You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 99 No. 4, October 1969 TABLE OF CONTENTS
  Archives
  •  Online Features
  ARTICLES
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citing articles on HighWire
 •Citing articles on Web of Science (14)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Histidine Decarboxylase Inhibitors and Second-Set Allograft Survival

Thomas C. Moore, MD

AMA Arch Surg. 1969;99(4):470-473.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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tissue, after skin allografting across this same histocompatibility barrier according to T.C. Moore and R.W. Schayer (unpublished data).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 . . . [Full Text PDF of this Article]


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).


Footnotes

Submitted for publication Feb 26, 1969.

Reprint requests to Department of Surgery, UCLA-Harbor Medical Center, 1000 W Carson St, Torrance, Calif (Dr. Moore).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1969 American Medical Association. All Rights Reserved.