BACKGROUND: We have previously shown that aspartate improves the tolerance of normal hearts to cardioplegia. The aim of this study was to investigate whether aspartate is also beneficial in the recently infarcted heart. METHODS: Myocardial infarction was produced in rats by left coronary artery ligation. Twenty hours later their hearts were perfused on an isolated working rat heart apparatus and underwent cardioplegic arrest for 30 min at 37 degrees C with or without 20 mM aspartate in the cardioplegic solution (n = 11 per group). Functional recovery and myocardial high energy phosphate levels were measured at the end of arrest and after 30 min of reperfusion. RESULTS: There was no difference in pre-arrest pump function between the untreated and aspartate-treated groups. However, after reperfusion the aspartate group generated more power (3.4 +/- 0.2 mJ/s per g) than the untreated group (2.5 +/- 0.3 mJ/s per g; P < 0.05) such that the percentage recovery of pre-arrest power in the aspartate group (67.7 +/- 3.5%) was greater than in the untreated group (53.6 +/- 4.9%; P < 0.05). The aspartate group also showed increases in aortic flow and myocardial oxygen consumption compared to the untreated group (P < 0.05). There were no between-group differences in high energy phosphate levels at the end of arrest or after reperfusion. CONCLUSION: Aspartate improves functional recovery of the recently infarcted heart during cardioplegic arrest, and therefore has potential as a useful adjunct to myocardial protection in patients with recent myocardial infarction undergoing cardiac surgery.
BACKGROUND: We have previously shown that aspartate improves the tolerance of normal hearts to cardioplegia. The aim of this study was to investigate whether aspartate is also beneficial in the recently infarcted heart. METHODS:Myocardial infarction was produced in rats by left coronary artery ligation. Twenty hours later their hearts were perfused on an isolated working rat heart apparatus and underwent cardioplegic arrest for 30 min at 37 degrees C with or without 20 mM aspartate in the cardioplegic solution (n = 11 per group). Functional recovery and myocardial high energy phosphate levels were measured at the end of arrest and after 30 min of reperfusion. RESULTS: There was no difference in pre-arrest pump function between the untreated and aspartate-treated groups. However, after reperfusion the aspartate group generated more power (3.4 +/- 0.2 mJ/s per g) than the untreated group (2.5 +/- 0.3 mJ/s per g; P < 0.05) such that the percentage recovery of pre-arrest power in the aspartate group (67.7 +/- 3.5%) was greater than in the untreated group (53.6 +/- 4.9%; P < 0.05). The aspartate group also showed increases in aortic flow and myocardial oxygen consumption compared to the untreated group (P < 0.05). There were no between-group differences in high energy phosphate levels at the end of arrest or after reperfusion. CONCLUSION:Aspartate improves functional recovery of the recently infarcted heart during cardioplegic arrest, and therefore has potential as a useful adjunct to myocardial protection in patients with recent myocardial infarction undergoing cardiac surgery.