Background: Ischaemia--reperfusion damage causes injury of all heart cells. Loss of endothelium function and biologically active substances secreted by it can be essential to development of the damage. Ischaemia and reperfusion decreases the release of nitric oxide, which influences postischaemic coronary flow and return of ventricular function. Administration of L-arginine to cardioplegic and reperfusion solution can improve protection of heart and cause the return of left ventricular function after hypothermic ischaemia through preservation of endothelial cell functions and increase of release of nitric oxide.
Objective: How addition of L-arginine to cardioplegic solution influences oxygen consumption by myocardium and its postischaemic haemodynamic function.
Methods: The research was conducted on isolated heart model of 56 rats, divided into seven equal groups. The hearts were prepared with modified Neely method and were perfused with the use of apparatus in accordance with modified Langendorf method. The research was carried out in the following order: initial perfusion of the non-working and working heart, perfusion with cardioplegic solution, cold cardioplegic arrest and reperfusion of the non-working heart.
Results: During initial perfusion, oxygen consumption was comparable in all groups. During cardioplegic perfusion, oxygen consumption was reduced in every group. At the time of reperfusion of non-working heart model, consumption of oxygen was increased. During reperfusion of the working heart, the lowest oxygen consumption was noted in group P, the highest in group DI. The decrease in cardiac output during postischaemic period was noted in control group and groups where L-arginine was added to reperfusion solution.
Conclusion: Addition of L-arginine to cardioplegic solution significantly decreases oxygen consumption by myocardium. L-arginine added to cardioplegic solution improves postischaemic haemodynamic function of heart.