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. 121 No. 1, January 1986 TABLE OF CONTENTS
  Archives
  •  Online Features
  PAPERS READ BEFORE THE FIFTH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, NEW ORLEANS, APRIL 29 TO APRIL 30, 1985-PART I
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (6)
 •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?

Degranulation Inhibition

A Potential Mechanism for Control of Neutrophil Superoxide Production in Sepsis

Joseph S. Solomkin, MD; Julia K. Brodt; Frank P. Zemlan, PhD

Arch Surg. 1986;121(1):77-80.


Abstract

• Previous studies with neutrophils from patients with intraabdominal sepsis have provided convincing evidence of in vivo exposure to C5a. However, in contradistinction to normal cells pretreated with C5a, patient cells showed depressed superoxide response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) and enhanced FMLP receptor affinity. To identify possible mechanisms responsible for these findings, we examined the effects of lysosomal alkalinization with the weak base clindamycin on normal neutrophils with and without C5a. Our results showed a specific suppression of FMLP-induced superoxide production and a loss of low-affinity FMLP receptors. These results occurred in the presence of clindamycin levels that did not interfere with other cellular processes. These findings suggest that regulation of neutrophil function during the course of intra-abdominal sepsis may be due to effectors active both at the cell surface (C5a) and within the lysosome. The clinical significance of our findings relates to a possible mechanism for specific pharmacologic suppression of oxide-radical production by neutrophils. Such oxide radicals are believed to be important in the capillary injury accompanying severe sepsis.

(Arch Surg 1986;121:77-80)



Author Affiliations

From the Departments of Surgery (Dr Solomkin and Ms Brodt) and Psychiatry (Dr Zemlan), University of Cincinnati College of Medicine.


Footnotes

Accepted for publication Sept 5, 1985.

Read before the Fifth Annual Meeting of the Surgical Infection Society, New Orleans, April 29, 1985.

Reprint requests to Department of Surgery, University of Cincinnati College of Medicine, ML#558, 231 Bethesda Ave, Cincinnati, OH 45267-0558 (Dr Solomkin).



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?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Prevention of body temperature reduction (afterdrop) following hypothermic perfusion
Jani et al.
Perfusion 1988;3:301-306.
ABSTRACT  

Neutrophil Activation in Sepsis: The Relationship Between fMet-Leu-Phe Receptor Mobilization and Oxidative Activity
Tennenberg and Solomkin
Arch Surg 1988;123:171-175.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1986 American Medical Association. All Rights Reserved.