Abstract
Following a brief definition of the new concepts of calcergy and calciphylaxis, experiments are reported which show that, in rats prepared by a single intravenous injection of lead acetate, topical connective tissue calcification can be prduced by minute doses of various mast cell components (histamine, 5-HT) or mast cell dischargers (compound 48/80, polymyxin). This form of calcergy can be inhibited by topical pretreatment with any one among the substances just mentioned. Here, both the production of cutaneous calcinosis and its prevention appear to depend upon compounds that can be liberated by mast cells and, hence, we speak of mastocalcergy.
In rats similarly prepared by an intravenous injection of lead acetate, the subcutaneous injection of formalin or crushing of the skin with a hemostat likewise produces topical calcification. However, this form of calcinosis cannot be prevented by pretreatment with mast cell dischargers, mast cell products, formalin or trauma. Apparently, here we are not dealing with mastocalcergy, but with an essentially different mechanism dependent upon the localization of blood-borne lead and subsequently of calcium salts owing to severe vascular leakage.
Footnotes
- Accepted July 1, 1964.
- The Williams & Wilkins Comapny
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