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Biomedical subjects

T Di Perri

Publications and source records attributed to T Di Perri.

At least 109 records · Page 6Linked to original sources
PubMed1984

Polymorphonuclear leukocyte as a model of Ca++ and Mg++-dependent cellular activation. Effect of flunarizine.

Flunarizine, a calcium entry blocker drug, concentration-dependently inhibited FMLP and A23187-induced aggregation, enzyme release and superoxide anion generation from human granulocytes. A23187-dependent granulocyte aggregation was also studied in media devoided of Ca++ or Mg++. Flunarizine (2.4 x 10(-5) M) significantly affected not only Ca++-supported but also Mg++-sustained granulocyte aggregation. The inhibiting effect of the drug was reversed by increasing extracellular level of Ca++ (1.2 mM) or Mg++ (2 mM). In this "in vitro" model, the role of flunarizine as a specific Mg++ entry blocker was suggested.

Calcimycin↗
PubMed1984

In vitro inhibition of granulocyte function by timegadine, a new anti-inflammatory agent.

Timegadine, a new non-acidic anti-inflammatory agent, inhibits in a concentration-dependent way the FMLP-induced release of beta-glucuronidase and lysozyme from human granulocytes. Superoxide generation and directed migration are also inhibited. As this effect on granulocytes occurs at drug concentrations inhibiting the lipoxygenase pathway of arachidonic acid metabolism, the hypothesis that these two phenomena could be related is discussed.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Placebo controlled double blind study with pentoxifylline of walking performance in patients with intermittent claudication.

A double blind placebo-controlled randomised crossover study was performed with Pentoxifylline (Trental 400 tablets with 400 mg active ingredient) in 24 patients (19 males, 5 females, aged between 40 and 71 years) suffering from peripheral occlusive arteriopathy of stage II severity (Fontaine's classification). In 12 patients (group I) the treatment was started with placebo, and in another 12 subjects with Pentoxifylline (group II). The dosage was 3 tablets of either formulation t.d.s., the treatment periods were 8 weeks each with a two week washout between. The standardised walking test (120 steps/min under metronome control) was used for the assessment of the walking capacity. There was a significant 60% increase in pain-free walking distance in either Pentoxifylline treatment periods, whereas there were no clinically relevant changes in the placebo periods. When comparing the two starting periods only, there was an increase in the Pentoxifylline group from 223 to 359 m on average and in the placebo group from 208 to 215 m, patients in both groups being comparable at basal level as to the distribution of sex, age, location of occlusion, duration of disease as well as in respect to the walking capacity. No adverse reactions were recorded during the trial.

Adult↗
PubMed1983

[The relation between erythrocyte filterability and platelet aggregation (in vitro studies in normal subjects and those with vascular disease before and after isotonic exercise)].

The aim of this study was to evaluate the possible action in vitro of the platelets on the rheological behavior of red blood cells in healthy subjects and in patients with peripheral obliterative arterial disease before and after an isotonic exercise. Red blood cells and platelets from control subjects and from patients were tested in several ratios before and after the exercise studying the erythrocyte filterability. beta-thromboglobulin, a platelet-specific protein, was determined in vivo in all subjects before and after the exercise and in vitro as percent of increase between PPP and PRP activated, to monitor the platelet release. The results showed the interrelationship between platelet activation and rheological behavior of red blood cells.

Adult↗
PubMed1983

[The effect of lysine acetylsalicylate on hemorrheological changes induced through ischemic exertion in patients with vascular disease].

This study has been performed to evaluate the in vivo effect of acetylsalicylic acid (ASA) i.v. infusion at two different dosages: 500 and 2,000 mg on the main hemorheological parameters (blood viscosity and filtrability, hematocrit) and on beta-thromboglobulin (a platelet-specific protein) in patients with peripheral obliterative arterial disease, before and after an ischemic exercise. The results obtained before and 3 and 24 h after the drug administration induced us to think that platelet-specific substances released during the ischemic exercise can affect the hemorheological parameters and that ASA may be able to interfere with these reactions by inhibiting the platelet release.

Adult↗
PubMed1983

Heparin inhibits FMLP and Con-A dependent activation of human polymorphonuclear leucocytes in vitro.

The effects in vitro of heparin on different functions of human neutrophilic leucocytes were assessed. Granulocyte aggregation, enzyme release and superoxide anion generation induced by FMLP (10(-6) M), ConA (30 micrograms/ml), and A 23187 (5 microM) were evaluated. Heparin was able to inhibit, in a dose-dependent way, FMLP-mediated and ConA-mediated granulocyte activation. Heparin inhibited cellular aggregation at the final concentration of 100-500 micrograms/ml, while the inhibiting effect on enzyme release and superoxide anion production was present at lower concentrations (10-100 micrograms/ml). No activity was observed on A 23187-induced granulocyte stimulation. The inhibiting effect of heparin on FMLP-induced granulocyte activation proved to be time-dependent. The hypothesis that an interaction of heparin with cells may possibly initiate the inhibitory effect is proposed.

Calcimycin↗
PubMed1983

[Hemorrheological changes in ischemic heart disease].

Ischemic cardiopathy in its various clinical manifestations, whether acute (angina pectoris or myocardial infarction) or chronic (chronic coronary insufficiency), has shown in recent years particular hemorheological characteristics of its own. The observation of patients with such diseases has allowed us to record the existence of modifications in the parameters indicative of rheological damage. Numerous studies have been made, many of which are still in progress, with the aim of clarifying the relationships between these data and the disease. In our experience an increase in blood and plasma viscosity and a decrease in red cell deformability are often present in a manner which is statistically significant, if these patients are compared with normal subjects. Hemorheological change is more evident in the acute forms of myocardial ischemia. In fact, in angina pectoris the occurrence of pain is always accompanied by an increase in blood viscosity and by a worsening of red cell deformability both during spontaneous crises and during provocative tests. The hemorheological damage tends to diminish fairly rapidly when the crisis is over, even if the level of stabilization proves to be still higher than normal. In myocardial infarction higher levels of viscosity appear for a brief period after the onset with a slight tendency to diminish up until the 30th day. With the aim of ascertaining whether the alteration is more evident precisely at the point where the ischemia occurs, we chose a necessarily limited number of subjects, undergoing coronarography and atrial pacing for diagnostic purposes, and decided to control the hemorheological data not only in the systemic venous blood but also in the blood taken from the coronary sinus. Our data has shown that the level of viscosity and of red cell filtrability, in the blood taken from the coronary sinus, is worse than those of the systemic venous blood and that, after atrial pacing, in negative pacing subjects the variations are of slight significance whilst in positive pacing subjects we observe a rapid increase in viscosity and a decrease in red cell filtrability. This seems to confirm what we have already observed in the limbs affected by peripheral ischemia, and to demonstrate the existence of a local hyperviscosity syndrome which, even in the myocardium, appears to be dependent on the tissue ischemia.

Adult↗
PubMed1983

[Methodological survey of whole blood filtration in the evaluation of erythrocyte deformability. III. Relative influence of various cellular components].

We have counted the different types of blood cells before and immediately after filtration. During filtration, an almost equal quantity of each type of cells remained in the filter, with a slightly higher percentage of leucocytes. The problem regarding occlusion of filter pores should be considered in the light of these findings.

Blood↗
PubMed1983

[Can normovolemic hemodilution really modify blood flow in the limbs?].

A clinical study on the effects of the normovolemic hemodilution on hemorheological and peripheral hemodynamic parameters has been carried out in patients with peripheral obliterative arterial disease. Two sessions have been performed: the acute test consisted in daily normovolemic hemodilutions for a period of 7 days in 10 patients with the determination of hemorheological and peripheral hemodynamic parameters before and after each treatment. A chronic study was then carried out in 8 patients by applying weekly normovolemic hemodilutions, by evaluating the hemorheological parameters as in the first session and by measuring the peripheral hemodynamic parameters at the beginning, after 5 weeks and at the end of the treatment. The results are reported and the possible mechanism of action of normovolemic hemodilution is discussed.

Arterial Occlusive Diseases↗
PubMed1982

Action of a new non-steroid anti-inflammatory drug, carprofen (Ro 20-5720) on activation of the complement system: an in vitro research.

Carprofen (Ro 20-5720), DL-6-chloro-alpha-methyl-carbazole-2-acetic acid, is a new non-steroid anti-inflammatory drug. We have studied the possible in vitro interference of the drug with the activation of human complement system. Carprofen exerts a constant inhibitory action of immunohaemolysis at a concentration of 4.5 X 10(-4)M. At the same concentration the drug is able to prevent the activation of the alternate pathway induced by insulin. Its specific site of action is on C1 and C3 components activation, according to the inhibiting activity on both classic and alternate pathway. However at a lower dosage (7.5 X 10(-6)M) carprofen is able to display an inducing action on the alternate pathway, thus confirming the complex in vitro interferences of the drug with the complement system.

Anti-Inflammatory Agents↗
PubMed1981

Influence of non-selective and selective beta adrenoceptor blockade on isoxsuprine-dependent hemodynamic and rheologic changes.

The infusion of isoxsuprine was followed by an increase of heart rate and calf blood flow and by a decrease of arterial diastolic pressure and blood viscosity both in normal controls and patients with peripheral obstructive arterial disease. The pre-treatment with a non-selective beta adrenoceptor blocker (propranolol) canceled all the isoxsuprine-dependent changes, while the pre-treatment with a selective beta adrenoceptor blocker (metoprolol) abolished only tachycardia and did not influence the increase of calf blood flow and the decrease of blood viscosity. These findings indicate the different role of vascular beta receptors in the regulation of muscular blood flow and suggest the pharmacologic possibility to unmask the beta2-dependent vasodilation.

Adult↗
PubMed1981

Inhibition of platelet aggregation in man by indobufen (K 3920).

A complete crossover trial was undertaken in six healthy volunteers to gain information on dose-effect responses to indobufen by assessing the intensity and duration of the effect of 3 single oral doses of the drug on platelet aggregation induced by threshold concentration of ADP and by 3 added doses of collagen. The results of the study confirm that the activity is dose-related and is reversible since 24 hours after administration it has practically disappeared. The effect of the same dose of indobufen differed significantly according to the amount of collagen added to plasma, whereas increasing doses of indobufen provoked a significantly more marked effect when the amount of inducer employed was the same.

Adenosine Diphosphate↗