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Ischemic Preconditioning, mitoKATP Channel and In Vivo Myocardial Oxygen Consumption
Author(s) -
He Guanglong,
Zhu Xuehai,
Liu Bin,
Zhou Shaotang,
Chen YeongRenn,
Zweier Jay L.
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a866-a
Ischemic preconditioning (IPC) protects the postischemic heart. We determine this protection is due to opening of mitoK ATP channel and thereby decreased formation of ROS/RNS after reperfusion. Four groups of mice: control (I/R, mouse heart subjected to 30 min ischemia followed by 60 min reperfusion), preconditioned (IPC+I/R, 3 cycles of 5 min coronary occlusion/5 min R), diazoxide and 5‐hydroxydecanoate (5‐HD) treated (DIZ+I/R, 5‐HD+IPC+I/R), N=7. In vivo myocardial PO 2 was monitored by electron paramagnetic resonance oximetry. No difference was found in PO 2 at baseline and during 30 min I among all the groups. Myocardial PO 2 at 60 min R increased significantly above the preischemic value in I/R but not in IPC+I/R. With treatment of diazoxide, there was no overshoot of PO 2 , but when treated with 5‐HD, the overshoot of PO 2 re‐appeared in the preconditioned group. After 60 min R, activities of cytochrome c oxidase (CcO) and NADH dehydrogenase (NADH‐DH) were reduced in I/R and 5‐HD+IPC+I/R but conserved in IPC+I/R and DIZ+I/R. Nitrotyrosine formation was observed in I/R and 5‐HD+IPC+I/R but undetectable in IPC+I/R and DIZ+I/R after 60 min R. Thus in vivo, IPC markedly attenuated ROS/RNS generation possibly through the opening of mitoK ATP channel, up‐regulated O 2 consumption, and conferred protection in the postischemic heart with preserved mitochondrial O 2 metabolism due to conserved CcO and NADH‐DH activities.