Anesthetic Preconditioning Attenuates Mitochondrial Ca2+ Overload During Ischemia in Guinea Pig Intact Hearts: Reversal by 5-Hydroxydecanoic Acid

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Abstract
Cardiac ischemia/reperfusion (IR) injury is associated with mitochondrial (m)Ca2+ overload. Anesthetic preconditioning (APC) attenuates IR injury. We hypothesized that mCa2+ overload is decreased by APC in association with mitochondrial adenosine triphosphate-sensitive K+ (mKATP) channel opening. By use of indo-1 fluorescence, m[Ca2+] was measured in 40 guinea pig Langendorff-prepared hearts. Control (CON) hearts received no treatment for 50 min before IR; APC hearts were exposed to 1.2 mM (8.8 vol%) sevoflurane for 15 min; APC + 5-hydroxydecanoate (5-HD) hearts received 200 μM 5-HD from 5 min before to 15 min after sevoflurane exposure; and 5-HD hearts received 5-HD for 35 min. Sevoflurane was washed out for 30 min and 5-HD for 15 min before 30 min of global ischemia and 120 min of reperfusion. During ischemia, the peak m[Ca2+] accumulation was decreased by APC from 489 ± 37 nM (CON) to 355 ± 28 nM (P 2+