Exhaled nitric oxide during acute changes of airways calibre in asthma. P. Garnier, I. Fajac, J.F. Dessanges, J. Dall'Ava-Santucci, A. Lockhart, A.T. Dinh-Xuan. ERS Journals Ltd 1996. ABSTRACT: It has been shown that endogenous nitric oxide (NO), measured in exhaled air, is increased in asthmatic subjects and after allergen challenge in sensitized animals. NO is also a paracrine molecule with some, though weak, bronchodilator effects. However, whether the amount of endogenous NO that originates in the lungs can reflect the degree of bronchial tone and airways calibre in asthmatic subjects has not yet been investigated. The aim of this study was, therefore, to determine whether NO production could be modified by acute changes of airways calibre in mild, nonatopic, asthmatic subjects.NO output was measured in the exhaled air of 14 steroid-free asthmatics, 8 steroidtreated asthmatics and 21 control subjects. In seven steroid-free asthmatics, exhaled NO was measured after methacholine challenge, and then after salbutamol-induced bronchial dilatation. Exhaled tidal breathing was collected for 30 s and NO in the exhaled air was measured with a chemiluminescence analyser.Both NO concentration and its output were significantly higher in the steroid-free asthmatic patients (15.6±1.5 parts per billion (ppb) and 6.3±0.7 nmol·min -1 , respectively) as compared with the control subjects (8.9±1.0 ppb and 3.5±0.3 nmol·min -1 , respectively; p<0.001 for both) and with the steroid-treated asthmatic patients (11.3±3.3 ppb and 3.7±0.9 nmol·min -1 , respectively; p<0.05 for both). Neither methacholine-induced bronchial obstruction nor salbutamol-induced bronchial dilatation caused a significant change in exhaled NO.We conclude that NO production is higher in steroid-free than in steroid-treated asthmatics and in control subjects. Furthermore, NO production is not affected by acute pharmacologically-induced changes of airways calibre in asthmatic subjects. Our results suggest that NO production is a marker of airways inflammation rather than an endogenous modulator of bronchial tone in asthma. Eur Respir J., 1996Respir J., , 9, 1134Respir J., -1138 The free radical gas nitric oxide (NO) is a potent pulmonary vasodilator [1], which is synthesized from the amino acid, L-arginine, and molecular oxygen through the action of constitutive and inducible NO synthase (NOS) isoforms [2]. Inducible NOS (iNOS) is expressed in various resident respiratory and inflammatory cells [3][4][5][6][7]. Its expression is enhanced after exposure to certain cytokines [7], and is inhibited by corticosteroids [8].There is a growing body of evidence that NO might play a role in asthma [9,10]. Exogenous NO, given by inhalation, reverses methacholine-induced bronchoconstriction in animals [11][12][13] and in humans, including healthy subjects [14] and asthmatic patients [15]. NO is a potent bronchial vasodilator in animal airways [16], and may either increase [17] or tonically suppress [18] airways plasma exudation in animals. Various investigators have fo...

The simplest and most natural route of drug delivery to the lungs is the inhaled one. From the historical and medical point of view, it was a Greek, Pedanus Discorides, the father of the science of pharmacy, who, during the first century prescribed inhaled fumigation. Pipes were also used to inhale hallucinogenic substances. All shamans knew the psychotropic effects of poisonous plants such as Datura stramonium, especially Red Indians, in their peace calumets; but Indians of Madras used fumigations of Datura ferox to treat asthma. Since 1803, this therapeutic was imported in Great Britain and cigarettes with leaves of datura were used by asthmatics until 1992. In the middle of the nineteenth century, to treat grapevines diseases and in response to the fashion of inhaling thermal waters, spray technology was developed for the effervescent waters at the thermal spas. The onslaught of tuberculosis, similar to AIDS a century later, brought back into practice the inefficacious use of antiseptic aerosol therapy. With the discovery of adrenaline, ephedrine aerosols enjoyed a rebirth. The perfecting of jet nebulizers by R. Tiffeneau, father of FEV1 and M.B. Wright, father of peak-flow, allowed a better practice of inhalotherapy. In 1949, the United States, ultrasonic nebulizers made their first appearance in the form of humidifiers, but doctors were quick to add medications to produce therapeutic aerosols. After 150 years, with the improvement of nebulizer systems and new nebulized medications, the nebulization story is still not concluded.

This is the first published study to calculate a reference equation for peak nasal inspiratory flow in North African subjects. This equation enables objective evaluation of nasal airway patency in patients of North African origin.

Femoral blood flow (FBF) was measured in seven dogs, simultaneously with both an electromagnetic perivascular probe and a transcutaneous range gated Doppler velocimeter. Measurements were made in basal conditions and during intraarterial infusions of noradrenaline (10 to 400 ng . kg-1 . min-1) and isoprenaline (10 to 400 ng . kg-1 . min-1) thus allowing comparisons of ultrasonic (DBF) and electromagnetic (EMBF) blood flow at 91 different blood flow rates ranging from 5 to 300 cm3 . min-1. The linear regression line through the data of ultrasonic and electromagnetic simultaneous measurement was: DBF = 0.8 + 1.016 EMBF +/- 19.0 cm3 . min-1 with a highly significant correlation (r = 0.96, p less than 0.001) but there was a wide scattering about the mean. Errors in DBF were mainly due to positioning of the probe and determination of arterial diameter.