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Biomedical subjects

G Davì

Publications and source records attributed to G Davì.

At least 73 records · Page 4Linked to original sources
PubMed1989

The relationship of insulin antibodies, platelet-fixing immune complexes and platelet-associated IgG to in vitro platelet aggregation and thromboxane B2 synthesis in childhood type 1 (insulin-dependent) diabetes mellitus.

The relationship of insulin antibodies, platelet-fixing soluble immune complexes and platelet associated IgG to in vitro platelet aggregation and thromboxane B2 synthesis was studied in a group of children with type 1 (insulin-dependent) diabetes mellitus. Insulin antibodies, through the formation of insulin anti-insulin platelet-fixing immune complexes, seem to increase the levels of platelet associated IgG and both insulin immunity and increased platelet associated IgG are associated with the highest degree of platelet aggregation and thromboxane synthesis. These data suggest a possible role of immune factors in the platelet disfunction of diabetic subjects. Both platelet abnormalities and immune factors have been thought to play a role in the pathogenesis of the late diabetic complications. In this paper data concerning a possible interaction between these two factors are presented.

Adenosine Diphosphate↗
PubMed1989

Platelet function in hypo- and hyperthyroidism.

Alterations in cardiovascular hemodynamics are found in patients with hypofunction of the thyroid. Frank hypothyroidism favours the development of coronary heart disease. Platelets are thought to be important in atherosclerotic lesions initiation and progression. We studied platelet sensitivity to several agonists and to a physiological antagonist, prostacyclin, and thromboxane production in patients with hyperthyroidism and hypothyroidism. No statistically significant differences were found between platelets activities in patients and control subjects. We conclude that increased platelet function is not a direct indicator of susceptibility to cardiovascular diseases in patients with hypothyroidism whereas the hyperdynamic state, cardinal manifestation of thyrotoxicosis, is not associated with platelet activation.

Adult↗
PubMed1989

[Effect of a long-term treatment with simvastatin, an inhibitor of HMG-CoA reductase, in dyslipidemic patients at high risk].

The reduction of total and LDL cholesterol (TC and LDLc), apoprotein B (ApoB) and in some instances triglycerides (TG) and the increase of HDL cholesterol (HDLc) and apoprotein A (ApoA) seem to be associated to a reduced coronary risk. Aim of our work was to evaluate the effects of a chronic treatment with the HMG-CoA reductase inhibitor simvastatin (MK-733), in a group of 8 dyslipidemic patients, 5 women and 3 men, aged between 48 and 69 years (mean age 59 +/- 8 years) at high risk being already affected by clinical compliances of atherosclerosis and not previously controlled by diet and/or other antidyslipidemic drugs. At the beginning and at the end (6 months) of this open study it was performed a clinical, ECG and ophthalmological examination, as well as an evaluation of the routine laboratory parameters. The initial dosage of simvastatin was a tablet of 10 mg/day, increased after a month to 20 mg and then to 40 mg/die. The mean dosage was 26.25 mg at the 3rd month and 21.25 mg at the 6th. Long-term simvastatin treatment was well tolerated (lack of important side effects as well as of significant changes of other clinical and laboratory parameters) and effective, reducing significantly (p less than 0.01) TC (317.9 +/- 30.8 vs 238.5 +/- 37.9 mg/dl), LDLc (210.6 +/- 48 vs 147.9 +/- 52 mg/dl), ApoB (144.7 +/- 17.5 vs 104.5 +/- 18), and TG (272.9 +/- 184 vs 200.5 +/- 117.6 mg/dl) and increasing in contrast HDL and ApoA values.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Platelet function in patients with type 2 diabetes mellitus: the effect of glycaemic control.

In the present study the effects of a short term intensive glycaemic control obtained with subcutaneous insulin therapy on lipids and apoprotein levels, platelet aggregation, platelet sensitivity to prostacyclin and platelet thromboxane production were investigated in 20 patients with type 2 diabetes and vascular disease. In 11 out of the 20 patients there was a significant improvement of glycaemic control (fructosamine reduction). Only with tight improvement of glycaemic control there was significant change in the concentration of ADP and collagen required to produce 50% of the maximum aggregation wave response, in the responsiveness of platelet to PGI2 and in the TxB2 synthesis. Lower Apo B levels were also shown in the tight control group suggesting that Apo B changes may have influenced platelet aggregation and thromboxane synthesis.

Adult↗
PubMed1989

[Antiplatelet effects of combined therapy with ticlopidine and low doses of aspirin on patients with ischemic cardiopathy].

The aim of study was to evaluate the effects on platelet function, in 8 patients with ischemic heart disease, of the following treatments administered consecutively: ticlopidine in a daily dose of 500 mg (10 days); aspirin in a daily dose of 50 mg (10 days); ticlopidine plus ASA, at the same dosages, for the last 10 days. Only ticlopidine plus ASA significantly inhibited EC 50 of ADP, collagen and arachidonate. Platelet activation and platelet sensitivity to prostacyclin was affected by ticlopidine and ticlopidine plus ASA but not by ASA alone. We conclude that in our ischemic heart disease patients the association of ticlopidine and low dose aspirin seems superior to each drug alone in inhibiting platelet activity.

Aged↗
PubMed1988

Complications of argon laser retinal buckling performed in myopic subjects presenting rhegmatogenous degenerations.

Twenty-two eyes of twenty-two patients suffering from retinal peripheral degenerations underwent preventive equatorial buckling with argon laser photocoagulation. The fellow eye was used as control. We evaluated the effects of laser photocoagulation on corneal sensitivity, on accommodation, on pupillary diameter and light reflex. In the postoperative period, up to the 3rd month, results were significant with respect to the control eye. The mechanisms to which the onset of these undesired alterations is due are discussed.

Accommodation, Ocular↗
PubMed1988

In vitro effects of gallopamil on platelet aggregation and thromboxane generation.

The in vitro effects of gallopamil, a highly specific calcium-channel blocker, on platelet function were investigated. Gallopamil caused a dose-dependent inhibition of platelet aggregation. In fact, the drug in concentrations as low as 0.5 microgram/ml inhibited platelet activating factor and epinephrine-induced platelet aggregation. Similarly, the inhibition of adenosine diphosphate and epinephrine-induced thromboxane generation was demonstrated. Since platelet activation and thromboxane release may be related to myocardial ischemia, it is conceivable that some of the antianginal effects of gallopamil may in part be due to platelet inhibitory effects.

Blood Platelets↗
PubMed1986

Are the vascular complications of diabetes mellitus preceded by an altered thromboxane/prostacyclin plasmatic ratio?

Although many data regarding the biosynthesis of thromboxane A2 and prostacyclin in diabetes mellitus have recently appeared in the literature, it is not clear whether an imbalance between the generation of the two prostaglandins might be connected to the vascular complications of diabetes. In the present review we have tried to emphasize the most significant aspects of these studies and we have focused on alterations of platelet prostacyclin receptors and on the effects of circulating immune complexes on platelets of diabetics. It is likely that studies on the release of platelet derived growth factor as well as more precise definitions of its action on vessel wall cells leading to a massive release of prostacyclin, will permit us to ascertain whether an alteration in prostaglandin ratio is linked to the genesis of the vascular complications in diabetics.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Enhanced platelet sensitivity to prostacyclin after isosorbide-5-mononitrate in patients with stable angina pectoris.

Recently the possibility that nitrates inhibit platelet function in man has been explored in vitro and in vivo. We have studied the effect of isosorbide-5-mononitrate (ISMN), a stable and long-acting organic nitrate, on platelet function in vivo. Given orally within the current therapeutic range, the drug has practically no effect on platelet aggregation nor thromboxane generation in platelet-rich plasma in response to ADP, collagen, arachidonate, epinephrine and PAF. Synergistic effects of prostacyclin and ISMN on inhibition of ADP-induced platelet aggregation have been observed. Thus, local inhibition of platelet aggregation might not have been detectable, due to the short half-life in vitro of prostacyclin.

Adult↗
PubMed1985

Platelet thromboxane production in liver cirrhosis.

To determine whether platelet prostaglandin production in patients with liver cirrhosis was as impaired as platelet aggregation, serum thromboxane production was studied in 52 patients with liver cirrhosis; 12 patients had consumed more than 80 gr of alcohol/day, for more than ten years; 13 patients had also had diabetes mellitus for more than two years. A reduced thromboxane synthesis by platelets of liver disease patients was observed; the parallel decrease of both platelet thromboxane and serum PGE2 formation may also suggest a decrease in arachidonic acid availability for prostaglandin and thromboxane production. A smaller reduction of thromboxane and PGE2 formation in cirrhotics with diabetes mellitus or chronic alcohol intake was also observed.

Adult↗
PubMed1985

Clinical pharmacology of platelet cyclooxygenase inhibition.

Nonsteroidal anti-inflammatory drugs and sulfinpyrazone compete dose-dependently with arachidonate for binding to platelet cyclooxygenase. Such a process closely follows systemic plasma drug concentrations and is reversible as a function of drug elimination. Peak inhibition and extent of its reversibility at 24 hr varies consistently with individual pharmacokinetic profile. Inhibition of platelet cyclooxygenase activity by these agents is associated with variable effects on prostaglandin (PG) synthesis in the gastric mucosa and the kidney. Aspirin acetylates platelet cyclooxygenase and permanently inhibits thromboxane (TX) A2 production in a dose-dependent fashion when single doses of 0.1 to 2.0 mg/kg are given. Acetylation of the enzyme by low-dose aspirin is cumulative on repeated dosing. The fractional dose of aspirin necessary to achieve a given level of acetylation by virtue of cumulative effects approximately equals the fractional daily platelet turnover. Serum TXB2 measurements obtained during long-term dosing with 0.11, 0.22, and 0.44 mg/kg aspirin in four healthy subjects could be fitted by a theoretical model assuming identical acetylation of platelet (irreversible) and megakaryocyte (reversible) cyclooxygenase. For a given dose within this range, both the rate at which cumulative acetylation occurs and its maximal extent largely depend upon the rate of platelet turnover. Continuous administration of low-dose aspirin (20 to 40 mg/day) has no statistically significant effect on urinary excretion of either 6-keto-PGF1 alpha or 2,3-dinor-6-keto-PGF1 alpha, i.e., indexes of renal and extrarenal PGI2 biosynthesis in vivo. Whether a selective sparing of extraplatelet cyclooxygenase activity by low-dose aspirin will result in increased antithrombotic efficacy, fewer toxic reactions, or both remains to be established in prospective clinical trials.

Aspirin↗