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Biomedical subjects

A Strano

Publications and source records attributed to A Strano.

At least 109 records · Page 6Linked to original sources
PubMed1985

[Evaluation of blood viscosity and erythrocyte filterability in chronic ischemic heart disease].

In 40 patients suffering from chronic ischemic heart disease (16 with history of myocardial infarction, 10 with unstable angina and 14 with stable angina) and in an equal number of sex-and age-matched control subjects, we have determined plasma and blood viscosity according to RAND et al. using a Wells-Brookfield Micro-Viscometer, shear rate 230 sec-1, and red cell filterability according to REID et al. Significant differences were found in patients suffering from ischemic heart disease, in comparison with the control group, for blood viscosity (p less than 0.01), plasma viscosity (p less than 0.001) and red cell filterability (p less than 0.001). The changes of hemorheological parameters in ischemic heart disease, especially in patients suffering from unstable angina and in those with history of myocardial infarction, point to the opportunity of a pharmacological treatment aiming at improving the district microcirculation.

Adult↗
PubMed1984

Double-blind, crossover study of the clinical efficacy and the hemorheological effects of pentoxifylline in patients with occlusive arterial disease of the lower limbs.

The effect of a 3 month daily administration of 800 mg pentoxifylline (Trental 400 bds) or placebo was assessed under double blind crossover design in 18 patients (12 males and 6 females) with peripheral occlusive arterial disease in respect of painfree walking distance and various hemorheological and hemostasiological variables, platelet aggregation, serum cholesterol and triglycerides. In first treatment period walking distance significantly increased with pentoxifylline by 46% from baseline 121 +/- 15 m and by 4% with placebo from baseline 134 +/- 18 m. Pentoxifylline administration furthermore yielded significant decrease in whole blood and plasma viscosity and significant increase in erythrocyte deformability. This was paralleled by distinct reduction of fibrinogen, platelet aggregation and euglobulin lysis time, also plethysmographic variables showed positive changes pointing to improvement of limb perfusion. The results of the study suggest that treatment of peripheral occlusive vascular disease by a drug improving blood fluidity through correction of hemorheological and hemostasiological factors turns especially promising and beneficial since the action centers finally on the languishing microcirculation in the ischemic tissue.

Adenosine Diphosphate↗
PubMed1984

Circulating immune complexes and platelet thromboxane synthesis in patients with insulin-dependent (type I) diabetes mellitus.

Platelets from diabetic subjects with circulating immune complexes (CIC) synthesized greater amounts of thromboxane than did platelets from CIC-negative patients or controls. In view of the known action of CIC on platelet function, a relationship between these two factors may be suggested in the initiation and progression of microangiopathy in diabetes.

Antibodies, Anti-Idiotypic↗
PubMed1983

The effect of two low doses of aspirin on whole blood thromboxane and prostacyclin generation in healthy subjects.

The effects of two low doses of aspirin (20 mg and 100 mg) on prostacyclin and thromboxane formation during whole blood clotting were studied in 8 healthy volunteers. A single 100 mg aspirin dose caused more than 90% reduction of both serum TXB2 and 6-keto-PGF1 alpha; a single 20 mg dose of aspirin inhibited serum TXB2 more than 6-keto-PGF1 alpha but effects on these two products could not be completely dissociated. However, the effect of a single 20 mg aspirin dose on serum TXB2, was of much longer duration than its inhibitory effect on PGI2 synthesis during whole blood clotting.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Plasmatic TXB2 and 6-keto-PGF1 alpha levels during charcoal hemoperfusion in chronic renal failure patients.

6 patients with end-stage renal disease underwent hemoperfusion with charcoal columns, for 60 min. Blood samples anticoagulated with 2% EDTA/aspirin solution were obtained from arteriovenous fistulas in the basal condition, 5 min after a bolus injection of heparin (7,500 U), at the end of hemoperfusion, and 30 min after. The study was repeated few days later, in the same patients, two hours after 100 mg aspirin by mouth. TXB2 and 6-keto-PGF1 alpha were assayed with RIA in unextracted (U) and extracted (E) and chromatographed platelet poor plasma (PPP). Platelet counts before and after hemoperfusion were also performed. Low levels of the two prostaglandins were found in plasma; this could be related to the procedures for collection and processing of plasma samples; no significant differences were observed between extracted and unextracted samples: there were slightly higher levels of 6-keto-PGF1 alpha in unextracted samples. After charcoal hemoperfusion there was only a slight and not significant increase of TXB2 and 6-keto-PGF1 alpha; low dose aspirin did not modify significantly plasma levels of the two prostaglandins before hemoperfusion but it reduced TXB2 and 6-keto-PGF1 alpha levels after charcoal hemoperfusion. The platelet count fell (-22%) after charcoal hemoperfusion with heparin alone and in similar manner after low-dose aspirin pretreatment (-24%, 7%).

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Platelet activation after adrenergic stimulation in hypertensive patients: effects of acebutolol.

In 12 patients with arterial hypertension (stages I and II according to WHO), adrenergic stimulation was induced by the immersion of a hand in ice water for 2 min. Blood samples were withdrawn before, at the end of, and 15 min after the cold application: the experiment was repeated 2 h after the ingestion of 200 mg acebutolol, a selective betablocking agent. The following assays were performed: serum nonesterified fatty acid (NEFA), plasma beta-thromboglobulin (BTG) and PF4 with specific radioimmunoassays; thromboxane B2 (TXB2) in plasma was also estimated with radioimmunoassay, platelet sensitivity to exogenous prostacyclin; furthermore, the thrombin-induced thromboxane production before and after acebutolol ingestion as well as serum TXB2-levels were measured. The blood pressure and the heart rate were also monitored. After cold stimulation, a significant increase of NEFA, BTG, and plasma TXB2 was observed, which was still discernible 15 min after the application of cold. After acebutolol, the cold treatment led to a lower increase of blood pressure with a reduction of the heart rate, as well as to a diminished release of BTG, PF4 and TXB2 no changes in the reduced platelet sensitivity to prostacyclin were noticed.

Acebutolol↗
PubMed1983

Platelet thromboxane formation and BTG levels after intensive charcoal HP in uremics or regular hemodialytic treatment (RHT).

Vascular tissues from uremic patients show increased prostaglandin synthesizing capacity while uremic platelets have decreased thromboxane synthesis. It has been suggested that the platelet defects in uremia are partially corrected by hemodialysis and a correlation with the levels of guanidinsuccinic acid, phenolic acid, creatinine or urea has been demonstrated. In our study 6 patients with end-stage renal disease on RHT, underwent, daily and for ten days, two-hours hemoperfusion, in order to obtain lower levels of toxic metabolites such as creatinine (less than 6 mg/dl.). Before and after this intensive treatment we have evaluated BTG plasmatic levels and thromboxane formation by platelets after thrombin and arachidonic acid stimulation. The thromboxane formation was not increased following this treatment, whereas BTG plasmatic levels were significantly diminished.

Adult↗
PubMed1983

[Behavior of various blood coagulation and hemorrheological parameters in arteriosclerotic vascular disease of the lower legs].

Red blood cell filterability was compared with some blood coagulation parameters in 50 patients suffering from atherosclerosis obliterans of lower limbs at stages II, III and IV. The reduced red blood cell filterability correlated positively with the stage of the arterial disease (r = 0.8185), with levels of plasma fibrinogen (r = 0.8366) and with the euglobulin lysis time (r = 0.8124), while negative correlations with platelet reactivity threshold (r = 0.6928) and with antithrombin III activity (r = 0.6557) were found. The authors believe that in the therapy of these vascular diseases it is necessary to modify the reduced red blood cell filterability together with the blood coagulation order.

Antithrombin III↗