Continuous warm versus intermittent cold cardioplegic infusion: A comparison of energy metabolism, sodium-potassium adenosine triphosphatase activity, and postischemic functional recovery in the blood-perfused rat heart

Abstract

We used metabolic, enzymatic, and functional end points to compare the protective properties of continuous warm and intermittent cold cardioplegic infusion in isolated, blood-perfused rat hearts. After excision, hearts ( n = 12 per group) were preserved for 3 hours by one of the following cardioplegic procedures: (1) continuous infusion of warm (37º C) blood cardioplegic solution prepared by mixing Fremes' solution with rat arterial blood in a ratio of 1:4, (2) continuous infusion of warm (37º C) crystalloid cardioplegic solution prepared by mixing Fremes' solution with bicarbonate buffer solution in a ratio of 1:4, or (3) intermittent infusion of cold (20º C) St. Thomas' Hospital cardioplegic solution number 2 infused for 3 minutes every 30 minutes during a 3-hour period of ischemia. In the continuous-infusion cardioplegic groups, the solution was infused through the aorta at a flow rate of 0.8 ml · min -1 · gm -1 heart. At the end of the 3-hour preservation period, myocardial sodium-potassium adenosine triphosphatase activity (an index of ion-exchange activity) was assessed in six hearts in each group. The remaining hearts in each group were then aerobically perfused at 37º C with arterial blood (from a support rat) for a further 50 minutes, during which time they were atrially paced at 320 beats/min. At the end of this period, left ventricular developed and end-diastolic pressures were assessed with an intraventricular balloon; the hearts were then freeze-clamped and taken for the measurement of tissue adenosine triphosphate and creatine phosphate content. Hearts ( n = 6) aerobically perfused with blood for 50 minutes (no cardioplegic infusion) served as control preparations. At a balloon volume of 180 μl, the mean final values for left ventricular developed pressure in the continuous warm blood, continuous warm crystalloid, and intermittent cold cardioplegic groups were 98 ± 5 mm Hg ( p < 0.05), 70 ± 5 mm Hg, and 78 ± 5 mm Hg, respectively. This was compared with 122 ± 5 mm Hg in control hearts ( p < 0.05 vs the rest). For left ventricular end-diastolic pressure, the corresponding values were 33 ± 3 mm Hg, 32 ± 6 mm Hg, and 14 ± 4 mm Hg ( p < 0.05), respectively. The control value was 16 ± 3 mm Hg ( p < 0.05 vs continuous warm blood and continuous warm crystalloid groups). Tissue content of adenosine triphosphate was similarly reduced to approximately 50% of control values in all groups, and creatine phosphate content fully recovered in all groups. Sodium-potassium adenosine triphosphatase activity was poorly preserved in continuous warm crystalloid–treated hearts (0.012 ± 0.003 vs 0.030 ± 0.008 μmol inorganic phosphate · mg -1 · min -1 in control preparations, p < 0.05), whereas in continuous warm blood and intermittent cold cardioplegic groups (0.032 ± 0.015 and 0.031 ± 0.013 μmol inorganic phosphate · mg -1 · min -1) there was no significant loss of activity. In conclusion, (1) none of the procedures conferred complete protection, (2) continuous warm blood cardioplegic infusion provided superior preservation of systolic function and intermittent cold cardioplegic infusion afforded superior protection with respect to diastolic function, and (3) both continuous warm blood and intermittent cold cardioplegic infusion similarly protected sodium-potassium adenosine triphosphatase activity and tissue adenosine triphosphate and creatine phosphate content, whereas continuous warm crystalloid cardioplegic infusion afforded poor preservation of sodium-potassium adenosine triphosphatase activity. In general, the poorest protection was afforded by continuous warm crystalloid cardioplegic infusion. (J T HORAC C ARDIOVASC S URG 1996;112:797-805)