Suppression of myocardial mitochondrial respiratory function in acute failing hearts made by a short-term Ca2+ free, high Ca2+ coronary perfusion.
We made acute cardiac failure in excised cross-circulated canine hearts by a new coronary perfusion protocol consisting of Ca2+ free Tyrode perfusion for the first 10 min, high Ca2+ (16 mmol/l) Tyrode perfusion for the next 5 min, and normal Tyrode perfusion for the last 5 min interrupting blood cross circulation. After 50 min from the blood recirculation, left ventricular contractility was stably depressed to 60% of control. We studied mechanoenergetics of these acute failing hearts for the next 1-3 h. Then, we prepared mitochondria from these excised failing hearts and the support dogs' normal hearts to examine their mitochondrial respiratory function by the respiratory control index (RCI) and the oxygen consumption rate in state III (State III O2). RCI and State III O2 were significantly smaller in the failing hearts than in the normal hearts. However, sham protocol consisting of normal Tyrode coronary perfusion for 20 min did not affect RCI and State III O2. These results revealed that the mitochondrial respiratory function was moderately impaired in these acute failing hearts made by the new short-term Ca2+ intervention. However, no ultrastructural injuries of mitochondria were detected in these failing hearts.
Second Department of Physiology, Okayama University Medical School, Japan.
M
M
Takaki
D D
DD
Zhao
L Y
LY
Zhao
J
J
Araki
M
M
Mori
H
H
Suga
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D019069:Cell Respiration / Q000187:drug effects; D004285:Dogs; D004579:Electron Transport / Q000187:drug effects; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000648:ultrastructure; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D010477:Perfusion
D002118:Calcium