Efecto antitusígeno del C02

Antitussive effect of CO2, is experimentally studied in dogs and guinea pigs. Cough is provoked by mechanic excitation of the trachea. CO2 5-12% in O2 is administered, during 10 to 15 minutes. In the majority of the experiences antitussive CO2, effect is evident. When light and brief coughing excitations are used in animals that easily respond, that is the case of the experiences with guinea pigs, breathing in CO2, suppress cough (fig. 1). With relative strong excitations, as those used in the majority of the experiences in dogs, although the complete suppression of cough is not reached, a more or less manifest diminution is indubitable. However in hiperpnea first moments, facilitation of response is observed: higher expiratory pleural pressure values and lenghtening of the access with a greater number of cough beats registered after excitation is ended (fig. 2). But this is followed of the cough depression, variable according to animals -as is variable the hiperpnea intensity, that possible depends on the animal conditions- that already appears during inhalation when it remains sufficient time and it is easily appreciated afterwards when the respiratory rythm normalizes. Results demonstrate that CO2, effect is a modification of the muscular expiratory activity: expiration lost its rough and in a certain form convulsive feature that is peculiar to cough. Experiences previous atropinization are most demonstrative in this sense because cough bronchioconstriction is avoid -so a factor is eliminated that makes assessment uncertain- that eases interpretation of CO2, effects on thoracic motility in response to tracheal excitation. On the neumotacogram during cough access -by comparation between grafics in CO2 and control- show the following results: under CO2 the maximal expiration speed is not so high, and its elevation is gradual at the beginning of expiration. Initial aceleration of expiratory velocity flow in CO2, cough -liters second, on 0,1 second- is lower than on the control (fig. 5). Diagrams relating the expiratory acceleration to pleural pression, measured at the same time, are obtained and also diagrams relating the initial expiratory acceleration to the final volume of precedent inspiration. These diagrams, supossed that bronchial tone remains sensibly constant with atropine, eases interpretation of predominant mechanism on initial expiratory acceleration. To a certain values of acceleration, when volume is relative low but pleural pressure is high -that is the case of control cough- it is possible to admit that acceleration fundamentally depend upon the strenght of expiratory muscular contraction. But when volume has much increased with relatively few increase of pleural pressure, acceleration must be a passive effect of elastic force with less influence to expiratory muscular contraction. That appears to happen on CO2 cough. That its say on CO2 cough, comparatively to control cough, inspiration volume-initial expiratory acceleration ratio is increased and expiratory pleural pressure acceleration decreased, which means that CO2 reduces cough expiratory muscular activity. On CO2 cough not only strenght of expiratory muscular contraction, but contraction does not appear so rude also. It is possible to say that on control cough expiratory contraction has a convulsive feature that has disappear in CO2 cough. This conclusion can be established on basis on increase pleural-time pressure graphics, in the first expiration phase (fig. 6). In CO2, initial pleural pressure increase is not so high, comparatively to control, in proof that muscular contraction is not so rough. Taking measure of pleural pressure increase time as an index of cough intensity, CO2 effect is most precisness valuated taking only the pleural pressure maxin. So when coughs of maximal pleural pressure are registered approximately as the controls, and maximal speed of highest expiratory flow thinking over this measures, it appears that cough is strongest. However in this case, measuring pleural pression increment time, cough appear decreased since in expiratory contraction is not so fast. Relative lenght of respiratory cicle phases on CO2 cough comparatively to control cough values, is another demonstrative fact of exposed interpretation. Is typical on cough the increase of inspiration expiration time ratio, and it is evident the contrast of lenghtening of inspiratory phase to fastness of phase (fig. 7). During CO2 respiration, and even after inhalation ends, this index decreases in relation to control cough and decreases herewith relation to respiratory movements of animal spontaneous respiration. Effect of CO2 respiration over glottis is quite characteristic and must have some relation to the antitussive action. Glottis expiratory constriction decreases shortly after inhalation begin and soon the rythmic oscilation of resistance characteristic of normal expiration disappear. Beginning of dilatation phase use to commeasure with cough increase, therefore foregoing to the depression phase. It means that glottis relax represents a manifestation of CO2 action that appears precociously to the antitussive effect relation. On the other hand this concurrence of cough increase to wide glottis dilation is significative -as well as other facts that have been, published by the authors- that in cough, against a classic, not only there is not glottis constriction, but the wide dilation appears as a component of the tracheal mechanical excitation reprise. Study of total pulmonary resistance diagrams shows a decrease of bronchial constriction in during respiration, but this results is constant. Results are discussed and the antitussive effect of CO2 is assumed it is a central action comparable its analgesic action.