Abstract 12215: Liposome-Encapsulated Hemoglobin, Artificial O2 Carrier, Preserves VO2 and Protects Myocardium after Myocardial Ischemia/Reperfusion in the Rat
Background: We tested the hypothesis that liposome-encapsulated hemoglobin (LEH) increases blood O2 content and maintains VO2 even at low cardiac output (LOS), simultaneously preserving hemodynamics and myocardium as assisting device/medication.
Method: Effect of LEH was tested in 52 rats undergoing myocardial ischemia for 40 min and reperfusion for 40 min. Rats were randomly assigned to 3 groups after pretreatment with 10 mL/kg of LEH with high O2 affinity (LEH, P50=10 mmHg, n=19), homologous RBC at the same amount as hemoglobin (RBC, n=15), or saline (SL, n=18). Cardiac function was determined by 1) monitoring pressure-volume relationship, 2) inspiratory and expiratory O2 and CO2 gas analyses, 3) A-V blood gas analyses, and 4) evaluating end-point immunohistochemi-cally-determined area of myocardial infarction (MI).
Results: After myocardial ischemia, stroke volume, ejection fraction, stroke work and cardiac output (CO, Figure) bounced back better in SL and RBC groups than in LEH-treated rats, in which these variables remained suppressed during ischemia and reperfusion. The suppression in hemodynamic variables became significant in LEH rats compared with the SL group 20 and 40 min after reperfusion (*), when CO reversely correlated with A-V O2 content difference as if to keep their products, or VO2 constant among the groups. LEH rats had a significantly smaller MI area (9.7±9.1 mm2, P<0.05) than SL (20.8±6.2 mm2) or RBC animals (26.4±14.2 mm2).
Conclusion: The results suggest that LEH pretreatment may preserve VO2 and spare the cardiac compensatory mechanism that further aggravates ischemia, thereby preserving myocardium undergoing ischemia and reperfusion, suitable for treating LOS and priming for ventricular assist device and cardiopulmonary bypass.
- © 2011 by American Heart Association, Inc.