Search PubMed⌕ Search

Biomedical subjects

G Audibert

Publications and source records attributed to G Audibert.

63 records · Page 4Linked to original sources
PubMed1989

[Hemolytic anemia and cardiac heterografts. Apropos of 2 cases].

Two cases of severe haemolytic anaemia developed after heterograft valve replacement are reported. In one case haemolysis was caused by prosthetic degeneration; in the other case the heterograft was not altered, but a ventricular septal defect had created a high turbulence around the valve which was in pulmonary position. In both cases anaemia subsided after surgical correction of the abnormalities responsible for periprosthetic turbulence. Haemodialysis can only develop in patients with heterograft valve replacement if a change in blood flow rate occurs around the valve, due to its alteration or to an associated cardiac disease.

Adult↗
PubMed1987

[Use of a low molecular weight heparin, CY 222, in the treatment of consumption coagulopathy].

UNLABELLED: Among the different treatments used for consumption coagulopathies, the most contested is classical heparin because of the risk of worsening of a hemorrhagic syndrome. A low molecular weight heparin was evaluated to determine possible improvement of this risk. METHODS: Treatment with CY 222 (Choay) was administered over 2 years to 29 patients (mean age 40 years, range 15-74) with coagulation coagulopathies. Diagnosis was based on the presence of 3 of the following 5 signs: platelets less than 150,000/mm, fibrinogen less than 2 g/l, QT less than 50%, ethanol test positive, PDF greater than 20 micrograms/ml. Etiology could be classed in 3 groups: gravido-puerperal (12 cases), medical disorders (15 cases), post-traumatic (2 cases). Dosage was 150 U/kg every 18 hours subcutaneously. The usual symptomatic treatment included: transfusion of red cells, frozen fresh plasma, platelets and antithrombin III as necessary. A hemorrhage syndrome was present in 16 cases. The course of the disease was evaluated on clinical findings and surveillance of hemostasis parameters; anti-Xa activity was determined in 15 patients. RESULTS: Hemorrhage was arrested and biological values normalized in 22 patients (76%) including 15 (52%) survivors. In the 7 cases where the coagulopathy was not improved, the hemorrhagic syndrome persisted in 4. In the 22 successful outcomes, the hemostasis was corrected within 48 to 72 hours, with the exception of the thrombopenia, which persisted up to the 6th day. Mean anti-Xa activity was 0.32 +/- 0.16 anti-Xa U/ml. CONCLUSION: Results of this preliminary, non-randomized study show CY 222 to be as effective as heparin in the treatment of consumption coagulopathies.

Adult↗
PubMedDate not supplied

In vivo and in vitro effect of cimetidine, inflammation, and hypoxia on propofol kinetics.

Propofol is rapidly cleared from the body by biotransformation; however, the repercussions of changes in cytochrome P-450 activity on propofol rate of elimination are unknown. To assess how changes in cytochrome P-450 activity affect propofol kinetics, one group of rabbits (N = 6) was pretreated with cimetidine, another (N = 6) had an inflammatory reaction produced by the subcutaneous injection of turpentine, and a third one (N = 6) was subjected to mild hypoxia. Propofol was infused (0.3 mg/min/kg) for 40 min; multiple blood samples were withdrawn before and once the infusion was stopped to assess propofol blood kinetics. Cimetidine did not modify propofol kinetics. An inflammatory reaction prolonged propofol half-life without changing significantly its clearance or volume of distribution. Hypoxia decreased propofol clearance and as a consequence, its half-life increased. Parallel studies were conducted in vitro, where propofol metabolism was documented in liver and lung homogenates prepared from controls (N = 6), and from rabbits that were pretreated with cimetidine (N = 3), had an inflammatory reaction (N = 5), or were hypoxic (N = 6). In controls, the lung biotransformed propofol as rapidly as the liver, and both organs generated an unidentified polar metabolite. Cimetidine did not affect the in vitro metabolism of propofol. The inflammatory reaction reduced the in vitro rate of elimination of propofol and, as a consequence, the production rate of the metabolite was also decreased in liver and lung homogenates. Hypoxia diminished hepatic metabolism of propofol but did not influence that in lung homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗