Search PubMed⌕ Search

Biomedical subjects

T Di Perri

Publications and source records attributed to T Di Perri.

197 records · Page 11Linked to original sources
PubMedDate not supplied

Complement-mediated polymorphonuclear leukocyte aggregation in vitro induced by levamisole.

In previous studies, we have demonstrated that levamisole was able to induce the activation of the alternate complement pathway as well as polysaccharide inductors inulin and zymosan. The knowledge that the activation of complement and the generation of C5a is followed "in vitro" and possibly "in vivo" by a rapid granulocyte aggregation suggested to study the levamisole-dependent changes of granulocyte aggregation "in vitro". Our findings showed that levamisole and inulin could induce granulocyte aggregation and granule-associated enzyme release through a specific triggering mechanism of complement activation. The possibility that a complement-induced granulocyte aggregation "in vivo" could operate in drug-dependent neutropenia was proposed.

Cell Aggregation↗
PubMedDate not supplied

Isradipine inhibits PMN leukocyte function. A possible interference with the adenosine system.

The dihydropyridine derivative isradipine is able to inhibit PMN leukocyte function, such as enzyme release and free radical generation, following the activation with specific stimuli. Moreover, the drug prevents calcium influx into the cells as detected by the specific fluorescent dye FURA 2/acetoxymethylester. The specific adenosine receptor antagonist theophylline is able to partially remove the inhibiting activity, thus suggesting a possible interference of isradipine with the adenosine system. Such a cell-protecting activity adds further rationale to the employment of isradipine in those conditions, such as acute and chronic ischaemia and reperfusion damage, in which PMN leukocyte-dependent tissue injury represents a relevant pathogenetic mechanism.

Adenosine↗
PubMedDate not supplied

[Action of dopamine on blood flow of the limbs and on blood viscosity (author's transl)].

The observation of several cases of gangrene in the lower limbs of subjects treated with an infusion of dopamine has encouraged the authors to study the action of the drug, in a dose capable of increasing the arterial pressure, on the blood flow in the lower limbs and on the viscosity of the blood in a group of normal middle aged subjects. A significant reduction in the values of the blood flow with a simultaneous increase in the blood viscosity was observed. There results confirm the ischemic action of the drug with the doses used at the muscular and cutaneous level in the lower limbs.

Blood Circulation↗
PubMedDate not supplied

Pathophysiology and pharmacology of the adenosine system.

Purine derivatives, especially adenosine and ATP, play an important role in the function of many organs, being released either as purinergic transmitters or as local modulators in a non-specific way from all tissues. Adenosine and adenine nucleotides act physiologically by interfering with specific cell membrane receptors (P1 and P2 respectively) that are associated with several signal transduction systems. The adenosine system seems to act in complex situations in which cells and tissues must deal with high energy consumption, maintaining or restoring an adequate balance between metabolic requirements and supply. This effect occurs by means of a series of events involving increased blood flow, an improvement in oxygen transport and utilization, as well as a cell protecting and energy saving mechanism. The activity of endogenous adenosine may be pharmacologically affected: a) by blocking cell receptors with methylxanthines or b) by inhibiting the specific cell uptake system and thus increasing interstitial concentration of adenosine and its metabolic half-life. Recently exogenous adenosine has been employed as a drug to induce controlled and stable hypotension during anesthesia, to reduce afterload in various forms of low cardiac output states, to cause platelet preservation during cardiopulmonary bypass and especially to reverse paroxysmal supraventricular tachycardias.

Adenosine↗
PubMedDate not supplied

Action of S 5682 on the complement system. In vitro and in vivo study.

Activation of the complement system during the early phase of inflammation is partly responsible for increased vascular permeability, white blood cell margination and stimulation of phagocytosis. The aim of this study was to evaluate the anti-inflammatory action of S 5682 in terms of inactivation of the serum complement system. Serum complement was measured by the method of Mayer modified. In vitro, S 5682 was tested on human and rabbit sera with increasing concentrations from 10 to 5.10(-8) g in the presence of different complement pathways activators. In vivo, serum anticomplement activity was evaluated is the N.Z. rabbit after administration of a single dose (100 mg/kg) of S 5682. In vitro, the anticomplement action of S 5682 was effective, starting at the concentration 1.10(-9) g for both classical (IC50 = 6.19.10(-9) g) and alternative pathways (IC50 = 7.69.10(-9) g). This dose-dependent anticomplement action was statistically significant (p less than 0.01) and involved fraction Clq and C3. In vivo, there was a statistically significant decrease (p less than 0.01) of complement activation which reached a maximum of 74%, 180 minutes after the administration of S 5682. This decrease was still significant after 5 hours (p greater than 0.01). These data suggest that the anti-oedematous effect of S 5682 can be partly explained by anti-inflammatory properties in relation with an anticomplement action.

Animals↗
PubMedDate not supplied

[The therapy of peripheral obstructive arteriopathies: rational bases].

The authors underline the relations among the anatomical lesion progression, the appearance of the clinical signs (claudicatio) of tissue ischaemia and the thromboembolic event in vascular districts like myocardium and brain, at high morbidity and mortality risk. They widely state the pathogenetic mechanism of the atherosclerotic arterial disease and the compensative mechanisms that may prevent the ischaemic effects of the vascular obstruction. It has been considered the importance of the hemorheologic changes and their influence on the development of the ischaemic syndrome. The therapeutic choice in relation to physiopathologic and hemorheologic events in the peripheral obstructive arterial disease is considered.

Arterial Occlusive Diseases↗
PubMedDate not supplied

Pharmacological preconditioning of ischaemia.

Five repeated submaximal treadmill exercises at 2 h intervals following a maximal test prolong walking distance and reduce haemorheological derangement in a second maximal test in patients affected with peripheral obliterative arterial disease (POAD). An increase in adenosine plasma levels is observed during maximal tests, thus suggesting the possibility of an ischaemic preconditioning of lower limbs. The intravenous infusion of 50-100-200 mg buflomedil, and the oral administration of 300-600-900 mg of the drug in POAD patients, also produce an increase in plasma levels of adenosine. Finally, 600 mg buflomedil orally at 12 h intervals produced pulse increase in adenosine plasma levels without any accumulation of the drug or adenosine for at least one week. The possibility of a pharmacological preconditioning of ischaemia is suggested.

Adenosine↗