AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 258: H85-H91, 1990;
0363-6135/90 $5.00
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, A.
Right arrow Articles by Ferro, T. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, A.
Right arrow Articles by Ferro, T. J.

AJP - Heart and Circulatory Physiology, Vol 258, Issue 1 85-H91, Copyright © 1990 by American Physiological Society

ARTICLES

Mechanisms of pulmonary edema induced by a diacylglycerol second messenger

A. Johnson, D. C. Hocking and T. J. Ferro
Research Service, Veterans Administration Medical Center, Albany, New York.

We investigated the effect of dioctanoylglycerol (DOG), a second messenger of protein kinase C (PKC) activation, in the absence and presence of neutrophils in isolated perfused guinea pig lung. DOG was given after a base-line isogravimetric steady-state period. Pulmonary capillary pressure (Ppc) and change in lung weight (delta W) were monitored at 15, 30, and 60 min. Capillary filtration coefficient (Kf,c, an index of vascular permeability) was measured during base-line period and at 30 min. DOG increased the Ppc and delta W at 30 and 60 min, and the Kfc at 30 min. Monooctanoylglycerol, a monoacylglycerol that does not activate PKC, had no effect on Ppc, Kf,c, and delta W. Pretreatment with two different PKC inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methyl piperazine or staurosporin, prevented the pulmonary response to DOG. With neutrophils present, DOG caused greater increases in delta W and the (wet-dry)-to-dry wt ratio compared with DOG group. Response to DOG+ neutrophils was due to oxygen radical production because it was prevented by pretreatment with catalase and because DOG increased superoxide release from neutrophils. PKC activation using DOG in the isolated lung results in pulmonary edema mediated by increases in capillary pressure and vascular permeability. Lung weight-gain response to DOG is greater in the presence of neutrophils. Response to DOG+ neutrophils is mediated by oxygen radicals.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
J. R. Klinger, J. D. Murray, B. Casserly, D. F. Alvarez, J. A. King, S. S. An, G. Choudhary, A. N. Owusu-Sarfo, R. Warburton, and E. O. Harrington
Rottlerin causes pulmonary edema in vivo: a possible role for PKC{delta}
J Appl Physiol, December 1, 2007; 103(6): 2084 - 2094.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
M.-F. Tsan, X. Cao, J. E. White, J. Sacco, and C. Y. Lee
Pertussis Toxin-Induced Lung Edema . Role of Manganese Superoxide Dismutase and Protein Kinase C
Am. J. Respir. Cell Mol. Biol., March 1, 1999; 20(3): 465 - 473.
[Abstract] [Full Text]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Q. Huang and Y. Yuan
Interaction of PKC and NOS in signal transduction of microvascular hyperpermeability
Am J Physiol Heart Circ Physiol, November 1, 1997; 273(5): H2442 - H2451.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online