Elements of surgical pathology / by Augustus J. Pepper.

  • Pepper, Augustus J. (Augustus Joseph)
Date:
1890
Catalogue details

Licence: Public Domain Mark

Credit: Elements of surgical pathology / by Augustus J. Pepper. Source: Wellcome Collection.

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    constructive in so far as it leads to an accumulation of indifferent cells, it is destructive as regards its influence on the tissues. The older views of the essential pathology of in- flammation now practically exploded may be briefly summarised : (1) The neuro-paralytic ; here it was sup- posed that irritation of the sensory nerves of the part brought about a dilatation of the vessels by inducing a reflex paralysis of the vaso-motor nerves. (2) The neuro-spastic, which was grounded on the belief that instead of being paralysed the arteries were stimu- lated through their nerves, and that, answering to the irritation, they contracted. The hypersemia was at- tributed to dilatation of the corresponding capillaries and veins. In refutation of these hypotheses it may be noted that inflammation of the cornea may not show itself for several hours after the part has been irritated, whereas if the injury acted through the nerves it ousjht to manifest itself much more quickly. It cannot be^denied that the calibre of the vessels and the vascular tension are altered by conditions that disturb the functional equilibriuQi of the vaso-motor nerves, and vary the amount of physiological contrac- tion of the muscular elements. Strieker has shown that certain fibres run in the sciatic nerve, which, on bein<^ stimulated, cause a direct dilatation ot the vessels by inhibiting the action of the vaso-motor nerves Again, division of the cervical sympathetic, in the rabbit, for example, is rapidly followed by a flux of blood to the ear, the vessels dilating on account of the paresis of tlieir walls. But these phenomena are mainly, if not entirely, dependent on a departure from the normal state of contraction of the m.iscular fibre cells by reason of disturbed innervation, and not from a molecular change, the result of damaged nutri- tion This molecular change may be taken, then, as the dilibrential sign between simple hypera^mia and