title: Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl.
abstract: 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 min global ischemia (30 degrees C) after infusion of 5 ml of cardioplegia. Cardioplegia consisted of either 30 mmol/l KCl (7 hearts) or nicorandil (100 micromol/l) in Tyrode solution (6 hearts). After a 30-min blood reperfusion, ESPVR and VO2-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 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 post-KCl arrest (73.9 +/- 8.2% of control) and post-nicorandil arrest (99.2 +/- 10.1% of control), however. Proteolysis of alpha-fodrin due to Ca2+ 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.
authors.affiliation: Department of Physiology II, Nara Medical University, Kashihara, Nara 634-8521, Japan.
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Yoshikawa
authors.forename: Susumu
authors.initials: S
authors.lastname: Sakata
authors.forename: Chikako
authors.initials: C
authors.lastname: Takenaka
authors.forename: Hiroji
authors.initials: H
authors.lastname: Hagihara
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Ohga
authors.forename: Takehisa
authors.initials: T
authors.lastname: Abe
authors.forename: Shigeki
authors.initials: S
authors.lastname: Taniguchi
authors.forename: Miyako
authors.initials: M
authors.lastname: Takaki
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D002352:Carrier Proteins / Q000378:metabolism; D004594:Electrophysiology; D004734:Energy Metabolism / Q000187:drug effects*; D006324:Heart Arrest, Induced; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D020108:Nicorandil / Q000494:pharmacology*; D010101:Oxygen Consumption; D010447:Peptide Hydrolases / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume; D016277:Ventricular Function, Left / Q000187:drug effects*; D013049:Spectrin
chemical_list: D002118:Calcium; D002314:Cardioplegic Solutions; D002352:Carrier Proteins; D008840:Microfilament Proteins; D020108:Nicorandil; D010447:Peptide Hydrolases; D011189:Potassium Chloride; D013049:Spectrin