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tractile tissues, and less of the purulent and opaque curdy deposits which originate in the corpuscles or sarcophytes.

In whatever way fibroid disease of the lung may have originated, its ultimate tendency is either to contract and condense the textures in which it is formed, or to degenerate and disintegrate into cheesy matter. The remarkably different effect of this condensation and contraction, according to its seat, has already been pointed out. When affecting the upper parts and root of the lungs, it contracts and constricts the large bronchi, causing an asthmatic difficulty of inspiration and expiration, and an emphysematous distention of the lower and peripheral vesicular texture. When, on the other hand, the condensation and contraction affects the lower lobes and obliterates the peripheral air cells, the bronchi become generally dilated by the pressure of the inspired air within their walls, as it cannot penetrate to the cells beyond. This is the explanation which I originally gave of the dilatation of the bronchi which follows contractile pleuro-pneumonia, and which was subsequently ascribed by Corrigan and his followers to a new tissue called cirrhosis, to which was imputed the paradoxical power of dilating the bronchi by contracting around them! But it is obvious that the dilating power is the pressure of the air in inspiration, which, failing to penetrate beyond the tubes, is exerted in distending them.

The contractile property of the fibroid tissue is manifest in the shrinking of the lung, and in the drawing towards it of the walls of the chest, the heart, and the opposite lung, to occupy its place. Thus, when the left lung is affected, in addition to the collapse of the ribs, the heart is drawn upwards, and may be felt with its apex beating at or above the fourth rib, and its body in contact with the ribs to the third costal cartilage; and the right lung may reach to the left of the sternum above. When the right lung is contracted, besides the flattening of the walls of the chest, the heart is drawn over to the right of the sternum, with its apex beating between the fourth and fifth costal cartilages, with the left lung sounding clear above it. So, likewise, other adjacent organs, the stomach and the liver, may be drawn up into the chest by the contractions of the lungs above them; and the upper and posterior walls of the chest may show depressions or flattenings from the same cause.

This contractile disease of the lung, consequent on inflammation, although an evidence of cacoplasis and degeneration, does not in all cases end in decay or consumption. In some instances, especially in young subjects, it may give way to a gradual re-expansion of the affected lung, and a restoration to the normal state. [Cases will be given afterwards.] Yet fibroid disease may properly be grouped among the varieties of phthisis; both because in most instances it is attended with symptoms of decline, and shows a tendency to degenerate further by its own caseation, and by the production of miliary tubercles in other parts of the lung; and also because in other varieties of phthisis, already tuberculous or caseous, inflammation of the lungs commonly produces more or less of this fibroid tissue in the more healthy parts of the decaying lung. It is, in fact, a modification of this which constitutes the scartissue around and between tubercles and their vomicae, and which tends, by its condensation and contraction, to pucker up and cobble together the wounds and breaches of the more destructive decay. In almost all of the more chronic kinds of phthisis there are proofs of the presence and operation of this contractile tissue during life, in flattening or hollowing of corresponding parts of the chestwalls, or in the signs of partial emphysema in the adjoining portions of lung; and after death, in puckered scars

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on the surface and in the substance of the lung, around, cavities or remains of caseous or tuberculous matters. In the more rapid forms of consumption there is neither time nor material for the formation of this fibroid scar-tissue. The exudations and deposits are corpuscular, more destitute of vitality, and therefore aplastic; passing speedily into disintegration and decay. But in chronic cases there is an attempt to limit and hedge in the work of destruction; and although this is done by a cacoplastic material, and in a clumsy and irregular manner, it may be looked on as a proof that nature is capable of exerting some resistance to the consuming malady.

In such cases the clinical history of the malady will show the symptoms and signs of partial emphysema and bronchitis in addition to those of phthisis. Occurring, as tuberculous lesions commonly do, mostly near the apex and root of the lungs, the puckering and contraction of the scar-tissue around them may shorten and narrow some of the chief bronchial tubes, with the effect of causing more rhonchi and wheezy prolonged breathing instead of tubular, and more emphysematous stroke-sound in patches, instead of the general dulness of consolidation. We were before led to this same conclusion, that chronic cases of consumption frequently assume more or less of an asthmatic character, which has some tendency to divert the disorder from the substance of the lungs to the bronchial surface.

But to complete the history of these fibroid productions, and to prove their connection with phthisis, we have to point to the other ulterior results mentioned in the table: they are themselves Uable to degeneration and caseation. In most cases of confirmed phthisis, even of the chronic kind, sooner or later there comes a break up— a failure of the vital powers and a sudden increase and prevalence of the work of decay. It may be occasioned by any weakening or greatly disordering influence—an


exhausting haemorrhage or diarrhoea; a harassing inflammation; any cause of severe mental depression or bodily weakness; or the decay may be gradual and progressive. But the change is manifest in the increasing weakness, pallor, emaciation, and colliquative sweats; in the occasional hard cough and wheezy breathing giving way to constant loose expectoration and panting breathlessness, the sputa being copious, opaque, and heavy; in the substitution of more moist and cavernous sounds in the breathing for the bronchial dr wheezing rhonchi which existed before. Then come increasing weakness of circulation, oedema and lividity, and the end is not far off. In the lungs of these genuine victims of chronic consumption are found the evidences of decay, not only in the old cavities spreading, and tubercles softening and forming new, but also in the opaque spots of caseation mottling the fibroid masses, and proving their degeneration; and in the numerous plump and soft (therefore newly-formed) miliary tubercles scattered through the less diseased parts of the lung. These are the signs and seeds of decay spreading and invading both the healthy tissues, and the frail barriers which nature had raised against it.



Inflammatory PhthinoplasmsCorpuscular, from change in the Sarcophytes Suppuration, if healthy, not Phthisical, but unhealthy often so; and also often part of the Consumptive processPurulent PhthisisCauses.

But although we thus find the fibrous element of hyperplasms amenable to the law of degeneration and decay, it is in the corpuscular element, the sarcophytes or bioplasts, that we can more commonly and constantly trace its workings. These, which in their healthy and vigorous state, are so lively in their moving, self-nutrient, assimilating, organising, and proliferating powers—in their unhealthy and enfeebled condition fail in these manifestations of vitality, and form a material more or less perishable and prone to decay, spreading degeneration and dilapidation in the adjoining tissues.

It will be an interesting subject for further investigation to trace the operation of this bioplasm in the more normal variations from healthy nutrition in mere determination of blood to a part, and in simple membranous inflammation, soon terminating in increased secretion, resolution, and the dispersion of its products; and still further to observe it working in adhesive inflammation, and in the healing of the simplest wounds by ' first intention.' In all these operations the bioplasm exercises its full vital properties, and the result is a living struc

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