This phenomenon evidently arises from the fact, that the lungs alone receive as much blood as the whole body, so that when an inflammation of this viscus interrupts the course of the fluids, a very great quantity of them can accumulate there in a given time. It is not however, properly speaking, the blood that is found crowding the lungs in pneumonia; the fluid appears whitish when pressed out; we should say that it was a kind of pus. Much has been said of vomicæ after pneumonia; but they are extremely rare; there is almost always effusion in the lungs; the fluid is not collected in a sac.
In pulmonary inflammation, does the blood pass through vessels that do not ordinarily circulate it, as happens so evidently upon the serous surfaces, or conjunctiva, &c. when inflamed? I do not think it does, for we do not know any vessels in the lungs, except the sanguineous. It appears evident that the blood or the other fluids are effused into the pulmonary texture, in which they are deposited by exhalation. There is no doubt that in some phlegmons, this fluid passes, as I shall say, into the cells of the cellular texture; now it appears that it happens here in the same way. By breaking or cutting inflamed lungs, we see clearly that its whole texture is crowded, and filled; whereas in examining an inflamed serous surface, we see that the blood is evidently contained in the capillaries.
It is a great mistake to try to represent inflammation as being everywhere the same, as exhibiting always the fluids, like their vessels, in the same state. Boerhaave for example thought, that there could be no inflammation without an error loci. There is according to the state of the parts, their structure, their vital properties, a thousand different modifications in the new anatomical order that this affection gives to the organs.
What constitutes the essence of inflammation is, 1st, the irritation of the inflamed part; 2d, the new modifications that its vital forces have taken in consequence of that irritation; 3d, the consequent stagnation of the fluids around it. But in what manner the fluids are arrested; how they stop in the capillary system; how they are taken up by the exhalants; how they are poured out, in extravasations, &c.; these are different effects that arise from the different organization of the parts; but the principle is always the same, it is always the same disease. If we could analyze thoroughly the state of all the systems in inflammation, we should see perhaps, that there was a difference in the inflammation of each. Besides, the diversity of the symptoms that it exhibits, a diversity of which I have already spoken, proves that the state of the solids and the fluids are not the same.
How is it that the blood can pass through the lungs of phthisical patients, in whom this organ is reduced nearly one half? I would observe upon this subject, that the blood in the great vessels is diminished in proportion to the ulceration of the lungs. The diminution of this fluid is remarkable in many organic affections, but especially in these, as Portal has observed. If a phthisical patient in the last stage had as much blood, as before the disease, the circulation certainly could not go on, or at least there would be a constant reflux towards the right auricle. Who is ignorant of the small pulse, feeble though frequent, particularly towards night, in phthisis? Compare it with the pulse of an inflammatory fever, in which there is evidently plethora; you will see that they are really the two extremes.
I will make a general observation upon this subject, it is this, that when the forces are weakened in our organs, or life languishes in them, the blood is diminished almost continually in proportion; so that this fluid being considered in the capillary system, as the resistance opposed to the power of the small vessels, the proportion remains always the same between this power and this resistance. It is necessary that the whole should be in relation. If blood was transfused into a phthisical patient, he would die, because the forces of the solids would not correspond with the increase of action to which they would be forced.
The circulation of the pulmonary capillaries, is, like that of the others, under the influence of the tonic forces of the part, and not under that of the impulse of the heart. This impulse terminates at the extremity of the branches of the pulmonary artery. In inflammation then of the lungs, the blood is not mechanically arrested in this organ; then, when you bleed, it is not to diminish the vis à tergo. You might draw ten basins from the patient, but the lungs most commonly would not empty themselves; they would be less fatigued by the entrance of the blood; but that which was stagnant in the capillary system would still remain there. So long as there is a point of irritation, it will be, if we may so say, a magnet which will attract the blood, and completely change its direction; which was before from the artery to the veins, it will now be only towards the irritated point. Bleeding acts then, 1st, by diminishing the blood that enters the lungs, and consequently by lessening the fatigue of this diseased organ; 2d, by diminishing the irritation of the solid, which attracts the blood, and retains it around the irritated place.
The constant excitement that the air gives to the pulmonary capillary system is favourable to its circulation; but the blood can traverse this system without this excitement, as is proved by my experiments mentioned elsewhere.
III. Alteration of the Blood in the Pulmonary Capillaries.
There takes place here the reverse of what happens in the general capillaries; the fluid changes from black to red. We have already some data upon the causes of this phenomenon; but I think new experiments should be made before a thorough explanation can be given. This is so much the more necessary, because if we knew how the black blood becomes red, it would seem that we might know how the red becomes black.