On hypertonicity of the diaphragm in the experimental asthmatic attack in the guinea pig

Abstract

Asthma is studied experimentally in the guinea-pig, by provoking attacks with histamine intravenously or in aerosol. It is noted that the histamine injection produces an increased rate of respiratory movements with a characteristic change in pleural pressure graph: pleural pressure at the end of expiration is more negative than in the respiratory niovements of the control group.

Figure 1 represents the beginning of a slight attack, due to a small dose of histamine. It is noted that one second after the end of the slow injection of 5 gammas of histamine Intravenously, as the rate of respiratory movements increases, the pleural pressure becomes more negative at the end of expiration. The graph registers a forced expiration followed by a deep inspiration after which expiratory descent of pleural pressure is accentuated. After a few respiratory movements the pleural pressure returns to its normal level.

In figure 3 the same phenomenon occurs with characteristics more demonstrable by the intraperitoneal pressure recording which helps clarify the interpretation. In the immeriate response to the intravenous injection of 5 gammas oi histamine the following is noted: increase in rate of respiratory movements ; pleural pressure becomes very negative at the end of expiration ; emphysema progressively develops, as can be shown by the spirogram obtained by integration and by plethysmographic recording ; the average level of intraperitoneal pressure increases as emphysema is produced. Pleural pressure descends notably during inspiration, but the value which depends on the point of fluid velocity changes relatively little with relation to normal movements. In the moments of maximum emphysema marked irregularities are observed in the graphs, characterised by rapid changes in pleural pressure at the end of expiration, wich simultaneous modification of the intraperitoneal pressure which diminishes somewhat at the same point in which the expiratory pleural pressure becomes least negative, and these changes occur without appreciable modification of the emphysema.

To explain these results it must be remembered that, given the marked degree of emphysema a pleural pressure at the end of expiration which is less negative than tile normal one, seems impossible without the presence of a force which opposes lung retraction during expiration. This force must be a consequence of the insufficient relaxation of inspiratory musculature during expiration. The fact that the average level of intraperitoneal pressure increases must be taken as a sign of increase in diaphragmatic tone, because if this increase in intraperitoneal pressure were due only lo contraction of the expiratory muscles, without simultaneous contraction of the diaphragm, pleural pressure would be less negative or positive. On the other hand the rapid changes observed can be taken as signs of momentary relaxation in diaphragmatic tone as such rapid effects are acceptable dealing with striped muscle but it does not seem so probable that modifications in the elastic properties of the lung which arise in hundredths of a second would be produced.

On the other hand, when histamine is given after previous injection of isopropylnoradrenaline, acceleration of the respiratory rate inmediately after injection of histamine is observed, but without modification of the pleural pressure, that is to say, without alteration in diaphragmatic tone. In this latter case there is no bronchial constriction, but there is pulmonary vasodilatation as isopropylnoradrenaline can even reinforce the vasodilatory action of histamine. Thus, in accordance with this, in the modification of respiratory movements provoked during the attack, two components can be distinguished : increase in rate ; and insufficient relaxation of the diaphragm. As hypertonicity of the diaphragm is not present when bronchial spasm is prevented, it can be considered related to bronchoconstriction and in consequence it can be admitted that it is a reflex of bronchial origin. As the increase in respiratory rate is not prevented by avoidance of bronchial spasm it is logical to consider it related to pulmonary vasodilatation, and as a consequence it may be supposed that it is a reflex originating in the lung parenchyma.

The results described confirm the theory that in the asthmatic attack one of the factors causing disturbance of respiratory movements is insufficient relaxation of the diaphragm.