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Ann Thorac Surg 1995;59:1541-1548
© 1995 The Society of Thoracic Surgeons

Articles

Differing protection with aspartate and glutamate cardioplegia in the isolated rat heart

DSc Oleg I. Pisarenkoa,b, FRACS Franklin L. Rosenfeldta,b,*, BApplSc Lesley Langleya,b, FRCPA Robert A.J. Conyersa,b, PhD Stephen M. Richardsa,b

a Baker Medical Research Institute, Melbourne, Australia
b Cardiology Research Centre, Moscow, Russia

Accepted for publication March 7, 1995.

* Address reprint requests to Dr Rosenfeldt, Baker Medical Research Institute, Commercial Rd, Prahran, Victoria 3181, Australia.

Aspartate and glutamate each have been shown to improve cardiac recovery after hypoxia or ischemia under normothermic conditions, but whether their effects are additive and to what extent they are modified by hypothermia has not been studied systematically. We set out to compare the individual and combined protective effects of aspartate and glutamate during cardioplegic arrest under normothermic and hypothermic conditions in the rat. Using isolated working rat hearts, functional and metabolic recovery was assessed after 0.5 hours of potassium arrest at 37°C or 5 hours at 2°C in control hearts (C) and in hearts in which 20 mmol/L glutamate (G), 20 mmol/L aspartate (A), or both (A + G) was added to the cardioplegic solution. Under normothermic conditions, percentage recovery of prearrest work (mean ± standard error of the mean) was as follows: C = 31.7 ± 2.8, G = 34.8 ± 0.2, A = 49.6 ± 2.8*, A + G = 53.7 ± 2.3*. Under hypothermic conditions, the values were as follows: C = 40.4 ± 4.0, G = 45.2 ± 2.3, A = 59.4 ± 1.8*, A + G = 54.1 ± 1.2* (*p < 0.01 versus C and G). Recovery of postischemic high-energy phosphate content followed the same pattern: A = A + G > G or C. Measurement of postischemic myocardial content of amino acids showed that recovery of function and energy status correlated with maintenance of myocardial levels of aspartate (r = 0.9; p < 0.01) but not glutamate. We conclude that aspartate cardioplegia is protective against ischemia under normothermic and hypothermic conditions due to its ability to augment postischemic myocardial aspartate levels.




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