Volume 1

Diseases of the arteries including angina pectoris / by Clifford Allbutt.

  • Thomas Clifford Allbutt
Date:
1915
Catalogue details

Licence: In copyright

Credit: Diseases of the arteries including angina pectoris / by Clifford Allbutt. Source: Wellcome Collection.

    542/560 page 522
    Thoma’s phrase the elastic-muscular layer of its intima. In the lesser arteries this musculo-elastic structure is seen rather at angles of stress, than in the lengths of them where, for the muscular, fine connective fibres are substituted. In the twigs the reduplication of the elastica tapers out; there we may see it degenerated simply. In youth the manifolding of the elastic elements, under the formative stimulation of stress, progresses likewise in the aorta and the small vessels respectively, but not identically nor pari passu in all the smaller vessels. Still, broadly speaking, in the smaller the elastica multiplies two to threefold ; in the aorta three to fourfold, a stage which in the third decade is, in health, constant. This mode of proliferation is the hyperplastic form of Jores, though I repeat that the prefix “ hyper ” is rather suggestive of a phase in which this process is beginning to slip from the physiological into the pathological mode, into phases which, when more definitely morbid, con¬ stitute Jores’ second form, called, not very happily, regenera¬ tive (reparative). Thus physiological growth is chiefly visible in the elastica, less so in the muscularis, and in connective fibre is distinct only in certain areas of stress ; at this stage it is that elastic resistance, resilience and, with them, stability are at the best. In this efficient form the structure should be stable for some twenty years ; not until about the end of the fourth decade does it begin to turn towards decline. In disease, these features preserve no less an importance, though degradation is manifested chiefly in the behaviour of the elastic fibres, and the hitherto tenuous connective strands. The first phase is no more than a normal increase would be ; in transition or suspensory phases we are guided by some inter¬ mediate and equivocal combinations. Diagnostic distinctions however can ordinarily be made plain enough ; slight degrees of splitting of the elastic lamina may be neglected, so long as no fatty reaction is given to Sudan. Dr. Cowan says that the elastica is peculiarly prone to suffer in the infections, such as tuberculosis, pneumonia, and typhoid fever, when it blurs, and loses stain characters (p. 285). Faber also lays much emphasis on this fragility of the elastica. When splitting of the elastica into layer after layer has evidently become a morbid activity, or a dilapidation (Herringham, Jores and others), we soon find
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