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1 Anesthesiology, UCSD, San Diego, California, United States; Anesthesiology, VA San Diego Healthcare System, San Diego, California, United States
* To whom correspondence should be addressed. E-mail: droth{at}ucsd.edu.
Delayed cardiac protection mediated by 12-lipoxygeanse (12-LO) expression and activity has been linked to opioid receptor stimulation. The role of 12-LO in volatile anesthetic-induced delayed cardiac protection has not been determined. We tested the hypothesis that expression and activity of 12-LO mediates delayed cardiac protection induced by isoflurane in the mouse heart in vivo. Mice were pretreated with 1.4% isoflurane for 30 min and allowed to recover for 1, 12 or 24 h. Immunoblot analysis showed isoflurane significantly enhanced 12-LO protein expression at 12 and 24 h post isoflurane exposure, and this induction of 12-LO was confirmed by immunohistochemistry of whole heart sections at 24 h. The induced protein expression appeared to be localized to intercalated disc regions adjoining adjacent cardiac myocytes. Additionally, mice ± isoflurane (24 h previously) were subjected to 30 min coronary artery occlusion followed by 2 hours of reperfusion in the presence and absence of a 12-LO inhibitor. Isoflurane reduced infarct size (27.1 ± 2.2% [n = 8] of the area at risk) compared to the control group (44.6 ± 3.6% [n = 8]). Baicalein (3 mg/kg), a selective 12-LO inhibitor, blocked the delayed protective effects of isoflurane pretreatment on infarct size (40.6 ± 3.6% [n = 8]). These data suggest that 12-LO is an important mediator of isoflurane-induced delayed preconditioning.
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