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Biomedical subjects

F Barbier

Publications and source records attributed to F Barbier.

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

Influence of pathological state on the acoustic attenuation coefficient slope of liver.

The acoustic attenuation coefficient slope (beta) of liver was estimated in vivo from the spectral difference of returned echoes. beta of normal young subjects was lower than that of older subjects (mean: 0.340 vs 0.418 dB/cm.MHz). Limited fluid withdrawal from the body by haemodialysis did not affect beta. In alcoholic liver disease beta was related to the amount of fat and of fibrous tissue in liver biopsy specimens. High values of beta were observed as soon as the degree of steatosis exceeded 5 vol%. There was a similar increase of beta in the presence of fibrous interlobular septa. In normal liver beta was related to the amount of triglycerides in the liver specimen.

Acoustics↗
PubMed1986

[Bilateral prosthesis of the knee in a hemophilia A patient with an inhibitor].

A forty-one year old severe haemophiliac A (factor VIII less than 1%) complicated by an antifactor VIII inhibitor was operated on for a bilateral arthroplasty of the knees. Substitutive treatment was started by giving anti-haemophilic A cryoprecipitate at a dose of 40 IU . kg-1. The anamnestic response occurred at day 6. Consumption of the inhibitor begun with the injection of 50,000 IU of concentrated factor VIII. This method proved to be insufficient for mastering the haemorrhagic syndrome, because the antibody titre quickly reached 10 IU Oxford. Treatment was continued with Autoplex (100 IU . kg-1), during three weeks, without any clinical or biological complications. It is suggested that Autoplex be used as the substitutive treatment in cases of major surgery in severe haemophilia complicated by a factor VIII inhibitor.

Adult↗
PubMed1986

Coagulant, fibrinolytic, and aggregating activity in ascitic fluid.

Ascitic fluid samples from 14 subjects with liver cirrhosis and from 13 patients with malignancy were investigated. Activated FX was present in ascitic fluid in small quantities with a mean value of 8.7 10(-3) IU/ml. The mean thrombin activity was 70.8 10(-3) IU/ml and the mean plasmin activity was 449.6 10(-3) CU/ml. High levels of fibrin/fibrinogen degradation products (mean 75.4 micrograms/ml) and of antithrombin III (mean 43.4%) were found. No statistically significant differences between values in liver cirrhosis and in malignancy were found. In 15 of 17 experiments 10-fold concentrated ascitic fluid caused irreversible platelet aggregation and [14C] serotonin release of normal platelet-rich plasma similar to collagen. The aggregating effect disappeared after addition of collagenase. These results do not support the concept that the coagulopathy after peritoneovenous shunting is a result of direct and rapid intravenous infusion of procoagulant substances. They rather point to a central role of collagen present in ascitic fluid.

Ascitic Fluid↗
PubMed1983

Quantitative gas chromatographic mass spectrometric determination of pinaverium-bromide in human serum.

A method has been developed for quantitative determination of pinaverium-bromide, a quaternary ammonium derivative with papaverine-like activity, in human serum. The method involves a chloroform extraction of serum spiked with N-(6,6-dimethyl bicyclo[3.1.1]2-heptenyl-ethoxyethyl) perhydro-1,4-oxazine as internal standard. After evaporation of the solvent, and reduction of the residue with Raney-Nickel, the internal standard and the reduced pinaverium-bromide are re-extracted from the reaction mixture with toluene and analysed isothermally on a fused silica column coated with OV-101. Although chemical ionization with methane revealed intense protonated molecular ions for both pinaverium-bromide and the internal standard, selectivity and sensitivity were significantly lower in comparison with electron impact ionization at 70 e V. Therefore, quantification was performed in the electron impact mode by single ion monitoring of the common fragment ion at m/z 100.2. A linear detector response was observed up to 160 ng ml-1. A within-run assay precision better than 2% CV (n = 5) was found, and a detection limit of 1 ng pinaverium-bromide ml-1 of serum was attained.

Autoanalysis↗
PubMed1983

[Not Available].

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Demography↗
PubMed1983

[Not Available].

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Demography↗
PubMed1983

Effects of oxametacin on coumarin anticoagulation and on platelet function in humans.

In 12 chronically anticoagulated patients the administration of 1-p-chlorobenzoyl-5-methoxy-2-methyl-3-indoacetohydroxamic acid (oxametacin, Flogar), three times 100 mg a day, decreased the thrombotest percentage from a mean of 11.2% to a mean of 8.3% after one week and of 7.8% after two weeks of treatment. A potentiating effect of oxametacin was also found when the prothrombin time or the activated partial thromboplastin time were used as parameters. In one third of our patients an adaptation of the coumarin dose or even an interruption in the warfarin administration was necessary. Although no severe bleedings occurred, care should be taken in prescribing oxametacin to anticoagulated patients. In a second part of this study we compared the ex vivo effects of a single oral dose of 1 g of acetylsalicylic acid, 50 mg of indometacin and 100 mg of oxametacin in human volunteers. Platelet aggregation and 5HT--14C release induced by collagen. Thrombofax, ADP, adrenaline (epinephrine), bovine plasma and ristocetin were measured before, 1 and 24 h after drug administration. A clear-cut inhibitory effect as induced by acetylsalicylic acid was not found for oxametacin.

Adult↗
PubMed1982

Alpha 1-antitrypsin in pancreatitis.

A possible relationship between alpha 1-antitrypsin deficiency and pancreatitis was studied. Pi phenotype distribution in a group of 90 patients with proven pancreatitis was compared to a control group of 549 randomly selected blood donors. No significant differences were found between the patient group and the controls, nor between acute and chronic forms of pancreatitis. It is concluded that alpha 1-antitrypsin phenotype does not play an important role in pancreatic disease.

Acute Disease↗