| First Author | Thomas JA | Year | 2002 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 283 |
| Issue | 4 | Pages | H1645-55 |
| PubMed ID | 12234819 | Mgi Jnum | J:108049 |
| Mgi Id | MGI:3622941 | Doi | 10.1152/ajpheart.01107.2001 |
| Citation | Thomas JA, et al. (2002) TLR4 inactivation and rBPI(21) block burn-induced myocardial contractile dysfunction. Am J Physiol Heart Circ Physiol 283(4):H1645-55 |
| abstractText | Both large burns and severe gram-negative sepsis are associated with acute myocardial contractile dysfunction. Because 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, postburn 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 4 (TLR4), a critical element of the mammalian endotoxin receptor, were resistant to postburn myocardial contractile dysfunction. In the second model, starting 30 min or 4 h after burn injury, rats were infused with recombinant bactericidal/permeability-increasing protein (rBPI(21)), a protein that binds and neutralizes endotoxin. Hearts from rBPI(21)-treated animals were completely protected from postburn contractile impairment. Because 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. |
