October 1969

Histidine Decarboxylase Inhibitors and Second-Set Allograft Survival

Author Affiliations

Los Angeles
From the Surgical Research Laboratory, Medical College of Virginia, Richmond, and the Department of Surgery, University of California, Los Angeles (UCLA-Harbor Medical Center, Torrance).

Arch Surg. 1969;99(4):470-473. doi:10.1001/archsurg.1969.01340160050012

A 33-fold increase in histidine decarboxylase (HDC) activity of allografted rat skin has been found during rejection.1 Full-thickness grafts were carried out from inbred Lewis to inbred PA rats and the peak elevation in HDC activity occurred ten days after grafting. No such change occurred in autografted skin.

An increase in HDC activity also has been encountered in rat spleen, but not in intestinal-tract Peyer's patches lymphoid tissue, after skin allografting across this same histocompatibility barrier according to T.C. Moore and R.W. Schayer (unpublished data). These observations, and the finding of an increase in 24-hour urinary histamine excretion in the rat during skin allograft rejection,2 suggest an involvement of intracellular histamine formation from increased HDC activity in the biologic mechanism of allograft rejection. Kahlson3 has found 24-hour urinary histamine excretion to be a useful means of monitoring intracellular histamine formation from increased HDC activity.

Histamine is formed

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