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Biomedical subjects

S Colli

Publications and source records attributed to S Colli.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of single oral administrations of non steroidal antiinflammatory drugs to healthy volunteers on arachidonic acid metabolism in peripheral polymorphonuclear and mononuclear leukocytes.

The effects of a single oral administration of acetylsalicylic acid (500 mg), indomethacin (50 mg) and piroxicam (40 mg) to healthy volunteers on functional and biochemical parameters of platelets, polymorphonuclear (PMN) and mononuclear (MNL) leukocytes were evaluated. Blood was collected before and two hours after the drug intake and blood cells separated according to conventional techniques. The considered drugs almost completely suppressed the aggregation of platelets, whereas they did not affect either PMN and MNL aggregation. Superoxide anion generation by leukocytes was (PMN), or no effect (MNL) was observed after piroxicam and indomethacin respectively. The formation of arachidonate metabolites via the 5-lipoxygenase pathway by PMN and MNL challenged with 10 microM A23187 was unchanged following aspirin and indomethacin. In this respect a selective increase of 5-HETE and LTC4 synthesis by MNL only was detected after piroxicam administration. The three drugs similarly reduced TXB2 synthesis by platelets and PMN (-80% for aspirin and indomethacin, and -40% for piroxicam). As far as MNL is concerned, aspirin inhibited this metabolite by 80%, while indomethacin reduced it by 40% only. In contrast piroxicam increased TXB2 synthesis by stimulated MNL. It can be concluded that the considered antiinflammatory drugs 1) differently affect the cyclooxygenase enzyme in platelets and leukocytes; 2) at variance with the situation in platelets, the inhibition of thromboxane formation by leukocytes is not related to modifications of cellular function; 3) the formation of arachidonate metabolites via the 5-lipoxygenase pathway is affected by piroxicam only.

Adult↗
PubMed1988

Proinflammatory lipoxygenase products from peripheral mononuclear cells in patients with rheumatoid arthritis.

The formation of 5-lipoxygenase products (5-hydroxyeicosatetraenoic acid [5-HETE], leukotriene B4 [LTB4], and leukotriene C4 [LTC4]) by polymorphonuclear and mononuclear leukocytes isolated from peripheral blood of patients with rheumatoid arthritis was evaluated and compared with the data obtained from a group of control subjects. Although the levels of arachidonic acid metabolites via 5-lipoxygenase pathway by stimulated polymorphonuclear cells were comparable between patients and controls, mononuclear leukocytes from patients synthesized, when stimulated, significantly greater amounts of 5-HETE, LTB4, and LTC4 than did cells isolated from normal subjects. In addition, the release of superoxide anion, stimulated by either a particulate or a soluble stimulus, was increased in mononuclear cells from patients. The enhanced capacity of peripheral mononuclear leukocytes isolated from patients with rheumatoid arthritis to generate proinflammatory metabolites of arachidonic acid and oxygenated species with bactericidal and tissue-damaging properties may contribute to the pathogenesis of this complex disease.

Arthritis, Rheumatoid↗
PubMed1988

[Inhibition of mitochondrial respiration by mepivacaine].

In the last years our researches on neurotropic drugs follow our hypothesis that the strong effects on nervous system have always hidden more widespread effects on all tissues and cells. It is often required to employ local anesthetics in practising dentistry and orthodontics, particularly when children have to be treated. We have assayed in vitro one of these dental anesthetics, mepivacaine, on liver rat mitochondria: it depresses the respiration coupled to phosphorylation in mitochondria having a good respiratory control; so respiratory control too is depressed, but P/O ratio is unaffected; also respiration uncoupled by 2.4-dinitrophenol is depressed. Depressing respiration cooperates with anesthesia; unchanging P/O is good for the health of the cells and tissues treated by the mepivacaine.

Adenosine Diphosphate↗
PubMed1987

Indobufen is a potent inhibitor of whole blood aggregation in patients with a high atherosclerotic risk.

The newly developed method, based on the quantitation of changes in electrical impedance, to determine platelet aggregation in whole blood was applied to the evaluation of the effects of Indobufen, a well known inhibitor of platelet rich plasma aggregation. The platelet antiaggregatory activity of the drug after single (200 or 400 mg) and repeated doses (200 mg or 200 mg b.i.d. for 1 week) was determined on whole blood aggregation and thromboxane B2 formation by platelet rich plasma of 16 patients with high risk of atherosclerosis. At 2 hr after the single dose treatments, Indobufen significantly reduced the whole blood aggregation induced by 0.5-2 micrograms/ml collagen. At 24 hr from the intake of the drug the aggregation was significantly inhibited in patients who ingested the 400 mg dose only. As far as the repeated administrations are concerned, it appears that the inhibition of whole blood aggregation and thromboxane B2 formation by platelets reached 12 hr after the last drug administration was comparable to the degree of inhibition achieved 2 hr after Indobufen intake. It is concluded that Indobufen orally administered to patients with high risk of atherosclerosis is a potent inhibitor of whole blood aggregation.

Adult↗
PubMed1987

[Action of a dental anesthetic on cell respiration].

It is often required to employ local anesthetics in practising dentistry, particularly when children have to be treated. Our researches on neurotropic drugs in the last years follow our hypothesis that the strong effects on nervous system have always hidden more widespread effects on all tissues and cells. In vitro essays carried out on rat liver mitochondria show that a dental anesthetic, lidocaine, depress respiration coupled to phosphorylation in mitochondria having a good respiratory control; so respiratory control too is depressed, but P/O ratio is unaffected; also respiration uncoupled by 2,4-dinitrophenol is depressed. Depressing respiration cooperates with anesthesia; unchanging P/O is good for the health of the cells and tissues treated by the lidocaine.

Animals↗
PubMed1987

Effects of gemfibrozil on plasma lipoprotein-apolipoprotein distribution and platelet reactivity in patients with hypertriglyceridemia.

The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)--associated triglyceridemia (respectively-32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)--associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.

Adult↗
PubMed1986

Dietary interventions in north Karelia, Finland and south Italy. Modification of thromboxane B2 formation in platelets of male subjects only.

The effects of dietary interventions, based on changes of total fat, saturated fatty acids and cholesterol contents and of the polyunsaturated/saturated (P/S) fatty acid ratio of the diet, were studied in normal male and female subjects, living in North Karelia, Finland, and South Italy. In North Karelia the increase of P/S ratio (from 0.15 to 1.2) of the diet for a 6-week period resulted in reduced thromboxane B2 (TxB2) production by collagen-stimulated platelets only in male subjects, whereas plasma total, LDL and HDL cholesterol were reduced in both sexes. After a 6-week return to the original diet, plasma lipid levels were restored in all subjects. In the South Italy study, changes in platelet TxB2 production were observed only after return to the original diet in male subjects. Total and LDL cholesterol were significantly increased during the dietary intervention and returned toward baseline levels after switch back to the original diet. These data indicate that the increase of the P/S ratio in the diet reduces platelet TxB2 formation only in men.

Adult↗
PubMed1986

In vitro assessment of mononuclear leukocyte aggregation in response to sodium arachidonate and calcium ionophore A23187: comparison with polymorphonuclear leukocytes.

The effects of ionophore A23187 and sodium arachidonate (AASS) on mononuclear leukocyte (MNL) aggregation were evaluated and the results compared to those obtained with similarly challenged polymorphonuclear leukocytes (PMN). MNL aggregated in response to both ionophore A23187 (8-40 microM f.c.) and AASS (0.05-0.5 mM f.c.) and the response was comparable to that of similarly challenged PMN. The AASS induced aggregation of the two leukocyte subpopulations was inhibited by the presence of bovine serum albumin (BSA) in the incubation media and by calcium exogenously added. In contrast, this cation stimulated ionophore induced aggregation. When PMN and MNL aggregation was induced by AASS, a marked release of lactic dehydrogenase (LDH) was detected. The thromboxane-synthetase inhibitor UK 37248, inhibited both leukocyte aggregation and LDH release. When the response of leukocytes from male and female subjects was compared, in terms of aggregation, it appeared that the response of PMN from female volunteers was higher than that of PMN isolated from male donors, whereas no sex-related difference was detected when MNL aggregation was evaluated.

Adult↗
PubMed1986

Controlled evaluation of fat intake in the Mediterranean diet: comparative activities of olive oil and corn oil on plasma lipids and platelets in high-risk patients.

Activities of low-fat diets with olive oil or corn oil on lipids and platelets were studied in 23 middle-aged patients with high atherosclerosis risk for 8 wk. The olive oil diet had a polyunsaturated-saturated ratio of 0.33 vs 1.28 for the corn oil diet. Plasma total cholesterol was reduced with corn oil, but high-density lipoprotein cholesterol levels were lower with corn oil and unchanged or raised by olive. Plasma apolipoprotein B levels were equally reduced by both diets; apolipoprotein AI and the apo AI:B ratio rose only with olive oil. Plasma-glucose levels were lowered significantly with olive oil. Changes in platelet function were characterized by a reduced sensitivity to arachidonic acid (particularly with corn oil) and to collagen (particularly with olive). An olive oil diet with a moderate fat intake (about 30% of total calories) leads to favorable plasma lipoprotein and platelet changes.

Adult↗
PubMed1985

Prostacyclin-lipoprotein interactions. Studies on human platelet aggregation and adenylate cyclase.

The in vitro effects of different lipoprotein fractions (VLDL, LDL and HDL) on human washed platelet aggregation, induced by collagen and thrombin, were evaluated in the presence and absence of PGI2. Although VLDL and LDL increased the platelet aggregation while HDL showed an opposite effect, none of the tested lipoprotein fractions affected the potency of PGI2 as inhibitor of platelet aggregation (IC50). In addition, studies were performed to evaluate the effects of lipoproteins on adenylate cyclase activity in human platelet membranes. The three lipoprotein classes inhibited both basal and PGI2-stimulated adenylate cyclase without affecting the EC50 for PGI2. This inhibitory activity was not specifically elicited by any protein or lipid since neither bovine serum albumin nor a lipid emulsion (Intralipid) displayed any inhibition. The effect on adenylate cyclase elicited by VLDL, LDL and HDL does not seem to be correlated with the activity on platelet aggregation. It is concluded that mediators other than cAMP might be involved in the control of platelet function by lipoproteins.

Adenylyl Cyclases↗
PubMed1985

Plasma lipoproteins affect platelet malondialdehyde and thromboxane B2 production.

Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30 degrees C for 30 min, 100 micrograms of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [14C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B2 production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B2 synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the in vitro platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B2 and malondialdehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.

Blood Platelets↗
PubMed1985

Differential effects of aspirin and indomethacin on platelet and leukocyte thromboxane A2 formation.

In this study, the in vitro inhibitory effects of aspirin and indomethacin on the arachidonic acid induced thromboxane B2 formation by human leukocytes, are evaluated. The results are compared to those obtained using similarly challenged human washed platelets. Acetylsalicylic acid inhibition, calculated as IC50 by a dose-response curve, is more than ten fold higher for leukocytes vs platelets. In fact, a concentration of aspirin as low as 5 microM almost completely suppresses thromboxane B2 formation by washed platelets, whereas a concentration of 50 microM is necessary to achieve the same inhibition with leukocytes. Indomethacin (0.001-100 microM), incubated with platelet and leukocyte suspensions acts similarly to aspirin. Leukocyte and platelet cyclooxygenases are, therefore, differently affected by both aspirin and indomethacin. These differences may be relevant in the understanding of the wide divergence between the aspirin doses used in thrombosis prevention and in the treatment of inflammatory disease.

Aspirin↗
PubMed1985

Control of human and animal platelet aggregation by a new prostacyclin analog.

The in vitro effects of ZK 36 374, a new chemically stable prostacyclin (PGI2) analog, on platelet aggregation were studied and compared to those of PGI2. Significantly lower concentrations of ZK 36 374, versus prostacyclin, were required to inhibit collagen and epinephrine-induced aggregation in human platelet-rich plasma. In contrast, in rat and rabbit platelet rich plasma, PGI2 was more effective than ZK 36 374 in inhibiting the aggregation elicited by ADP and collagen. It is concluded that ZK 36 374 is a potent antiaggregatory compound and may be useful in the prevention of cardiovascular disorders.

Adenosine Diphosphate↗
PubMed1984

Increased platelet sensitivity and thromboxane B2 formation in type-II hyperlipoproteinaemic patients.

Platelet aggregation induced by collagen, ADP and epinephrine, was monitored in 150 type-II patients (115 type IIA and 35 type IIB) and compared with a reference group of normolipidaemic controls; in addition, malondialydehyde formation and thromboxane B2 were examined in a subsample of the type-IIA patients. Threshold aggregatory concentrations were significantly lower in the whole group of type-II patients for all three aggregating agents; no difference in terms of aggregatory response was detected between platelets from type-IIA and -IIB patients. Only 56% of type-II patients, however, exceeded the 95th percentile of the threshold aggregatory concentrations in controls. The formation of malondialdehyde in platelet-rich plasma stimulated with thrombin and collagen, was significantly higher in platelets from type-IIA patients. The production of thromboxane B2 by platelets, from endogenous arachidonic acid in type-IIA patients, was significantly higher and exceeded the highest level found in controls.

Adolescent↗
PubMed1984

Acute effects of ethanol, caffeine, or both on platelet aggregation, thromboxane formation, and plasma-free fatty acids in normal subjects.

The acute effects of ethanol (0.5 ml/kg b.w.) and caffeine (200 mg), alone or in combination, on platelet function and plasma lipid-lipoprotein levels, were tested in four healthy volunteers according to a Latin Square design. The effects of ethanol alone on platelet function (adrenaline- and collagen-induced aggregation, thromboxane B2 formation induced by arachidonic acid) were negligible. Conversely, caffeine significantly reduced maximal aggregation of platelets following adrenaline and collagen, 3 hours after administration; it also significantly increased thromboxane B2 formation 1 hour from administration. The intakes of caffeine and, to some extent, of ethanol at doses in the common daily range, although not profoundly affecting platelet function or lipid parameters, should be given consideration when treatments with platelet-active drugs are prescribed.

Adult↗
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↗