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Biomedical subjects

A Craveri

Publications and source records attributed to A Craveri.

At least 37 records · Page 2Linked to original sources
PubMed1987

[Hemorrheologic disorders in obese patients. Study of the viscosity of the blood, erythrocytes, plasma, fibrinogen and the erythrocyte filtration index].

Risk factors for atherosclerosis are often associated with haemorheological changes. On this point, obesity (recently advocated as an independent risk factor) was not much studied and with not univocal results. We have studied 70 obese patients (BMI greater than 30) and 50 healthy subjects (BMI less than 25). Among obese 26 had no more pathologies, 29 had hypertension, 3 suffered from ischemic heart disease, 3 suffered from occlusive arteriopathy, 9 were hyperlipidemic, 10 were smokers. We determined plasma viscosity and whole blood viscosity (at haematocrit corrected to 45% too). Washed erythrocytes, poor in leucocytes and platelets and resuspended in phosphate-buffered saline, were used for study of erythrocyte viscosity and deformability. Obese patients showed raised mean blood viscosity values when compared to healthy controls (p less than 0.01); an even more significant increase (p less than 0.001) was found concerning plasma viscosity and fibrinogen. Erythrocyte viscosity and red blood cell filterability index did not show any significant difference. We found no significant correlation between viscosity values and presence of hypertension, hyperlipidemia and smoking habit among obese. In conclusion, the higher vasculopathy incidence might be caused by an increase in blood viscosity, mostly due to plasmatic component. This fact appears to be independent from the presence of atherosclerosis complications or other risk factors.

Adult↗
PubMed1987

[Increase in erythrocyte and plasma viscosity in patients with atherosclerotic vasculopathy of different sites].

Peripheral atherosclerotic arteriopathies are characterised by increased blood viscosity and, according to some, by a reduction in red blood cell deformability. Red blood cell viscosity was studied in 40 atherosclerosic patients (14 carotid and 26 aortoiliacofemoral lesions). All patients were subjected to the standard diagnostic examination (Doppler velocimetry, etc.). Fifty healthy non-smokers of the same sex and 20 heavy smokers were studied as controls. The viscosity of the whole blood, and plasma and blood fibrinogen were assayed. In studying erythrocyte viscosity, cells poor in leucocytes and platelets suspended in a saline phosphate buffer were employed. The atherosclerotic patients presented significantly higher mean levels of erythrocyte viscosity (p less than 0.01) and the increase in plasma viscosity and blood fibrinogen was also statistically significant. The viscosity of the whole blood was also increased in these patients (p less than 0.001). The increase in blood viscosity in subjects with peripheral arteriopathies therefore appears to be attributable to the plasma and to rheological alterations in the red blood cells.

Adult↗
PubMed1987

[Blood, plasma, erythrocyte viscosity and index of erythrocyte filtration in subjects with hyperlipemia].

40 hyperlipidaemic patients (26 type II a and b, 14 type IV) and 50 healthy controls were studied. The patients were not suffering from any other pathology of note and were under no drug treatment. Blood viscosity at natural Ht and at Ht 45% and plasma viscosity were measured. Red blood cell viscosity and deformability was studied on washed red cells, poor in leucocytes and platelets and suspended in a saline phosphate buffer. The patients with hyperlipidaemia had blood viscosity higher than healthy people. Red blood cell and plasma viscosity were higher in subjects with hyperlipidaemia. There was no difference in the filtration index between the people under study. The increased blood viscosity found in people with hyperlipidaemia appears to be attributable to changes in both the plasma and the erythrocytes.

Adult↗
PubMed1986

Prolactin lowering effect of dihydroergokryptine in rat and in man.

The prolactin lowering activity of dihydroergokryptine was investigated both in rats and in humans. The drug was administered orally at the doses of 0.2, 1 and 5 mg/Kg to intact or reserpinized male rats. Nine male adult volunteers were given 300 mg cimetidine iv 90 min after receiving 2, 3 or 4.5 mg of dihydroergokryptine and 3, 4.5 and 6.75 mg of dihydroergocristine or placebo per os in a randomized, cross-over design. Eight young adult males were injected im with 10 mg sulpiride 120 min after randomly receiving dihydroergokryptine 2.5 and 5 mg or placebo in a cross-over manner. Finally, five healthy young women were given dihydroergokryptine 2.5 and 5 mg, bromocriptine 2.5 mg and placebo in a cross-over design. Dihydroergokryptine caused a strong, long-lasting, dose-dependent fall of plasma prolactin concentrations in both rats and humans. Moreover, it inhibited the reserpine-induced rise of plasma prolactin in rats, as well as the cimetidine-or sulpiride-induced hyperprolactinemia in humans. Dihydroergokryptine proved twice as potent as dihydroergocristine and about half as potent as bromocriptine. Effective doses of both dihydrogenated ergot alkaloids were much better tolerated than bromocriptine.

Adult↗
PubMed1984

Controlled evaluation of pantethine, a natural hypolipidemic compound, in patients with different forms of hyperlipoproteinemia.

Pantethine (P), the stable disulphate form of pantetheine, major component and precursor of coenzyme A, was evaluated within a double-blind protocol (8 weeks for P or for a corresponding placebo) in 29 patients, 11 with type IIB hyperlipoproteinemia, 15 with type IV, and 3 with an isolated reduction of high density lipoprotein cholesterol (HDL-C) levels. In type IIB patients, P (300 mg t.i.d.) determined a highly significant lowering of plasma total and low density lipoprotein (LDL) associated cholesterol (-13.5% for both parameters). In the same patients, HDL-C levels increased about 10% at the end of treatment. Switching from P to placebo was associated with a rapid return to the baseline cholesterolemia. Both in type IIB and type IV patients, plasma triglyceride levels were reduced around 30%, when P was given as the first treatment; when it was preceded by placebo, reductions were less striking (respectively, -17.8% for type IIB and -13.0% for type IV, at the end of P treatment). HDL-C levels were not increased by P, either in type IV, and in the patients with low HDL cholesterolemia. In type IV, LDL cholesterol levels showed a variable response to P: they tended to increase when below 132 mg/dl, prior to treatment, and to be reduced when above this level. This study provides evidence for a significant hypocholesterolemic effect of P, a natural compound free of overt side effects. It also indicates that P may raise HDL-C levels in type IIB patients, while moderately reducing triglyceridemia.

Adult↗