Adenosine, added to St Thomas' hospital cardioplegic solution, improves functional recovery and reduces irreversible myocardial damage

St Thomas' Hospital cardioplegic solution is commonly used to arrest hearts during surgery. Pursuing the hypothesis that the cardioprotective properties of adenosine could be beneficial adjunct to a solution containing high K⁺ and Mg²⁺, we tested a low and a high adenosine concentration added to this cardioplegic solution, aiming at improved recovery of function and energy status. We arrested 18 working rat hearts by a 3-minute infusion with the solution without or with 50μM or 5mM adenosine. We induced 30 minute stop-flow ischemia at 37°C, followed by 10 minute washout (Langendorff mode) and 20 minute reperfusion (working heart). Control cardioplegia induced electrical arrest in 19.8 ± 5.5 s. This took 9.1 ± 0.9 (*) and 12.7 ± 1.8 s in the presence of 50 μM and 5 mM adenosine, respectively ((*)p<0.05 vs no adenosine). During reperfusion a regular electrocardiogram appeared after 1.9 ± 0.3 minutes in controls, after 1.0 ± 0.0(*) and 1.7 ± 0.2 minutes in hearts treated with low and high-dose adenosine, respectively ((*)p<0.05 vs no adenosine). After 20 minute reperfusion, the pressure-rate product had recovered to 65 ± 17% in controls, and to 107 ± 11 (*)* and 72 ± 11% of preischemic values in hearts treated with 50 μM and 5 mM adenosine, respectively ((*)*p < 0.05 vs other groups). There was a good correlation between reperfusion function recovery and the postischemic release of creatine kinase, an index for irreversible cellular damage. This association was absent with ATP content, which increased with the adenosine concentration. Our data indicate a cellular protection by adenosine with the low but not with the high-dose, unrelated to high-energy phosphate levels. Conclusion: Fifty μM adenosine, added to St. Thomas' Hospital cardioplegic solution, accelerated cardioplegic arrest, reduced creatine kinase release, and improved reperfusion function in isolated working rat hearts.