Adenosine cardioplegia: Reducing reperfusion injury of the ischaemic myocardium?

Hyperkalaemia-induced hypopolarization of the sarcolemnal membrane during standard crystalloid cardioplegic arrest potentiates calcium influx during reperfusion and is associated with depletion of high-energy phosphate reserves. Adenosine has been shown to induce fast cardiac arrest whilst preserving membrane hyperpolarization in an isolated rat heart model [14]. In this study we compared the efficacy of adenosine, both as an arresting agent and as an ultrastructural, haemodynamic and high-energy phosphate preserving agent, in an in situ global ischemia model in the baboon with St. Thomas’ Hospital solution No. 2 (ST2; n = 8) and with Krebs-Henseleit buffer (KHB; n=7). The addition of 10 mM adenosine to the non-cardioplegic KHB (ADO; n = 8) improved haemodynamic recovery significantly in terms of cardiac index (91.6% +7.2 vs 59.9% ±9.9) and stroke volume index (101.6% +8.9 vs 55.6% ±10.0) and was not statistically distinguishable from the ST2 with regard to cardiac index (91.6% ±7.2 vs 94.8% ±5.8), stroke volume index (101.6% ±8.9 vs 114.0% ±8.3) or left ventricular dP/dt (73.1% ±9.9 vs 87.0% ±12.4). Adenosine triphosphate was best preserved with ADO (103.5% ± 21.1 vs 67.9% ± 9.3 and 48.5% ± 8.7) although this was not statistically significant. This suggests therefore that the mechanism of cardioprotection by adenosine occurs by means other than its role as high-energy phosphate precursor. © 1991 Springer-Verlag.