Cardioprotection of CPB-Induced Injuries by EGCG and Pulsatile Blood Flow

Background: Severe inborn cardiac malformations are typically corrected in cardioplegia. That implies the connection to a cardiopulmonary bypass (CPB). Negative effects can occur due to the global low-flow perfusion and the arrested heart, which may lead to ischemia-reperfusion injury. The aim of our study was to investigate the impact of pharmacologic intervention (EGCG) and different flow modulations (pulsatile vs. nonpulsatile flow) on cardiac cell damage.

Methods: We examined five experimental groups of 4-week-old piglets: control group (n = 9), control group + EGCG (n = 7), CPB pulsatile flow (n = 8), CPB nonpulsatile flow (n = 9), and CPB nonpulsatile flow + EGCG (n = 6). The CPB groups were subjected to a 90-minute CPB and a 120-minute reperfusion phase. Hemodynamic and blood parameters as well as ATP measurements were assessed. Moreover, a histological evaluation of the heart muscle was performed.

Results: Markers of apoptosis, hypoxia, nitrosative, and oxidative stresses were significantly elevated in hearts of the CPB group. Nevertheless, addition of epigallocatechin-3-gallate and CPB with pulsatile flow significantly reduced markers of myocardial damage. Furthermore, cardiac ATP levels and blood lactate were significantly lower and creatine kinase was significantly higher in the three CPB groups.

Conclusion: Epigallocatechin-3-gallate supplementation and pulsatile flow are capable to reduce CPB-induced myocardial damage.