The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.
Various types of inflammatory exudates have been obtained either by the introduction into normal tissues of a chemical irritant, or by a burn, or by bacteria in either dogs or rabbits. A study has also been made on an exudate of human origin.
These exudates have all been found to contain a factor which induces prompt increase in the permeability of normal skin capillaries, demonstrable by the almost immediate accumulation from the circulation of trypan blue into areas of skin injected with the cell-free exudate.
The active factor may be carried down with the precipitate resulting from the interaction of the exudate with either saturated ammonium sulfate or 20 per cent sodium sulfate.
The active factor passes through a dialyzing membrane. It can be recovered from the dialysate as a protein-free crystalline material.
The active factor manifests no property in common with histamine or presumably with the hypothetical H substance assumed to be closed related to histamine.
This is indicated by the following considerations: (a) difference between the tissue staining pattern of the exudate or of its active fraction and that of histamine; (b) opposite effects by histamine and the active factor found in exudates on the tonicity of the isolated strip of guinea pig intestine.
The observations presented in this report do not substantiate Lewis' hypothesis of histamine or of its closely related H substance as the primary cause of increased capillary permeability in inflammation.
The present studies are being continued in an endeavor to free of its impurities and to identify the active crystalline-like material isolated from an inflammatory exudate. The details of this investigation will form the subject of a separate future communication.
Trypan blue injected into normal subcutaneous tissue passes rapidly to the regional lymphatic node and is found in lymph drawn from its efferent lymphatic.
When the dye is injected into the normal peritoneal cavity it rapidly appears in the lymph of the retrosternal lymphatics and stains deeply the retrosternal lymphatic nodes.
Trypan blue injected into the site of inflammation in the subcutaneous tissue or in the peritoneal cavity is fixed in the inflamed area and fails to reach the regional lymphatic nodes.
If an inflammatory reaction has been produced in the dermis or in the subcutaneous tissue, trypan blue injected into the circulating blood enters the site of inflammation and is fixed so that the tissues are deeply stained.
India ink or graphite partides injected into an area of inflammation fail to disseminate to the tributary lymph nodes. When injected into a normal peritoneal cavity they rapidly appear in the retrosternal lymph nodes. When injected into an inflamed peritoneal cavity they are fixed in situ and fail to reach the regional lymph nodes.
Graphite particles injected in the circulating blood stream enter an inflamed area both as free particles owing to increased capillary permeability and also as phagocyted material within leucocytes.
Bacteria (B. prodigiosus) injected into inflamed tissue are fixed at the site of inflammation and fail to disseminate to the regional lymph nodes as readily as when injected into normal tissue.
Bacteria (B. prodigiosus) injected at the periphery of an inflamed area do not readily penetrate into the site of inflammation. The experiments furnish evidence, in addition to that already provided, that fixation of foreign substances by the inflammatory reaction is primarily due to mechanical obstruction caused by a fibrin network and by thrombosed lymphatics at the site of inflammation.
Bacteria (B. prodigiosus and B. pyocyaneus) injected intravenously rapidly enter an inflamed area. It is suggested that localization of bacteria in a locus minoris resistentiae may be explained as the result of increased capillary permeability with subsequent accumulation and fixation of bacteria from the blood stream at the point of injury.
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