Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl

Departments of 1 Physiology II and 2 Surgery III, Nara Medical University, Kashihara, Nara 634-8521, Japan Submitted 9 February 2004 ; accepted in final form 21 April 2004 We hypothesized that there are no differences in left ventricular (LV) mechanoenergetics between after hyperpolarized cardioplegic arrest by nicorandil (nicorandil arrest) and after depolarized one by high potassium chloride (KCl arrest). The aim of the present study was to test this hypothesis using LV curved end-systolic pressure-volume relation (ESPVR) and linear pressure-volume area (PVA)-myocardial oxygen consumption per beat (V O 2 ) relation. All hearts underwent 30 min global ischemia (30°C) after infusion of 5 ml of cardioplegia. Cardioplegia consisted of either 30 mmol/l KCl (7 hearts) or nicorandil (100 µmol/l) in Tyrode solution (6 hearts). After a 30-min blood reperfusion, ESPVR and V O 2 -PVA relation were assessed again. Mean end-systolic pressure (ESP mLVV ) and mean PVA at midrange LV volume (PVA mLVV ) significantly ( P < 0.05) decreased to 79.1 ± 13.4% and 85.4 ± 17.1% of control after KCl arrest and to 85.3 ± 14.8% and 86.4 ± 16.9% of control after nicorandil arrest. There were no significant differences in both decreases of mean ESP mLVV and PVA mLVV between each arrest. The slopes of V O 2 -PVA relations were also unchanged after each arrest. There was a significant ( P < 0.005) difference in the decreases of mean V O 2 intercepts of V O 2 -PVA relations between post-KCl arrest (73.9 ± 8.2% of control) and post-nicorandil arrest (99.2 ± 10.1% of control), however. Proteolysis of -fodrin due to Ca 2+ overload was significantly marked after KCl arrest. The present results indicate that the total calcium handling in excitation-contraction coupling is transiently impaired after KCl arrest, whereas it is unchanged after nicorandil arrest. This suggests the possibility that nicorandil is a better cardioplegia than KCl. excitation-contraction coupling; -fodrin; left ventricle; myocardial oxygen consumption Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp ).