Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction
| Autor: | Damien Barraud, Batric Popovic, Pierre Labroca, Frederique Groubatch, Sébastien Gibot, Jérémie Lemarié, Nguyen Tran, Amir Boufenzer, Marc Derive |
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| Rok vydání: | 2015 |
| Předmět: |
Cardiac function curve
0303 health sciences medicine.medical_specialty Ejection fraction biology business.industry Ischemia 030204 cardiovascular system & hematology medicine.disease 3. Good health 03 medical and health sciences 0302 clinical medicine Internal medicine Heart failure Troponin I medicine Cardiology biology.protein Creatine kinase Myocardial infarction Cardiology and Cardiovascular Medicine business Reperfusion injury 030304 developmental biology |
| Zdroj: | ESC Heart Failure. 2:90-99 |
| ISSN: | 2055-5822 |
| DOI: | 10.1002/ehf2.12029 |
| Popis: | AIMS: Limitation of ischemia/reperfusion injury is a major therapeutic target after acute myocardial infarction (AMI). Toll-like receptors are implicated in the inflammatory response that occurs during reperfusion. The triggering receptor expressed on myeloid cells (TREM)-1 acts as an amplifier of the immune response triggered by toll-like receptor engagement. We hypothesized that administration of a TREM-1 inhibitory peptide (LR12) could limit reperfusion injury in a porcine model of AMI. METHODS AND RESULTS: AMI was induced in 15 adult minipigs by a closed-chest coronary artery occlusion-reperfusion technique. Animals were randomized to receive LR12 or vehicle before reperfusion (LR12 n = 7, vehicle n = 8), and were monitored during 18 h. AMI altered hemodynamics and cardiac function, as illustrated by a drop of mean arterial pressure, cardiac index, cardiac power index, ejection fraction, and real-time pressure-volume loop-derived parameters. TREM-1 inhibition by LR12 significantly improved these dysfunctions (P |
| Databáze: | OpenAIRE |
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