| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print June 13, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01107.2001
Submitted on December 20, 2001
Accepted on June 7, 2002
1 Pediatrics, The University of Texas Southwestern Medical Center, Dallas, Texas, USA; Molecular Biology, The University of Southwestern Medical Center, Dallas, Texas, USA
2 Pediatrics, The University of Texas Southwestern Medical Center, Dallas, Texas, USA
* To whom correspondence should be addressed. E-mail: james.thomas{at}utsouthwestern.edu.
Both large burns and severe Gram-negative sepsis are associated with acute myocardial contractile dysfunction. Since others have reported that burn injury may be followed by transient endotoxemia, we hypothesized that bacterial endotoxin induces contractile impairment after burn trauma. We tested this hypothesis in two rodent models. In each model, post-burn myocardial contractility was assessed using Langendorff preparations of excised hearts. In the first model,mice expressing either a mutant form of or no Toll-like receptor (TLR)4, a critical element of the mammalian endotoxin receptor, were resistant to post-burn myocardial contractile dysfunction. In the second model, starting 30 minutes or 4 hours after burn injury, rats were infused with recombinant bactericidal permeability-increasing protein (rBPI21), a protein that binds and neutralizes endotoxin. Hearts from BPI21-treated animals were completely protected from postburn contractile impairment. Since burn-induced contractile dysfunction can be prevented either by blocking signaling through the endotoxin receptor or by neutralizing circulating LPS,bacterial endotoxin may contribute to impaired myocardial contractility after burn injury.
This article has been cited by other articles:
|
|
 |
|
  J. W. Horton, D. L. Maass, D. J. White, and J. P. Minei Bactericidal/permeability increasing protein attenuates the myocardial inflammation/dysfunction that occurs with burn complicated by subsequent infection J Appl Physiol, September 1, 2007; 103(3): 948 - 958. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Carlson, D. L. Maass, J. White, P. Sikes, and J. W. Horton Caspase inhibition reduces cardiac myocyte dyshomeostasis and improves cardiac contractile function after major burn injury J Appl Physiol, July 1, 2007; 103(1): 323 - 330. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Willis, D. L. Carlson, J. M. DiMaio, M. D. White, D. J. White, G. A. Adams IV, J. W. Horton, and B. P. Giroir Macrophage migration inhibitory factor mediates late cardiac dysfunction after burn injury Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H795 - H804. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Horton, J. Tan, D. J. White, D. L. Maass, and J. A. Thomas Selective decontamination of the digestive tract attenuated the myocardial inflammation and dysfunction that occur with burn injury Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H2241 - H2251. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Thomas, S. B. Haudek, T. Koroglu, M. F. Tsen, D. D. Bryant, D. J. White, D. F. Kusewitt, J. W. Horton, and B. P. Giroir IRAK1 deletion disrupts cardiac Toll/IL-1 signaling and protects against contractile dysfunction Am J Physiol Heart Circ Physiol, August 1, 2003; 285(2): H597 - H606. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
