The dyspnoea of asthma & bronchitis : its causation, and the influence of nitrites upon it / by Thomas R. Fraser.

  • Fraser Thomas R. (Thomas Richard), Sir, 1841-1920.
Date:
1888
Catalogue details

Licence: Public Domain Mark

Credit: The dyspnoea of asthma & bronchitis : its causation, and the influence of nitrites upon it / by Thomas R. Fraser. Source: Wellcome Collection.

Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.

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    urticaria-like character—whose most prominent upliolders are Weber and Sir Andrew Clark—presupposes for the production of the swellings a dilated state of the bloodvessels of the bronchial tubes. The means which I have successfully employed, however, for controlling and checking the asthmatic paroxysm are the very means which should, according to this theory, be the most efficient that could have been selected for increasing the paroxysm and rendering it more prolonged. There is no fact in pharmacology more certain and undoubted than that nitrites produce rapid and great dilatation of the bloodvessels throughout the body.^ In the first observation I brought forward, and I have others of a like kind, this dilatation was produced at the moment when the dyspnoea disappeared; it was maintained while the dyspnoea was absent; and it gave place to a normal condition of the blood- vessels when the dyspnoea returned. It seems, therefore, to have been abundantly shown that the theory of the production of asthmatic dyspnoea, by swellings of the bronchial mucous mem- brane of a hyperaemic or inflammatory kind, can no longer be maintained. The conceptions of the conditions that immediately produce the asthmatic dyspnoea or orthopnoea have been obscured by the numerous and unharmonizing theories that have been propounded. If the results of the observations I have brought forward should produce the impression upon others which they have produced upon me, I believe these obscurities will to a great extent dis- appear, and the old doctrine, that the asthmatic paroxysm depends immediately upon spasm of the bronchial muscles, will be more firmly established in the position which it had formerly occupied. At the same time, it is not to be supposed that this doctrine is incompatible with the view that, in a secondary manner, and as a result probably of the dyspnoea which has already been caused by contractions of the bronchial muscles, spasmodic contractions may also be originated in the diaphragm and in other of the ordinary muscles of respiration. The success in any disease of a therapeutic agent, whose action is a known one, affords valuable evidence of the correctness of the theory of the causation of that disease. Such evidence appears to be afforded in a very incisive manner by the influence of nitrites in a.sthma. In this disease many other remedies have also been found to produce benefit. Probably this benefit has been more markedly associated with the inhalation of the smoke of certain solanaceous plants, of nitre, and ol several patent medicines in the ‘ Although it ha.s not been proved by direct ob.servntion tliat nitrites dilate the bloodves.sels on the surface of the bronchi, there is no reason o c ou i that they do so ; while tl.e fact that these bloodvessels are derived from the aorta and interco.stal arteries, and that they possess the same stnictuie ^ other bloodvessels of the systemic circulation, afford a favour of their being dilated by nitrites in common wi i vessels of this system.