Submitted on February 9, 2004
Accepted on April 21, 2004
Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl
Shuichi Kobayashi1, Yoshiro Yoshikawa2, Susumu Sakata1, Chikako Takenaka1, Hiroji Hagihara3, Yoshimi Ohga1, Takehisa Abe2, Shigeki Taniguchi1, and Miyako Takaki1*
1 Department of Physiology II, Nara Medical University, Kashihara, Nara, Japan
2 Department of Surgery III, Nara Medical University, Kashihara, Nara, Japan
3 Department of Physiology II, Nara Medical University, Kashihara, Nara, Japan; Department of Surgery III, Nara Medical University, Kashihara, Nara, Japan
* To whom correspondence should be addressed. E-mail: mtakaki{at}naramed-u.ac.jp.
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 (VO2) relation. All hearts underwent 30-minute global ischemia (30°) 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 30-minute blood-reperfusion, ESPVR and VO2- PVA relation were assessed again. Mean end-systolic pressure (ESPmLVV) and mean PVA at midrange LV volume (PVAmLVV) 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 ESPmLVV and PVAmLVV between each arrest. The slopes of VO2-PVA relations were also unchanged after each arrest. There was a significant (P<0.005) difference in the decreases of mean VO2 intercepts of VO2-PVA relations between after KCl arrest (73.9 ± 8.2% of control) and after nicorandil arrest (99.2 ± 10.1% of control), however. Proteolysis of 
-fodrin due to Ca2+ overload was significantly marked after KCl arrest. 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.
