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DIPHASIC INCREASE OF VASCULAR PERMEABILITY IN TURPENTINE‐INDUCED INFLAMMATION IN SKIN AND MUSCULATURE OF MICE
Author(s) -
Svanes Knut
Publication year - 1971
Publication title -
acta pathologica microbiologica scandinavica section a pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0365-4184
DOI - 10.1111/j.1699-0463.1971.tb01829.x
Subject(s) - inflammation , dermis , vascular permeability , turpentine , necrosis , medicine , pathology , subcutaneous tissue , erythema , chemistry , anatomy , surgery
Inflammation was induced in the abdominal skin and musculature of mice by subcutaneous injection of turpentine. The leakage of serum proteins estimated by the trypan blue technique was found to be diphasic, both in the skin and musculature. The early phase was completed in about 2 hours. The late phase started at about 3 hours and reached a maximum 12 to 16 hours after turpentine injection. However, even at 48 hours considerable dye leakage was present. By means of the colloidal carbon technique, turpentine was found to induce a diphasic labelling of venules in the, skin and musculature, the early phase being slight and short‐lived, the second marked and prolonged. Labelling of capillaries occurred in the panniculus carnosus in the first half hour of inflammation. At 36 and 48 hours capillary labelling occurred in a ringshaped area of the skin. In the musculature capillary labelling occurred in the first 3 hours of inflammation. Tissue necrosis was present in the panniculus carnosus at 14 hours, in the dermis at 24 hours and in the epidermis at 48 hours of inflammation. Necrosis was also present in a thin layer of the musculature close to the abscess wall after 14 hours of inflammation. Inflammatory oedema developed rapidly during the second hour of inflammation and slowly during the following 22 hours. Some relations between protein leakage, vascular carbon labelling, tissue necrosis and oedema formation are discussed.