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Biomedical subjects

T Di Perri

Publications and source records attributed to T Di Perri.

At least 127 records · Page 7Linked to original sources
PubMed1980

Pharmacological induced depression of E-rosette forming cells (RFC) of normal healthy subjects. Restoration by levamisole and thymopoietin pentapeptide.

The authors describe a pharmacological inhibition of E-Rosette formation by the "in vitro" addition of adenosine and theophylline. In the same experimental conditions TP5 and levamisole are able to reverse this inhibiting activity. The role of the cyclic nucleotides (cAMP and cGMP) in the regulation of the lymphocytes response is discussed.

Adenosine↗
PubMed1980

Effects of prostaglandin A1 on renal handling of salt and water in congestive heart failure.

Prostaglandin A1 (PGA1) was infused at the rate of 1/microgram/kg/min in 10 patients with decompensated heart failure under conditions of water loading (5 patients) or water deprivation (5 patients). During water loading, PGA1 increased urinary excretion of sodium, potassium, chloride, calcium, and magnesium, as well as free-water clearance. During water deprivation, it increased free-water reabsorption. Gomerular filtration rate was increased slightly by PGA1 only when it was given with an infusion of hypertonic mannitol during water deprivation. This selective action of PGA1, which increased the excretion but not the reabsorption of free water, suggests its use to correct certain hypo-osmolar conditions. The site of action of PGA1 on the kidney seems to be in the tubules and mainly in the proximal tubules. These findings might be important in the understanding of the role of renal prostaglandins.

Adult↗
PubMed1980

Immunokinetics of a single dose of thymopoietin pentapeptide.

14 patients with classical or definite rheumatoid arthritis and a low number of E-rosette forming cells were given single doses of 5 mg and 50 mg of thymopoietin intravenously. Thymopoietin pentapeptide produced a dose-related sustained increase in E-rosette forming lymphocytes as shown by the decrease of thymopoietin dependent rosetting ratio. A single dose of 50 mg restored the number of E-rosette forming cells to normal after 12 h and this effect lasted 60 to 7 days. With the administration of 5 E-rosette forming cells markedly increased after 12 h and returned to the pretreatment level on the 2nd day. These immunokinetic data clarify some aspects of the clinical pharmacology of thymopoietin pentapeptide and must be considered for a rational schedule of treatment with the drug.

Adult↗
PubMed1979

Action of cinnarizine on the hyperviscosity of blood in patients with peripheral obliterative arterial disease.

Cinnarizine, a drug capable of improving blood flow, was studied for its action on blood viscosity and its main components in patients affected by peripheral obliterative arterial diseases (POAD). Both acute and chronic administration of the drug diminished the increased whole-blood viscosity in patients, without affecting plasma and serum viscosity, hematocrit, plasma fibrinogen concentration, and plasma osmolality. Since cinnarizine also led to a significant increase of peripheral muscular blood flow, it was hypothesized that this action may be due to an increased deformability of the red cells, and may play a considerable role in the therapeutic approach to POAD.

Arterial Occlusive Diseases↗
PubMed1979

Action of levamisole on E-rosette forming cells and serum adenosine deaminase in Hodgkin's disease.

The interaction of levamisole and/or adenosine in vitro on E-rosette forming cells (RFC) of healthy subjects and on low RFC of patients affected with various diseases was investigated. Levamisole did not enhance normal RFC. The drug enhanced low RFC in some patients (responders) but not in others (non-responders). Adenosine inhibited normal and low RFC and this inhibition could be reversed by levamisole. Further, levamisole 150 mg 2 days a week was given to 12 Hodgkin's disease (HD) responders for 2 weeks, then 150 mg 1 day weekly for 2 1/2 months. After one week of treatment RFC increased and the enhancement could be maintained during the whole treatment period. Lastly levamisole in vitro and in vivo diminished serum adenosine deaminase activity in normal subjects and HD patients.

Adenosine↗
PubMed1979

Immunokinetics of a single dose of levamisole.

Ten patients with classical or definite rheumatoid arthritis and a low number of E-rosette forming lymphocytes were given single doses of 50, 100 and 150 mg of levamisole. Levamisole produced a dose-related sustained increase in E-rosette forming cells. A single dose of 150 mg restored the number of E-rosette forming cells to normal within 24 hours and this effect lasted 6 to 7 days. These immunokinetic data provide a rational basis for the once-a-week administration of levamisole.

Adult↗
PubMed1979

Inhibition of platelet aggregation by a new synthetic compound: 2-[p-(1-oxo-2-isoindolinyl)phenyl] butyric acid (K 3920).

The effect of the new synthetic compound 2-[p-(1-oxo--2-isoindolinyl)phenyl] butyric acid (K 3920) on platelet aggregation was assessed in vitro on human platelets. ADP, epinephrine and collagen at different concentrations were employed as inducing agents. From the results of the present study it appears that K 3920 inhibits human platelet aggregation in vitro, probably by acting on the release reaction.

Adenosine Diphosphate↗
PubMed1978

The effects of intravenous isoxsuprine on blood viscosity in patients with occlusive peripheral arterial disease.

1 Blood viscosity is thought to be a major factor in disorders of the peripheral circulation. 2 Ten patients with obliterative arterial disease received an infusion of isoxsuprine of 20 micrograms kg-1 for 30 min. The infusion was followed by a highly significant and prolonged fall in blood, plasma and serum viscosity, in haematocrit and in plasma fibrinogen concentration. Blood lipid levels were also studied: total lipids and total cholesterol did not alter; triglyceride level was significantly lowered at the end of, and after, drug infusion. 3 There was no change in blood, plasma or serum viscosity in the four patients receiving a control infusion 2 days before the infusion of isoxsuprine. 4 The relationships between lowered viscosity and increasing peripheral tissue perfusion are discussed.

Aged↗
PubMed1977

Inhibition by cinnarizine of the properdin-dependent activation of complement.

Cinnarizine (1-benzhydryl-4-cinnamylpiperazine dihydrochloride), a well-known antagonist of vasoactive agents, has previously been shown to inhibit the activation of complement at the level of the fourth component. Cinnarizine was now tested in a system of complement activation by the properdin-dependent alternative pathway. At the concentration of 7.10(-5) M the compound completely inhibited the hemolytic reaction, which is the consequence of human complement activation in the presence of inulin or zymosan. This in vitro effect of cinnarizine was abolished by the addition of 1 mM MgCl2. These findings extend the anticomplementary activity of cinnarizine to the properdin pathway and support its interaction with the magnesium-dependent steps of the activation sequence.

Animals↗