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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2013 May;61(5):369–377. doi: 10.1097/FJC.0b013e318285f55b

Figure 7.

Figure 7

Effect of APC with isoflurane on H2O2 induced stress and survival of isolated cardiomyocytes from WT (n=9) and Kir6.2 KO (n=6) hearts. Percent cell death was determined in four experimental groups: time control (Time Ctrl), oxidative stress with H2O2 (Stress), stress following cell exposure to isoflurane (APC), and stress in isoflurane-pretreated myocytes during blockade of KATP channels with 5HD (APC+5HD). Data are mean±SEM, *P< 0.05 vs. Time Ctrl; #P< 0.05 vs. Stress; §P< 0.05 vs. APC. Left panel: Pretreatment with isoflurane protected WT myocytes from stress. Blockade of mitoKATP channels with 5HD abolished this protection. Right panel: Pretreatment with isoflurane protected Kir6.2 KO myocytes from stress. However, isoflurane-induced protection of Kir6.2 KO myocytes was not altered by 5HD (APC vs. APC+5HD).