Effects of -glutamine on Post-ischaemic Cardiac Function: Protection and Rescue

We investigated the effects of -glutamine (0–20 m ) on cardiac function. The isolated perfused working rat heart (left atrial and aortic pressures of 5 and 70 cm H2O, respectively) was subjected to 20 min of normothermic low-flow ischaemia followed by reperfusion for 35 min. In the absence of glutamine, ischaemia-reperfusion caused an immediate significant (P<0.01) fall in cardiac output from 46 to 20 ml/min, with a further deterioration to 17 ml/min at 35 min reperfusion. Ischaemia also caused a significant (P<0.05) fall in myocardial glutamate from 2.6 to 1.8μmol/g wet weight; and ischaemia-reperfusion caused significant (eachP<0.05) diminutions of myocardial ATP from 3.5 to 1.0μmol/g wet weight and phosphocreatine from 4.8 to 1.5μmol/g wet weight and resulted in significant (P<0.05) accumulation of myocardial lactate from 0.9 to 4.3μmol/g wet weight. Glutamine, present throughout the perfusion protocol (i.e. prior to ischaemia), at or above 1.25 m , prevented the post-ischaemic diminution of cardiac output and the deleterious changes in myocardial metabolites. Post-ischaemic treatment with glutamine at 2.5 m completely prevented the post-ischaemic diminution of cardiac output and restored the myocardial metabolites to normal. Conclusions: glutamine may be suitable as a cardioprotective and rescue agent. These effects may be mediated by maintenance of myocardial glutamate, ATP and phosphocreatine; and prevention of lactate accumulation.