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Biomedical subjects

A Craveri

Publications and source records attributed to A Craveri.

50 records · Page 3Linked to original sources
PubMedDate not supplied

Effect of indobufen on whole blood platelet aggregation recorded in the morning in patients with ischaemic heart disease.

Platelets are involved in the progression of coronary atherosclerosis as well as in the development of the acute precipitating event. Recently, it has been shown that normal subjects present increased platelet aggregation between 6.00 a.m. and 9.00 a.m.; epidemiological studies have shown a higher incidence of myocardial infarction between these times. This study evaluated, by an impedence method using whole blood, platelet aggregation induced by ADP (3 microM) and collagen (2 microM/ml). Measurements were made at 6.00 a.m., 9.00 a.m. and 12.00 noon, the day before and the day after evening administration of 200 mg indobufen, a platelet aggregation inhibitor, in 12 patients with ischaemic heart disease. Patients showed a significant increase of platelet aggregation between 6.00 a.m. and 9.00 a.m. which was inhibited by the prior evening administration of indobufen.

Adenosine Diphosphate↗
PubMedDate not supplied

Effects of defibrotide after oral and parenteral administration in patients with peripheral obliterative arterial disease (POAD).

Defibrotide (D) a polidesoxyribonucleotidic derivative provided with fibrinolytic and antithrombotic activity has already proven effective when administered by parenteral route in patients with peripheral obliterative arterial disease (POAD). Bioavailability studies gave evidence that the drug is absorbed by 50-70% when administered orally. Thus, aim of this trial was to evaluate whether the drug might exert similar clinical and biological effects after oral/parenteral dosing in a 2:1 ratio. This was a randomized cross-over study including 17 out patients with POAD (Leriche stage II). D was administered by oral (400 mg b.i.d.) and intramuscular route (200 mg b.i.d.), both treatments lasting 15 days. In basal conditions and at the end of both treatments the following evaluations were made: (1) absolute walking distance (tread mill); (2) Doppler ultrasonographic examination (Winsor index); (3) strain-gauge plethysmography (rest flow and peak flow). In addition in the same occasions plasma samples were collected for the assessment of plasminogen (chromogenic assay) and fibrinolytic activity (fibrin plates). Defibrotide administration was followed by a significant increase in walking distance both after oral and parenteral administration [basal conditions (IRL): 232.7 +/- 23.0 meters; oral: 273.1 +/- 28.1 m; i.m.: 277.9 +/- 26.8 m, p less than 0.01 - (IRA) basal conditions: 380.1 +/- 25.6; oral: 437.1 +/- 31.5 m; i.m.: 442.5 +/- 34.0 m, p less than 0.01] and by a significant increase in peak flow (basal conditions: 9.66 +/- 1.04; oral: 10.90 +/- 0.90; i.m.: 11.12 +/- 0.98, p less than 0.05), while Winsor index and rest flow were unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMedDate not supplied

[Relations between overweight, thrombophilia and cardiovascular risk].

Seventy-one healthy subjects, aged 20 to 60, 19 males and 52 females, body mass index (BMI) 19 to 40, were enrolled in the study. None of them were smokers, or affected by hyperlipidemia, arterial hypertension or impaired glucose tolerance. We measured plasminogen activators inhibitor (PAI) activity, C-peptide levels, plasma fibrinolytic activity. We found a correlation between BMI and plasma fibrinolytic activity (r = -0.382, p less than 0.005), between BMI and PAI (r = 0.353, p less than 0.005), between BMI and C-peptide (r = 0.694, p less than 0.001) and between PAI and C-peptide (r = 0.404, p less than 0.02). Our data show a correlation between obesity and low fibrinolytic activity, probably due to high PAI levels. In obesity impaired fibrinolytic activity, maybe linked to hyperinsulinemia, could induce thrombophilic state.

Adult↗
PubMedDate not supplied

[Factor VII and cardiovascular risk in obese subjects].

We investigated whether or not obesity is related to increased factor VII activity. We studied 70 obese subjects (aged 25 to 50 years, 25 males and 45 females, body mass index (BMI): mean +/- SD = 32.44 +/- 5.44) and 33 non-obese subjects (aged 25 to 50 years, 12 males and 21 females, BMI: mean +/- SD = 21.80 +/- 1.70). None of them were smokers or affected by hyperlipidemia, diabetes mellitus, impaired glucose tolerance or arterial hypertension. Factor VII activity was measured by the coagulometric method. We found higher factor VII activity in obese subjects (115.74 +/- 26.10%) than in healthy subjects (98.55 +/- 23.49%, p less than 0.005). Increased factor VII levels could determine a thrombophilic state involved in the genesis of cardiovascular accidents in obesity.

Adult↗