spacer gif spacer gif spacer gif spacer gif spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by MacIntyre, D. E.
Right arrow Articles by Gordon, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by MacIntyre, D. E.
Right arrow Articles by Gordon, J. L.

Journal of Cell Science, Vol 28, Issue 1 211-223, Copyright © 1977 by Company of Biologists

JOURNAL ARTICLES

Endotoxin-induced platelet aggregation and secretion. I. Morphological changes and pharmacological effects

DE MacIntyre, AP Allen, KJ Thorne, AM Glauert and JL Gordon

Endotoxin lipopolysaccharide (LPS) from Acinetobacter 199A induced aggregation of blood platelets from immune adherence-positive species (rat, rabbit) but not from immune adherence-negative species such as pig and man. Aggregation occurred in 2 phases: the first was not accompanied by secretion of platelet constituents, was apparently a consequence of C3 activation, and was selectively inhibited by EGTA. The second phase of aggregation was associated with secretion of platelet granule contents, and with a lesser amount of cytoplasmic leakage. Secondary aggregation was abolished by the sulphydryl alkylating agent N-ethylmaleimide, and by agents which increased the level of cyclic AMP in platelets, such as prostaglandin E1 (a stimulator of adenylate cyclase) and methyl xanthines (inhibitors of phosphodiesterase). Secondary aggregation was partly inhibited by agents which block platelet prostaglandin biosynthesis (e.g. aspirin, indomethacin). Primary aggregation was unaffected by these inhibitors at concentrations which blocked secondary aggregation.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
F. Moulin, B. L. Copple, P. E. Ganey, and R. A. Roth
Hepatic and extrahepatic factors critical for liver injury during lipopolysaccharide exposure
Am J Physiol Gastrointest Liver Physiol, December 1, 2001; 281(6): G1423 - G1431.
[Abstract] [Full Text] [PDF]


© The Company of Biologists Ltd 1977