TITLE

MICROCIRCULATORY STASIS AND THE PRODUCTION OF TISSUE NECROSIS IN THE HAMSTER CHEEK POUCH INDUCED BY HISTAMINE OR A HISTAMINE LIBERATOR

AUTHOR(S)
Taichman, Norton S.; Goldhaber, Paul
PUB. DATE
December 1964
SOURCE
Angiology;Dec1964, Vol. 15 Issue 12, p515
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
In the present study it was shown that 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 48/80. The mechanism of this protective influence appears to be dependent on preventing microcirculatory stasis in response to high concentrations of histamine.
ACCESSION #
16366581

 

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