PubMed Health⌕ Search

Biomedical subjects

R Matran

Publications and source records attributed to R Matran.

63 records · Page 4Linked to original sources
PubMed1988

Effects of noradrenaline on the isolated human bronchus. Comparison with the isolated guinea pig trachea.

The pharmacodynamic activity of noradrenaline was evaluated comparatively in vitro on isolated human bronchi and on guinea pig tracheal spirals. Noradrenaline exerted a contractile effect on both preparations under resting tone and in the presence of propranolol 10(-6) M; maximal noradrenaline-induced contraction was 15-20% of maximal acetylcholine (ACh)-induced contraction. Without propranolol, the contractile effect of noradrenaline was negligible when the preparations were under resting tone and absent when they were precontracted with ACh. In contrast, noradrenaline exerted a strongly relaxant effect on both human bronchi (-log ED50 5.24 +/- 0.17; N = 5) and guinea pig tracheae (-log ED50 6.15 +/- 0.29; N = 8). With maximal contraction induced by ACh 3.10(-3) M the -log ED50 of both preparations were shifted to the right by functional antagonism and became 4.72 +/- 0.17 and 5.31 +/- 0.11, respectively. The pKD values of noradrenaline, calculated according to Furchgott and Bursztyn (1967), were 4.79 +/- 0.04 in human bronchi (N = 5) and 4.77 +/- 0.16 in guinea-pig tracheae (N = 8). In the presence of cocaine plus phenoxybenzamine these values were not significantly modified in human bronchi and only slightly modified in guinea pig tracheae. It is concluded that noradrenaline induces a strong beta-adrenergic response and a negligible alpha-adrenergic response from both human bronchi and guinea pig tracheae in vitro.

Animals↗
PubMed1988

Influence of epithelium on the responsiveness of guinea-pig isolated trachea to adenosine.

1. The influence of epithelium removal on the effects of adenosine on airway contractility was investigated on the guinea-pig isolated trachea. 2. In preparations under resting tone or precontracted with histamine 10(-5) M, removal of the tracheal epithelium resulted in similar shifts to the left of the adenosine concentration-response curves (0.61 +/- 0.18 (P less than 0.05) and 0.80 +/- 0.09 (P less than 0.001) log units; n = 5), corresponding to 4.07 and 6.31 fold potentiations of the relaxant effect of adenosine. 3. In the presence of dipyridamole 10(-5) M the relaxant effects of adenosine were potentiated 85.1 fold on tracheae with epithelium; removal of the epithelium did not produce a significant additional shift to the left of the adenosine concentration-response curves (0.07 +/- 0.03 log units; n = 5; NS). 4. In the absence of dipyridamole, the theophylline-adenosine antagonism was not of the competitive type, irrespective of whether the tracheae were with or without epithelium. 5. In the presence of dipyridamole, this antagonism was likely to be of the competitive type and its characteristics were the same when the epithelium was present or absent. Regression slope and pA2 values were 0.84 and 5.07, respectively, in the presence of epithelium and 0.76 and 4.89, respectively, in its absence. 6. It is suggested that, at least in the guinea-pig isolated trachea model, the airway epithelium seems to be involved only in the uptake and metabolism of adenosine.

Adenosine↗
PubMed1988

[The nonadrenergic, noncholinergic neuropeptide system and asthma].

An understanding of the non adrenergic non cholinergic nervous system and its implication in the pathogenesis of asthma would benefit by the identification and localisation of the numerous natural bioactive peptides at the pulmonary level. In the past few years two components of the non adrenergic non cholinergic nervous system have been characterised. A bronchodilator component which would be mediated by "vaso-active intestinal peptide" (VIP) and the "peptide histidine methionine" (PHM). A broncho-constrictor component which would be mediated by the neurokinins (substance P (SP), neurokinin A (NKA) and the "calcitonin gene related peptide" (CGRP)). These neuropeptides, in vitro as well as in vivo, have effects which are not limited to the regulation of bronchial smooth muscle tone. In effect, they may intervene in the regulation of vascular tone, in the production of mucous and in the expression of immediate hypersensitivity reactions at pulmonary level. Several neuropeptides are present or co-exist with classical neurotransmitter in the afferent nerve endings of the pulmonary efferents. This co-existence of several neurotransmitters in the same nervous fibres raised the questions as to their interactions at the pre or post synaptic level. The implication of these neuropeptides in the pathogenesis of asthma rests on numerous experimental arguments. This recent aspect in the pathophysiology of asthma allows us to hope for new therapeutic approaches.

Asthma↗
PubMed1988

Effects of clonidine on bronchial responses to histamine in normal and asthmatic subjects.

Our aim was to examine the effects of clonidine (C), an agonist of central and peripheral alpha-2 adrenoceptors, on bronchomotor responsiveness to histamine (H). In a double-blind study, we compared on two different days the effects of pretreatment with placebo (P) and with 200 micrograms or 150 micrograms of C given orally, in ten normal (NS) and eight asymptomatic asthmatic subjects (AS) respectively, the response to inhalation of serially increasing doses of H. On each day, five doubling doses of H (first dose = 3.5 and 1.1 mumol in NS and AS, respectively) were administered every 5 min; forced expiratory volume in one second (FEV1) was measured after each dose. The dose-response curves were compared by an analysis of variance. Clonidine caused hypotension with bradycardia in all subjects. Baseline values and pre-challenge values of FEV1 after P and C were identical on the two study days. Compared to P, C did not modify the response to H in NS but significantly increased it in AS (p less than 0.01). Our results suggest that the neural control of the airways differs in AS compared to NS and could be explained either by a decrease in sympathetic inhibitory activity or a greater responsiveness of the airways to parasympathetic stimulation and/or a higher parasympathetic tone in AS.

Asthma↗
PubMedDate not supplied

Bronchial response to hyperventilation of dry air at room temperature in normals and asthmatics.

The bronchial effects of three levels (25, 40 and 60 1 X min-1) of voluntary isocapnic hyperventilation of dry air at room temperature (20-22 degrees C) have been studied in 18 normal, non-atopic subjects and in 25 nonperennial asthmatics who were asymptomatic and whose airway obstruction at the time of the study was mild, with a peak expiratory flow rate of 6.1 +/- 1.5 (SD) 1 X s-1 vs a predicted 8.4 +/- 1.3 1 X s-1. The bronchial response was assessed by use of maximal expiratory flow-volume curves obtained before and 1, 5, 10 and 15 min after the 5 min hyperventilation challenge. In normal subjects, there was a minimal though significant (p less than 0.001; two-way analysis of variance) fall in maximal expiratory flows which did not increase with the level of hyperventilation and was not accompanied by a fall in forced vital capacity. The bronchial response of asthmatics differed from that in normal: the fall in maximal expiratory flows was significantly greater, associated with a significant fall in forced vital capacity and increased with the level of hyperventilation. Results in 10 asthmatics studied on two different study days were highly reproducible. Sensitivity and specificity are excellent (approximately equal to 1) for the 40 1 X min-1 hyperventilation challenge. Our results suggest that isocapnic voluntary hyperventilation of dry air at room temperature (20-22 degrees C) is a highly satisfactory screening test to detect bronchial hyperreactivity.

Adolescent↗