O vazomotornim reakcijama u plućima pasa

Abstract

The authors report on 157 vasomotor pulmonary reactions in 47 dogs after asphyxia. From the total, 109 reactions were observed in summer months (35 dogs), and 48 in winter months (12 dogs); from the latter, 21 dogs had been curarized, while the other reactions were observed on 45 dogs after opening up the chest and ­ in a few cases only ­ before doing so.

On the basis of results in 157 cases the authors claim (I) that in asphyxia of the summer months pulmonary vasomotors react in a uniform typical way only if opening up of the thorax is followed by vagotomy of both vagi. In this case the vasomotors always react by a distinct vasodilatation. With the vagi intact however the depresor reflex intervenes in vasomotor reactions, disturbing ­ in different forms and degrees ­ the manifestation of reaction, owing to an accumulation of metabolites in the blood. If the chest is not opened up, the basic reactions become even more masked through the interference of a negative intrathoracic pressure, in addition to the depressor reflex. The results of tests and experiments in the course of three years clearly show that in the region of pulmonary vasomotors the metabolites can ­ after elimination of all other concurrent stimulants ­ operate effectively as the sole activators.

If besides the metabolites the aortic depressor reflex operates during the aspyxia, then reactions occur which should be treated as a result of a concurrence between two effects of two different factors in the region of pulmonary vasomotors. The final result may be the victory of either activator, or again, combined efforts of both activators may become manifest. Graph. No I shows numeral proportions of the outcome of this fight, as well as consequences of vagotomy when either of the participants is moved away. Similar results were obtained during winter experiments (Graphic table II) where, besides the depressor, the effect of cold appears as an antagonistic activator.

Graph. No I shows that during the summer experiments effects become manifest in following proportions:

1. In 15 dogs the metabolites manifest themselves as only and dominating factors, causing vasodilatation, as if the depressor reflex were eliminated (Picture 2). In summer months reactions of this kind are most frequent.

2. In 14 dogs both activators are manifest in three forms, i.e. besides the metabolites the depressor reflex too (Pictures 3, 4, 5).

3. Only in 6 dogs out of 35 the effect of the depressor reflex is completely dominant (Picture 6). See graph. 1.

4. On all of the 20 dogs with partly or completely masked vasodilatation, vagotomy of both vagi was subsequently performed with the result: (a) in 18 dogs vasodilatation was complete (Picture 8), and (b) in 2 dogs only there was a postasphyctic jump ­ pro­ bably a third reaction intervened, the cause of which we did not investigate (Picture 9).

II. The results of winter experiments vary according to the air­temperature of the room, as follows:

1. At a room temperature of 18° to 20° C the reactions are characterized by the absence of vasodilatation, without exception, and with an absolute domination of the depressor reflex in all cases where reactions were brought about by vagotomy.

Vagotomy does not change the direction of reaction, though it does eliminate the depressor reaction of the aortic as well as of the pulmonary curve of blood pressure (See graph. II).

30 reactions of this kind in 4 dogs were recorded, vize,

a) 10 records with manifest depressor reactions; in all of these the influence of depressor is predominant without mar ed hypo­ tension (See picture 10). From the data obtained, the domination occurred because the low respiratory air temperature helps the depressor reaction through its vasoconstricting effect, and hinders the reaction caused by the effect of metabolites;

b) following vagotomy in all 4 dogs the depressor reaction disappeared in 20 records, with the cold however hindering the appearance of the effect of metabolites (fig. 11). See graphic table n. Cosequently, there is no hypotension.

2. In a room with the air temperature of 20° to 300° C, tests were made on; 8 dogs: on 2 of these after curarization, and on the rest of them in the usual way after opening up the thorax. From the curarized dogs one reaction only was recorded in order to prove that even under these circumstances adequate changes were obtained during asphyxia. On 16 dogs 18 asphyxies were performed with the thorax opened up, 15 with saved depressor reflex, and 3 after vagotomy.

Reactions in cases with the thorax unopened are analogous with those of the summer experiments (See picture 12). 

With an opened-up thorax and saved depressor reflex, the reactions in general are analogous to the type and reactive direction of pulmonary vasomotors (See fig. 13 and 14) during the summer. The only difference to be seen in the group of positive hypotensions as compared with the sommer reactions is the shift of the numerical proportion of particular types. While the number of negative reactions is proportional to the number of negative reactions in summer, the number of clear hypotensions observed in winter experiments is considerably less, even at a. high room­temperature. In summer tests, clear hypotension is the most frequent reaction­ form, with a saved depressor (ab. ~7%). As a contrast to this, in winter experiments the concurrence between the metabolites and depressor generally results in a compromise (ab. 60%). No attempts were made to account for the difference.

The data reported here represent only a fraction of the findings from a total of 348 recorded vasomotor pulmonary reactions, i. e. the results obtained through asphyxia. Another report dealing with reactions obtained through other means is to appear shortly; it will be seen, for instance, that our results concerning hormones show complete analogy with the findings of many other investigators in that they are just as heterogenous and contradictory as theirs, in other words, chaotic. Still, some of our results lead us to believe that we are possibly on the way to discover the causes am.di to find a means for obtaining equal reactions. Therefore our present conclusions are limited to the material dealing with cases in connection with asphyxia.

Our experiments and the tests made go to prove that an accumulation of metabolites in the blood brings about typical vasomotor reactions. In general the results correspond with the findings of Loehr and other investigators concerning the effect of C02 on the reaction of pulmonary vasomotors. In this report the relation bet­ ween C02 and adrenalin, according to Loehr, was not investigated; nevertheless, as we did not inhibit the effect of adrenalin by any agents, it is evident that it was always present in the blood during our investigations; accordingly Loehr's condition was fulfilled, viz., for the effect of CQ the presence of adrenalin is indispensable. Some of our experiments, to be reported. on later, similarly point out that the effect of C02 was probably determined by the presence of adrenalin.

Manifestation of the depressor reflex in the region of pulmonary vasomotors and, moreover, the acute effect of traumatic demolition of the vagus (See picture 7) show analogies with the fin­ dings of Carlson and Luckhardt (7) in respect of pulmonary blood vessels and stimulation of the vagus, as well as with those of Wearn, Ernstene and Bromer (55), and Wearn, Barr and German (54), viz., that most pulmonary capillaries are in a state of vasoconstriction when at rest, but that vasodilatation occurs when they are in motion. 

Some of the conclusions to be drawn from our experiments concerning the reaction of pulmonary vasomotors against asphyxia would be as follows:

1. The basic reaction of the pulmonary vasomotors under the effect of asphyxia consistently manifests itself in undoubted! and pure hypotension which in all probability comes about owing to vasodilatation of the pulmonary arterial. branches;

2. This basic reacting course may be increased, concealed or suppressed, even reversed, by simultaneous superposition or inter­ position of one or more effects. These effects may originate from the respiratory tract itself (thorax motions), or from the circulatory system (depressor reflex), but they also may come directly from the surrounding nature in the form of temperature of the air inhaled (ecological effects);

3. The reacting course of these effects, both accessory and secondary, corresponds to the basic course (thoracic motion, increased air temperature), but it can be reversed in opposition to the basic reaction (depressor reflex, cold, irritation of the vagus). Final effect depends on the predominance of a single stimulant, or their united effects, in this conflict for support of different influences.

4. Our observations so far have disclosed the presence of at lea.st 4 participants in the start of vasomotor pulmonary reactions:

a) the group of metabolites, as the principal activator, whose circulation proceeds directly through the breathing function. This follows from the fact that a discoutinuation of the breathing function and elimination of other effects upon pulmonary vasomotors makes the reaction/ itself manifest. Intervention of other participants in our experiments is proving itself as a hindrance in determining the basic type of the reaction. This interference in the basic reaction leads to a heterogeneousness or indifference of reacting forms of the pulmonary vasomotors. After removing all interfering factors, we succeeded in bringing to light the basic reaction. At the same time, this effect upon the vasomotors can only be characterized as disturbing from the standpoint of our investigations, for from the stand­ point of the organism itself it· rather represents an expression of a realization o~ correlative connections within its functions;

b) thoracic respiratory motions greatly affect the blood circulation of the lungs; however, this intervention is external and passive, consequently the reaction of the vasomotors is not affected either through hormones or nerves, and acts quite mechanically through changes of intrathoracic pressure;

c) the depressor reflexes no doubt is involved in the pulmonary circulation by way of cardiac bradycardia and increased filling up of the right ventricle; one might suppose also a direct involvement of the depressor reflex in the vasomotor reaction, causing vasoconstiction (?) ­ Asphyxias produced directly after vagotomy and the reactions that follow at any rate, seem to suggest this idea.

Opposing the direction of effect of the basic vasomotor reaction the depressor reflex may change ­ in various ways and different degrees: ­ the basic character of reaction, may vary from clear domination of asphyctic reaction, over transitional f orms, to clear domination of depressive reactions. Hence the variety of forms when both factors act simultaneously. After vagotomy and consequent suspension of depressor reflex metabolites remain as the only stimulants being exchanged trough the breathing function (unless for some other reason a third effect asserts itself);

d) cold respiratory air, inducing a vasoconstrictor reaction of pulmonary blood vessels, seems to disturb the effects of metabolites accumulated during asphyxia; at the same time, it facilitates the domination of depressor reflex in the pulmonary arterial region. No attempts were made to test the influence of air temperature itself, outside of asphyxia;

It looks as if each of the stimulants mentioned! were involved in the reaction trough these steps of the process, in whose accomplishment participates itself. Acting upon pulmonary vasomotors each activator adequately brings to bear its reaction in the direction of its process. One has the impression that the pulmonary vasomotors, simultaneously and seem to effect reactive relations with several functional systems, providing for each reactive course ­ in proportion to its momentary importance to the organism ­ conditions indispensable for realization of its reaction. Our investigations probably revealed only a small number of such correlations between the pulmonary region and other parts of the organism. Our method of studying these correlations consists essentially successively pre­ venting the involvement of particular functional courses with the reaction of pulmonary vasomotors, thus ensuring perexclusion em an increasingly simpler and more specific reaction of the pulmonary vasomotors.

It is for this reason that we considered. it indispensable to establish conclusively the direction of the effect in the region of pulmonary artery and the reaction type for each of the activators of pulmonary vasomotors; further, to establish conditions promo­ ting an adequate reaction to the effect of a given activator; moreover, to ascertain how a certain reaction is included in the common response and to what extent the corresponding activator outside the lung participators in the basic process, etc.

5. Curarization and opened thorax followed by vagotomy showed the same results, except that the former inhibits the depressor reflex, i. e. it acts as a vegetative poison.

6. Vasodilatory reacting course of pulmonary artery during asphyxia is consistent with the general physiologic rule that an in­ crease in function of an organ brings about a corresponding vasodilatation.

7. The response of pulmonary vasomotors to the influence of carbonclioxyde ·and other metabolites, accumulated in the blood du­ ring asphyxia, occurs at the same time and under the same conditions, producing maximum activation of the respiratory centre, as seen from the highly increased rate of thoracic motions (See pictures 1 and 12). No doubt the same activators that induce pulmonary ventilation also determine adequate changes in the region of pulmonary artery, i. e. just where the elimination of CO from the organism takes place ­ the cause of pulmonary ventilation.