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Biomedical subjects

M Perrin-Fayolle

Publications and source records attributed to M Perrin-Fayolle.

At least 37 records · Page 2Linked to original sources
PubMed1993

Behaviour of leukocyte membrane fluidity in presence of anaesthetic drugs. Comparison between allergic patients and control subjects.

1. In this study we compared the effects of two anaesthetic drugs on the leukocyte membrane fluidity in allergic patients versus control subjects. 2. Fluidity was assessed by means of the fluorescence polarization technique. 3. We report that the treatment of the whole leukocytes with thiopental or pancuronium enhanced membrane fluidity in the allergic group as well as in the control one, but the effect was more pronounced in allergics. 4. This finding suggests a different biophysical behaviour of the leukocyte membrane towards anaesthetic drugs in allergic diseases. 5. This agrees with the hypothesis of the existence of an intrinsic abnormality in allergic cells, expressed as an initial hyperreactive state.

Adult↗
PubMed1993

In-vitro concentration of azithromycin in human phagocytic cells.

The in-vitro intraphagocytic uptake and retention of azithromycin in both human polymorphonuclear leucocytes (PMN) and alveolar macrophages was measured by an improved high-performance liquid chromatography (HPLC) method that was approximately three-fold more sensitive than previous methods. Azithromycin was accumulated in PMN and alveolar macrophages (about 300-fold), with maximum uptake being obtained after incubation for 60 min. Azithromycin was eliminated only partially from the cells during the washing process, and was released slowly during re-incubation of phagocytic cells in antibiotic-free medium. This intracellular retention distinguishes azithromycin from most of the macrolides and quinolones which, in spite of high I/E ratios, are released rapidly from cells.

Azithromycin↗
PubMed1993

Impaired G-proteins and cyclic nucleotide phosphodiesterase activity in T-lymphocytes from patients with sarcoidosis.

Among the various immune abnormalities which characterize active sarcoidosis, a low proliferative response of peripheral blood lymphocytes to mitogenic lectins has long been observed. Since membrane-associated G-proteins are very likely to be crucial elements in lectin signal transduction, we investigated the binding of 5'-guanylylimidodiphosphate (GppNHp), a non hydrolyzable GTP analogue, to blood total lymphocyte membranes and to blood T-lymphocyte membranes from patients with active sarcoidosis, and from healthy control subjects. GppNHp binding was markedly decreased in peripheral cells from patients with sarcoidosis as compared to controls, suggesting the occurrence of a defect at the level of G-protein(s). A further characterization of G-proteins in these cells by means of ADP-ribose-labelling in the presence of bacterial toxins brought forward a significant decrease in the labelling of a 40 kDa protein, the major pertussis toxin substrate, in membranes from sarcoid patients, while the labelling of the major 44 kDa cholera toxin substrate proved to be unchanged with respect to control membranes. It is hypothesized that, in sarcoid lymphocytes, a defect in the negative control of adenylate cyclase mediated by the inhibitory G-protein Gi, prevents the lowering of cAMP necessary to normal mitogenic response of blood lymphocytes to stimulation. cAMP degradation by the specialized enzyme phosphodiesterase constitutes another critical step in the control of cAMP levels. Both cAMP and cGMP phosphodiesterase activities were found decreased in blood total lymphocyte preparations from sarcoid patients. With purified T-cells, although the mean cAMP and cGMP phosphodiesterase activities from sarcoid patients were found more markedly decreased with respect to healthy donors, only the decrease in cGMP phosphodiesterase was found statistically significant. The role these defects in cyclic nucleotide degradation potentially play in the disturbance of blood lymphocytes response associated with sarcoidosis is discussed.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1993

Increased plasma levels of atrial natriuretic factor, renin activity, and leukotriene C4 in chronic obstructive pulmonary disease.

We studied atrial natriuretic factor (ANF), plasma renin activity (PRA), and plasma levels of leukotrienes (LTs) B4 and C4 in 23 patients with COPD undergoing right cardiac catheterization for suspected pulmonary hypertension. Hemodynamic measurements together with concomitant ANF levels (both in venous and pulmonary artery blood and right atrial and pulmonary artery plasma levels of LTC4 and LTB4, were determined at rest (T0), after 30 min of breathing oxygen (3 L/min) (T1), and after 30 min recovering and breathing air (T2). Patients with effective exacerbation or definitive evidence of left ventricular disease, hypertension, arrhythmias, or vasodilator or diuretic therapy were excluded. Increased levels of ANF, both in peripheral venous blood (117 +/- 65 pg/ml) and the pulmonary artery (153 +/- 75 pg/ml), were found in patients with COPD, with or without pulmonary hypertension. Levels of LTC4 were also significantly increased (366 +/- 406 pg/ml) when compared with our control values. No correlations among ANF, LTC4 values, functional tests, and hemodynamic measurements were found. Brief increased levels of oxygen did not modify ANF or LTC4 plasma levels, either in patients with or without pulmonary hypertension.

Atrial Natriuretic Factor↗
PubMed1993

Concentrations of cefodizime in bronchial secretions after single intravenous administration.

UNLABELLED: The concentrations of cefodizime (HR 221, CAS 69739-16-8) in bronchial secretions were measured after administration of a single intravenous bolus of 2 g in 19 patients requiring fibreoptic bronchoscopy for diagnostic purposes or as therapeutic follow-up. These concentrations, which were obtained in absence of inflammation of the mucosa, were compared to serum concentrations obtained simultaneously. The penetration into bronchial secretions was rapid, maximum levels of between 1 and 5 mg/kg being already observed 1 h after injection. Most concentrations remained about 1 mg/kg throughout the whole observation period of about 5.5 h. The percent penetration amounted to about 1.5% of the corresponding serum concentrations. CONCLUSION: Concentrations well above the MIC90s of the relevant respiratory pathogens--S. pneumoniae, M. catarrhalis, H. influenzae, K. pneumoniae--and Enterobacteriaceae were reached in bronchial secretions after intravenous injection of a single 2 g dose of cefodizime. Even higher levels may be expected in the usual condition of inflamed bronchial mucosa as found in respiratory infections.

Adult↗
PubMed1992

Leukotriene B4 level in stimulated blood neutrophils and alveolar macrophages from healthy and asthmatic subjects. Effect of beta-2 agonist therapy.

Leukotriene B4 levels were measured after stimulation by calcium ionophore A23187: (i) in peripheral, neutrophils (PMN) from allergic asthmatics, rhinitis and healthy subjects; (ii) in macrophages collected by bronchoalveolar lavage. LTB4 levels in PMNs were significantly higher in non-treated allergic asthmatics and non-treated subjects with rhinitis compared to controls. Beta-2 agonist-treated asthmatics showed a significantly decreased LTB4 production which was not different from those of controls. In vitro, LTB4 production decreased significantly after PMN incubation with Salbutamol (10(-6) mol l-1). LTB4 produced by AM collected by BAL was measured in non-treated (n = 5) and treated (n = 11) asthmatics with inhaled beta-2 agonist. AM collected from all controls and non-treated asthmatics produced LTB4. By contrast, no production of LTB4 was observed in the treated group. LTB4 production decreased when normal AM were incubated in vitro with Salbutamol (10(-8) mol l-1). These results suggest that biochemical differences occur in PMN and macrophages from subjects treated with beta-2 agonist, presumably in changing the 5-lipoxygenase pathway.

Adult↗
PubMed1991

Leukotriene B4 level in neutrophils from allergic and healthy subjects stimulated by low concentration of calcium ionophore A23187. Effect of exogenous arachidonic acid and possible endogenous source.

Peripheral blood neutrophils from patients with allergic rhinitis and from normal subjects were incubated for 5 min at 37 degrees C with 0.15 microM calcium ionophore A23187 in the absence or presence of exogenous arachidonic acid (2.5 to 10 microM). In neutrophils from allergic patients, the leukotriene B4 (LTB4) level was significantly increased by exogenous arachidonic acid in a concentration-dependent manner (16.2 +/- 4.2 and 38.1 +/- 6.8 pmol/5 min per 2 X 10(6) cells in the absence and presence of 10 microM arachidonic acid, respectively; P less than 0.005; n = 8). The LTB4 level in neutrophils from healthy subjects was only 0.97 +/- 0.17 pmol/5 min per 2 x 10(6) cells (n = 5) and was not enhanced by exogenous arachidonate. When cells from allergic patients were challenged in the presence of exogenous [1-14C]arachidonic acid, released LTB4 was radiolabeled and the incorporated radioactivity increased with the labeled arachidonate concentration. Labeled LTB4 was never detectable after incubating neutrophils from normal donors with exogenous labeled arachidonate. When neutrophils were incubated with [1-14C]arachidonate for 1 h, the different lipid pools of the two cell populations were labeled but both types of neutrophils produced unlabeled LTB4 in response to ionophore stimulation. The hydrolysis of choline and ethanolamine phospholipids into diacyl-, alkenylacyl- and alkylacyl-species revealed that solely the alkylacyl-subclass of phosphatidylcholine was unlabeled. We conclude (i) that neutrophils from allergic patients stimulated by low ionophore concentration produce more LTB4 than neutrophils from healthy subjects and incorporate exogenous arachidonate, (ii) that endogenous arachidonate converted to LTB4 by the 5-lipoxygenase pathway may provide only from 1-O-alkyl-2-arachidonoyl-glycero-3-phosphocholine.

Adult↗
PubMed1991

[Asthma and infection: interrelations].

The frequent interaction of infection in asthma is a result of a complex interrelationship. Infectious agents are capable both of inducing asthmatic crises and, at least for viruses, of initiating the asthmatic process. They also favour a specific IgE response to allergens. Similar immunity is involved in defence against these infectious agents but this immunity can be disturbed in asthmatic subjects; as seen with defects in immunoglobulin subclasses, disturbance in T lymphocyte function, monocytes and blood neutrophils. The determination of the genetic or acquired character of these disturbances is pre-condition for the development of a therapeutic substitute.

Asthma↗
PubMed1990

Cyclic nucleotide phosphodiesterases and methyltransferases in purified lymphocytes, monocytes and polymorphonuclear leucocytes from healthy donors and asthmatic patients.

Cyclic nucleotide phosphodiesterase and phospholipid N-methyl-transferase activities were simultaneously measured in purified polymorphonuclear cell-, mononuclear cell-, lymphocyte- and monocyte-homogenates from control subjects, from patients with atopic asthma and from patients with non-atopic asthma. Whereas cyclic AMP and cyclic GMP phosphodiesterase activities were found to be about 10-fold lower in polymorphonuclear than in mononuclear cells, phospholipid N-methyltransferase proved to be rather similar in each cell type from control donors. Cyclic AMP phosphodiesterase and phospholipid N-methyltransferase were significantly decreased in polymorphonuclear cells and monocytes from asthmatic patients compared with the control group while cyclic GMP phosphodiesterase was significantly impaired only in the monocyte subpopulation.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1990

[T-lymphocytes disorders in pulmonary sarcoidosis].

Sarcoidosis is a granulomatous disorder of unknown aetiology accompanied by variable immunological changes which concern both the monocyte and lymphocyte cell line. During the course of this disease anomalies of distribution (with accumulation in the disease tissue contrasting with a peripheral lymphopenia) and also of T cell functions (a predominance of CD4 T lymphocytes within the lesions and spontaneous expression of activation criteria) have been described. Recent works show some disturbances of T cell function and evoke the possibility of the initial pathology being related to this cell. Some current hypotheses place the T cell receptor for the antigen and the interleukin 2 receptor whose dysfunction will lead to an anomaly of the transduction of the activating signal of the T lymphocyte. The intrinsic origin (genetically determined) or extrinsically (retroviral) of these disturbances remains however to be determined.

Animals↗
PubMed1990

[Penetration of antibiotics in alveolar macrophages compared by in vitro and in vivo data in man].

Optimal therapy of infections caused by intracellular organisms requires an active antibiotic prone to intracellular penetration. This phenomenon has been studied on alveolar macrophages as well in vitro as in vivo for most groups of antibiotics. The comparison of data shows that the values obtained by incubation are not predictive of what happens in situ. These results must be taken in account for the choice of an antibiotic in pulmonary infections as well as its spectrum, pharmacokinetic, and possible side effects.

Anti-Bacterial Agents↗
PubMed1990

[Chiasmal radionecrosis after irradiation of the sella turcica using a conventional dosage. Contribution of magnetic resonance imaging].

A 47 year-old man developed rapid visual loss, visual field defects and memory disturbances after radiotherapy with conventional doses for a pituitary metastasis from a renal carcinoma. CT and MRI did not show recurrent tumour, pituitary apoplexy or empty sella. Eventually, T2-weighted MRI images showed abnormal high signals in the optic chiasm, the left mesial temporal lobe and the right inferior frontal lobe, supporting the diagnosis of delayed radionecrosis. The role of chemotherapy associated with radiotherapy is discussed.

Female↗