Microcirculatory Stasis and the Production of Tissue Necrosis in the Hamster Cheek Pouch Induced By Histamine or a Histamine Liberator

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Abstract
In the present study there is a critical relationship between microcirculatory stasis and the development of subsequent tissue necrosis. The topical application of relatively high concentrations of either histamine or 48/80 in "surgical pouch preparations" (SPP) of the hamster cheek pouch resulted in the production of "irreversible" vascular stasis. The injection of identical concentrations of these agents into the "intact cheek pouch" (IPP) led to ischemic necrosis. Lower concentrations of either agent which did not produce irreversible vascular stasis in the SPP did not result in necrosis when injected into the IPP. Since the dose of histamine needed to produce stasis and necrosis was far beyond presumed physiologic levels in the tissues, these experiments would tend to support the contention that endogenous histamine cannot in itself mediate these phenomena. Triprolidine hydrochloride and cortisone acetate prevented irreversible vascular stasis and hence necrosis in many animals exposed to necrotizing doses of histamine but failed to inhibit the necrotic response to p-methoxyphenethylmethylamine condensation product with formaldehyde (48/80). The mechanism of this protective influence appears to be dependent on preventing microcirculatory stasis in response to high concentrations of histamine.

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