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Biomedical subjects

E Bursaux

Publications and source records attributed to E Bursaux.

66 records · Page 4Linked to original sources
PubMedDate not supplied

[Hyperalaninaemia during acute hypoxia in the anesthetized rabbit (author's transl)].

Blood alanine (Ala), an important glucose precursor, has been demonstrated to result mainly from the transamination of pyruvate derived from glucose in muscle [10]. A positive relationship between blood pyruvate and blood alanine was reported during muscular exercise and fasting. The alanine/pyruvate relationship in arterial blood has been studied in male fasted anesthetized rabbits before, during and after a short term hypoxic stress (50 minutes). Three groups of animals were studied : normoxic control (FIO2 = 0.28 ; n = 3) (C), hypoxic hypoxia (FIO2 = 0.10 ; n = 4) (HH) and hypoxia induced by respiring the animals with a carbon monoxide containing gas mixture (FIO2 = 0.28, FICO = 0.002 ; n = 6) (HCO). The hypoxic stress was of similar magnitude in HH and HCO groups. During the hypoxic periods an increase of [Ala] was observed along with hyperlactatemia and hyperpyruvatemia. Hyperalaninemia and hyperlactatemia was higher in HH than in HCO groups and hyperglycemia was observed only in HH group (adrenergic stimulation). In normoxic conditions [Ala] correlates positively with pyruvate. This relationship vanishes during the hypoxic and post hypoxic periods. The percentage increase of [Ala] during hypoxia was larger than that of pyruvate. These data, as well as recent reports in the literature, suggest that elevated [Ala] during hypoxia may result from increased muscular production from glycolytic pyruvate and other amino acids and decreased hepatic utilization (gluconeogenesis).

Acute Disease↗
PubMedDate not supplied

Hereditary spherocytosis (HS) due to loss of anion exchange transporter.

BACKGROUND: Hereditary spherocytosis encompasses a heterogenous group of inherited disorders due to alteration of r.b.c. surface/volume ratio. Spectrin deficiency is the most common observed defect. We analyzed a case of HS associated with band 3 deficiency without spectrin reduction. METHODS: In the study of a family originating from southern Italy, we show that a 20% deficiency of band 3 with normal spectrin content may be responsible for dominantly inherited hereditary spherocytosis (HS). The proband is a 12 years old girl consulting for jaundice, chronic anaemia and splenomegaly. Her mother had a similar haematologic phenotype. RESULTS: Electrophoretic analysis of erythrocyte membrane proteins showed a deficiency in band 3 protein. Band 3 protein chymotryptic fragments, deglycosylated band 3, and its isolated cytoplasmic domain, all displayed normal electrophoretic migrations. Furthermore, the tryptic peptides profile of the cytoplasmic domain of the protein did not demonstrate any abnormality, nor did the amino acid composition of the peptides. Analysis of the membrane proteins during erythrocyte ageing, evaluated in density-fractionated red cells, showed that band 3 content was normal in the lighter fraction, whereas in the denser fraction band 3 deficiency was more pronounced than in membranes from non fractionated red blood cells. CONCLUSIONS: This case describes HS due to anion exchange transporter deficiency. Our results on fractioned red cells support the hypothesis that the defect was probably due to a band 3 protein loss during cell ageing and not to a primitive quantitative defect.

Adult↗
PubMedDate not supplied

[Structural and functional alterations of the erythrocyte membrane in sickle cell anemia].

The low solubility of deoxyhemoglobin S is responsible for sickle cell disease. Membrane alterations associated with intracellular polymerization of HbS are progressively irreversible, leading to shortened red cell viability, abnormal rheologic behaviour of blood in the microcirculation, disseminated vascular occlusion and hypoxic organ damage. The alterations in membrane molecular architecture include mainly cell shape abnormality (sickle shaped cytoskeleton), loss of membrane material, changes on the red cell surface (adherence to vascular endothelium) and loss of lipid bilayer asymmetry (exposition of procoagulant phospholipids). Functional alterations of the membrane permeability to cations lead to dehydration of the red cells. The resulting increase in HbS concentration and polymerization is responsible for the irreversibility of the lesions.

Anemia, Sickle Cell↗
PubMedDate not supplied

Cardiorespiratory adjustments in chronic sickle cell anemia.

During the intercrisis periods, patients homozygous for sickle cell anemia (SS) show clinical symptoms of severe impairment of oxygen transport mechanisms. We have determined respiratory lung function tests, arterial and venous blood gases and cardiocirculatory parameters in 39 SS patients (mean age 22 +/- 5 yr) at distance from any vaso-occlusive crisis or blood transfusion. The patient group was compared to subjects homozygous for HbA (AA) of the same ethnic origin. Determinations were made at rest and after a 5 min mild exercise period. The main alterations in oxygen transport parameters observed in SS patients were: 1) a moderate reduction in vital capacity and maximal ventilation (pure restrictive syndrome), 2) an arterial hypoxemia which worsened the already low oxygen content of blood due to anemia, and 3) a low arterio-venous oxygen saturation difference which is very surprising in anemic patients. The normal oxygen consumption rate was thus insured by a 70% increase of the cardiac output at rest. A particular abnormality found in SS patients was the high Po2 in mixed venous blood. The decreased affinity of blood for oxygen resulting from the polymerization of HbS in the erythrocytes led to an almost normal venous blood unsaturation and thus a decreased release of oxygen from this anemic blood. These results indicate that peripheral blood flow was permanently increased in SS patients. This may be in part at the origin of the arterial hypoxemia induced by an increased pulmonary blood shunting. Sickle cell anemia is more severe than other anemias of comparable intensity as, due to the sickling process, these patients appear to be at the upper limit of physiological compensatory mechanisms usually encountered in chronic anemia.

Adolescent↗