), without affecting the platelet cyclo-oxygenase system. This study indicates that dipyridamole may be beneficial in pathological conditions, which are characterized by increased platelet turnover, possibly leading to frequent thromboembolic complications.

Adult↗
PubMed1982

Metformin reduces platelet hypersensitivity in hypercholesterolemic rabbits.

The effects of Metformin treatment on platelet responsiveness to aggregating agents was studied in cholesterol-fed rabbits. Three groups of animals were fed, for one month, either a normal (N), or a hypercholesterolemic (HC), or a hypercholesterolemic + 0.5% Metformin diet (HC + Met), Platelets from the HC rabbits required significantly lower collagen and arachidonic acid concentrations to aggregate, as compared to platelets from N rabbits. The platelet response from the HC + Met rabbits was not significantly different from that of normals. The cholesterol/phospholipid ratio in platelets was increased in both dietary groups (HC, HC + Met). The serum thromboxane B2 concentrations did not show any significant difference between the groups. Plasma exchange experiments failed to indicate a specific effect of the plasma environment on platelet behaviour. In view of the inactivity of metformin on the platelet cyclo-oxygenase pathway, the reported results suggest that metformin may act by an as yet unexplored mechanism.

Animals↗
PubMed1982

Platelet function in rheumatoid arthritis.

Platelet function tests were evaluated in 20 patients with rheumatoid arthritis (RA), 9 of whom displayed thrombocytosis (greater than 400,000 platelets/microliter). Most patients had an enhanced sensitivity to collagen and epinephrine induced aggregation, as compared with a reference group. In contrast, malondialdehyde (MDA) production, an index of platelet arachidonic acid metabolism, was in the normal range for all the patients except 3, who were LE phenomenon positive. The hypersensitivity of platelets to aggregating stimuli was particularly marked in thrombocytotic patients, who also showed the most striking biochemical and clinical abnormality. These findings indicate the crucial role of platelets in the development and self-sustaining of RA.

Adult↗
PubMedDate not supplied

5-Lipoxygenase gene expression in HL60 cells during differentiation with DMSO.

The model of promyelocytic leukemia cells HL60 was utilized to study the accumulation of 5-lipoxygenase mRNA during the cellular differentiation induced by DMSO. In the present study a strict correlation between the increase in state of differentiation of HL60 and accumulation of 5-lipoxygenase mRNA is demonstrated, indicating that HL60 cells are an interesting model for the study of drugs which could interfere with the synthesis of the enzyme.

Arachidonate 5-Lipoxygenase↗
PubMedDate not supplied

Atherosclerosis and thrombosis. Old and new drugs.

Thanks to the increasing knowledge of the pathogenesis of atherosclerosis, much effort has been made in the last years to develop new drugs aimed at controlling risk factors correlated with the disease as well as to investigate more deeply their mechanism of action. In particular, this brief review will describe some new aspects of the mechanism of action of drugs widely used in the control of risk factors like hyperlipemia, hypertension and blood viscosity. Among drugs active on plasma lipid profile, HMG-CoA reductase inhibitor are, at present, under study for their promising activity in the modulation of the interaction between the cells of the arterial wall and circulating blood elements. Indeed, these compounds have been found to control the proliferation of smooth muscle cells and other events related to the formation of atheroma. As far as antithrombotic drugs are concerned, the efficacy of low doses of aspirin has emerged by recent clinical trials. The successful use of low doses of aspirin has been possible following the comprehension of the mechanism by which this compound inhibits TXA-dependent platelet function, thus allowing a dose-dependent dissociation of the antithrombotic activity from other undesirable effects. Also for calcium antagonist an antiatherogenic effect which deserves further investigations has been recently clarified. Indeed it has been demonstrated that calcium antagonists have a protective effect against vascular lesions because they inhibit smooth muscle cell proliferation, lipid uptake by macrophages and the production of collagen and elastin. Another class of drugs which represents a new approach in the control of some risk factors is represented by n-3 fatty acids. Besides their activity on triglycerides, these compounds exert a positive effect on hemostatic and thromboembolic event, by reducing platelet aggregation and blood viscosity. Also for those molecules which appear to exert promising antiatherosclerotic and antithrombotic action, further studies will define their exact mechanism of action.

Journal Article↗
PubMedDate not supplied

Oxidized LDLs influence thrombotic response and cyclooxygenase 2.

Oxidative modification of low-density lipoproteins (LDLs) plays a key role in the development of atherosclerosis and the onset of coronary artery disease. LDL oxidation alters the antithrombotic balance of human endothelial cells inducing surface tissue factor (TF) pathway activity, which results in enhanced fibrin deposition. Fibrinolysis, which is strictly regulated by plasminogen activator inhibitor-1 (PAL-1) and tissue-type plasminogen activator (tPA). Is also dysregulated by LDL oxidation with a net increase in the inhibitory rate. Oxidized LDLs (oxLDLs) also affect many aspects of macrophage function linked to the inflammatory response of these cells, In particular, oxLDLs downregulate inducible cyclooxigenase (Cox-2) in human monocyte-derived macrophages exposed to bacterial lipopolysaccharide. This observation may support the hypothesis that, within atheromata, the transformation macrophages into foam cells results in the attenuation of the inflammatory response, thus contributing to the progression of athrogenesis. Among lipid constituents of oxLDLs, Ox-PAPC, a mixture of oxidized arachidonic acid-containing phospholipids, prevents Cox-2 expression, suggesting that it could be considered responsible for the biological activity of oxLDLs.

Arteriosclerosis↗