Biomedical subjects

J Rami

Publications and source records attributed to J Rami.

27 records · Page 2Linked to original sources

PubMed1989

Alveolar phospholipids, hyperventilation and temperature of conservation of rat lungs.

Hyperventilation has been found to increase the phospholipid content of broncho-alveolar lavage fluids. Had the temperature of conservation of the lungs an influence? Two groups of rats were allowed to ventilate normally (NV), and two groups (HV) were induced to hyperventilate for 1 h by addition of a dead space. After sacrifice, the isolated lungs were kept for 25 min at 37 degrees C (NV37 and HV37), or 10 degrees C (NV10 and HV10), and then washed at the same temperatures. The phospholipid content of lavage fluid was only found to be increased in the HV37 group (P less than 0.05). Neither hyperventilation followed by conservation of lungs at 10 degrees C nor normal ventilation followed by conservation of lungs at 37 degrees C led to an increase in phospholipid content. It was the association of hyperventilation and conservation of lungs at 37 degrees C that led to the increase. In vivo hyperventilation is thought to lead to an equal increase in secretion and reabsorption of alveolar phospholipids, and conservation of the lungs at 37 degrees C was thought to lead to an imbalance between these two processes.

Animals↗

PubMed1988

[The effect of cytochalasin A on the composition of subcellular fractions of hyphae in the growth of Mucor mucedo L. I. Composition of the plasmalemma].

The plasma membrane of young hyphae of Mucor mucedo L. growing in presence or absence of cytochalasine A was isolated by continuous density gradient centrifugation using Percoll at 10% or on discontinuous sucrose density gradient. Isolated membranes were characterized by enzymatic markers and cytochemical reactions, using electron microscopy. Lipid composition and protein content were determined. From the enzymatic point of view, the cytochalasine A induced a decrease (60%) in ATPase activity and with regard to the chemical composition of the membrane, a decrease in sterol content and in the sterol-phospholipid ratio as well as a decrease in protein content and an increase in the proportion of cysteine relative to other amino acids.

Adenosine Triphosphatases↗

PubMed1988

[The effect of cytochalasin A on the composition of subcellular fractions of hyphae in the growth of Mucor mucedo. II. Composition of the cell wall].

Walls of young hyphae of Mucor mucedo L. growing in the presence or absence of cytochalasin A were isolated and their chemical content determined. Cytochalasin A induced modified proportions of various monomers resulting in a reduction of the (neutral sugars + glucuronic acid)/glucosamine ratio. The walls contained less proteins but more chitin-chitosan and phosphate. These modifications are discussed in relation to ultrastructural changes described previously.

Amino Acids↗

PubMed1984

[Effects of pneumogastric nerve stimulation and injection of a beta 2 stimulant (terbutaline) on the lipid composition of the alveolar lining fluid and on pulmonary compliance in the rat].

The effects of vagal stimulation and of terbutaline injection on lipidic composition of alveolar fluid and pulmonary compliance were studied. Three groups of rats were used: control, after right vagus nerve stimulation, after 0.2 mg terbutaline injection. The lungs of the rats were isolated. We studied pulmonary pressure-volume curves with air and we measured pulmonary compliance. We realised an alveolar lavage to obtain alveolar lipids. We observed: Vagus nerve stimulation and beta 2 agonist significantly increased fatty acids of total lipids respectively by 52.5% and 25.5% and phospholipids, respectively by 43.6% and 25.7%. beta 2 agonist did not change fatty acid composition of total lipids and phospholipids. Right vagus nerve stimulation increased the percentage of palmitic acid in phospholipids and decreased the percentage of saturated fatty acids and of palmitic acid in total lipids. Terbutaline injection induced more significant changes in pressure-volume curves and in pulmonary compliance than right vagus nerve stimulation. Our results suggest that both vagal stimulation and beta 2 agonists increase lipid release in alveolar lining, but only vagal stimulation modifies the composition of these lipids. These modifications could be, at least in part, correlated with the changes observed in the pressure-volume curves.

Animals↗

PubMed1982

[Acute experimental bone marrow necrosis in the rabbit induced by aortic ligation. Ultrastructural and biochemical study].

The authors study the effects of ligation of the infra-renal aorta on the bone marrow in the femoral shafts in ten rabbits, from a histopathological and biochemical standpoint. Histology revealed marrow necrosis in nine cases out of ten. They describe the appearances of this necrosis by light and electron microscopy. In five cases it was focal and partial and in four cases total. It sometimes involved only the haematopoietic tissue, leaving fatty tissue unaffected. The latter would thus seem to be more resistant to ischaemia. Study of lipids showed a decrease in polyunsaturated fatty acids, a decrease which was more marked in the ischaemic femurs than in the humerus of the same rabbits.

Adipose Tissue↗

PubMedDate not supplied

Failure of L-nitroarginine to inhibit the activity of aortic inducible nitric oxide synthase.

Nitric oxide (NO) is produced by a family of three isoenzymes: the endothelial, inducible and neuronal NO synthases. L-Nitroarginine methyl ester (L-NAME) is the most commonly used inhibitor of NO synthase activity. The goal of the present study was to evaluate to what extent L-nitroarginine (L-NA), the in vivo circulating metabolite of L-NAME, blocks NO production in the rat aorta depending on the NO synthase isoform expressed (and evidenced by Western blotting) and on the presence or absence of the extracellular NO synthase substrate L-arginine (100 microM, i.e. the plasma concentration). Intact [endothelium present (E+)] control aortic rings express mainly endothelial NO synthase. L-NA (30--100 microM) induced a dose-dependent contraction (due to blockade of the relaxant properties of NO) irrespective of the presence or absence of L-arginine. In deendothelialized (E-) control aortic rings, the three isoforms of NO synthase are virtually absent (as demonstrated by Western blotting) and L-NA does not elicit any contractile effect. E- aortic rings from lipopolysaccharide (LPS)-treated rats express mainly inducible NO synthase. In these rings, L-NA induced a dose-dependent (0--100 microM) contraction in the absence of extracellular L-arginine, whereas L-arginine (100 microM) completely abrogated the contractile effect of the NO synthase inhibitor. Chronic L-NAME administration (50 mg/kg/day for 4 weeks) elicited the aortic expression of inducible NO synthase, but to a lesser extent (about 5-fold) than in LPS-treated rat aorta. The average plasma concentration of L-NA was 50 +/- 10 microM in these rats. In E- rings from these L-NAME-treated rats, L-NA induced a similar contractile response (but smaller in magnitude) to that observed in LPS-treated rat aorta. Altogether, these data suggest that (1) in the presence of a physiological concentration of extracellular L-arginine, L-NA fails to inhibit inducible NO synthase, and (2) chronic L-NAME administration, at a dose commonly given to block NO production in vivo, leaves the activity of inducible NO synthase unaffected.

Animals↗

PubMedDate not supplied

Effect of quinacrine on lipid content of bronchoalveolar lavage fluid in guinea pigs sensitized to ovalbumin.

In both ovalbumin-sensitized and ovalbumin-challenged guinea pigs, the phospholipid content of bronchoalveolar lavage fluid is decreased with respect to that of controls. In the sensitized guinea pig, the activity of lung membrane phospholipase is increased and the phospholipid content of lung membranes is decreased. In determining whether alveolar phospholipids are metabolized in a similar way, quinacrine, a phospholipase A2 inhibitor, was administered (10 mg/kg intravenously) to control, sensitized, and challenged animals before inhalation of ovalbumin. Pulmonary ventilation and lung mechanics were measured both before and after the injection of quinacrine and inhalation of ovalbumin. Phospholipid content was measured in the bronchoalveolar lavage fluid. In the control and sensitized groups quinacrine had no effect on pulmonary ventilation and lung mechanics, and in the challenged group it reduced the intensity of anaphylactic bronchospasm. In control animals it did not change the phospholipid content, whereas in the sensitized and challenged animals it suppressed the decrease of phospholipid content. The results suggest that in the sensitized and challenged guinea pigs alveolar phospholipids are degraded by phospholipase A2, the activity of which is increased.

Animals↗

PubMedDate not supplied

[Effect of estrogens on arterial physiology and mechanisms of their atherosclerosis-protective effect in animals].

Two isoforms of oestrogen receptors (alpha and beta) have been identified in the cells of the arterial wall, and a heterogeneity of their expression according to the animal species, the vascular beds and the sex has been reported. Oestrogens can thus directly influence the vascular physiology through a 'genomic' mechanisms, but 'extra-genomic' mechanisms responsible for a short-term effect have also been suggested. Oestrogens potentiate endothelium-dependent relaxation through an increase in nitric oxide bioavailability (increase in its production and/or decrease in its degradation by superoxide anion according to the vascular beds). Endothelial 'dysfunction' (abnormality of the endothelium-dependent vasodilation) occurs in atheromatous arteries. Oestrogen replacement prevents and even corrects this endothelial dysfunction. In monkeys, this beneficial effect of oestrogens is not altered by coadministration of progesterone, but is abolished by coadministration of medroxyprogesterone. Finally, oestrogens prevent fatty streak deposit, and the mechanisms of this atheroprotective effect are being studied.

Animals↗

PubMedDate not supplied

[Effects of sensitization to ovalbumin on the lipid content of the bronchoalveolar lavage fluid in guinea pigs].

Four groups of guinea-pigs were studied (l1: control, l2: sensitized to ovalbumin, l3: sensitized and challenged by aerosol of ovalbumin, l4: challenged by aerosol of histamine). In urethane anaesthetized guinea-pigs, pulmonary resistances and dynamic compliance were measured (before and after aerosol of ovalbumin in l3 and aerosol of histamine in l4). The lungs were removed and the static pressure-volume curves were performed to determine lung compliance. In the pulmonary lavage fluids, surface tension and total fatty acids and phospholipids were measured by Cahn's electrobalance and gas chromatography respectively. In l2 guinea-pigs, the mean value of total fatty acids and of phospholipids was significantly decreased in pulmonary lavage fluid, by 24.5% and 40.2% respectively. Surface tension was increased while lung mechanics was identical to control. In l3 guinea-pigs, the mean value of total fatty acids and of phospholipids was significantly decreased in pulmonary lavage fluids, by 55.7% and 53.2% respectively. Surface tension was increased. In vivo, lung mechanics was changed: dynamic compliance decreased, pulmonary resistances increased. Pressure-volume curves were flattened and pulmonary compliance of isolated lungs was decreased since bronchial obstruction remained after death. In l4 guinea-pigs, the mean value of total fatty acids and of phospholipids was increased in pulmonary lavage fluid but not significantly, by 26.6% and 9.2%. Surface tension was not changed. Lung mechanics was very significantly affected by bronchospasm, but after death the mechanics of the isolated lung and of control lung was identical. Finally, the decrease of surface-active lipids in pulmonary lavage fluid originates in the sensitization and is enhanced by antigen-induced bronchial anaphylaxis but not by histamine-induced bronchospasm.

Aerosols↗