The fibrin-derived peptide Bbeta(15-42) significantly attenuates ischemia-reperfusion injury in a cardiac transplant model

Transplantation. 2010 Apr 15;89(7):824-9. doi: 10.1097/tp.0b013e3181ccd822.

Abstract

Background: The inflammatory response after prolonged ischemia and subsequent reperfusion leads to increased risk of primary organ dysfunction after cardiac transplantation. It has been demonstrated that the fibrin-derived peptide Bbeta(15-42) (also called FX06) reduces infarct size in coronary artery occlusion/reperfusion models by inhibition of leukocyte migration. Further, Bbeta(15-42) preserves endothelial barrier function. The purpose of this study was to investigate whether Bbeta(15-42) has a protective effect in cardiac allografts exposed to prolonged global ischemia and subsequent in vivo reperfusion.

Methods: Hearts of male Lewis rats were flushed and stored in cold Bretschneider preservation solution for 4 or 8 hr. Bbeta(15-42) was administered before being transplanted into syngeneic recipients. Serum samples were collected for troponin-T measurements. Hemodynamic performance was evaluated after a reperfusion period of 24 hr. Morphologic quantification of myocardial necrosis was performed in hearts exposed to 24 hr or 10 days of reperfusion.

Results: Allografts from Bbeta(15-42) treated animals showed less myocardial necrosis (2.5% +/- 2.5% vs. 18.4% +/- 9.2%, P=0.0019) and decreased values of cardiac troponin-T (1.1 +/- 0.6 ng/mL vs. 2.7+/-2.3 ng/mL, P=0.0045), reduced number of infiltrating leukocytes (7.2 +/- 13.6 vs. 49.2 +/- 34.9 per high powerfield, P=0.0045), and superior cardiac output (78.1 +/- 1.8 mL/min vs. 21.7 +/- 4 mL/min, P = 0.0034). Hearts exposed to 0 and 4 hr of ischemia showed no severe signs of myocardial damage.

Conclusion: Bbeta(15-42) ameliorates the ischemia-reperfusion injury in transplanted hearts during extended cold ischemia by reduction of infiltrating leukocytes. This experimental protocol provides evidence that Bbeta(15-42) may play a useful role in organ preservation, but clinical evaluation is warranted.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / blood
  • Cardiac Output / drug effects
  • Cardiotonic Agents / pharmacology*
  • Cell Movement / drug effects
  • Cold Ischemia / adverse effects*
  • Fibrin Fibrinogen Degradation Products / pharmacology*
  • Heart Transplantation / adverse effects*
  • Leukocytes / drug effects
  • Leukocytes / pathology
  • Male
  • Models, Animal
  • Myocardial Reperfusion Injury / blood
  • Myocardial Reperfusion Injury / etiology
  • Myocardial Reperfusion Injury / physiopathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Myocardium / metabolism
  • Myocardium / pathology
  • Necrosis
  • Organ Preservation Solutions / pharmacology
  • Peptide Fragments / pharmacology*
  • Rats
  • Rats, Inbred Lew
  • Time Factors
  • Transplantation, Homologous
  • Troponin T / blood
  • Ventricular Function, Left / drug effects
  • Ventricular Pressure / drug effects

Substances

  • Biomarkers
  • Cardiotonic Agents
  • Fibrin Fibrinogen Degradation Products
  • Organ Preservation Solutions
  • Peptide Fragments
  • Troponin T
  • fibrinogen Bbeta (15-42)