cardiovascular system
• following ischemia-reperfusion, hearts of untreated mice exhibit a slightly higher % of lactate dehydrogenase (LDH) release than those of wild-type controls, indicating more heart injury
• hearts are resistant to diazoxide-induced cardioprotection from reperfusion damage, showing a significantly higher % of LDH release and infarct size than similarly treated wild-type hearts
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cellular
• whereas energized mitochondria from wild-type livers show ATP- and diazoxide-sensitive K+ uptake, neither ATP nor diazoxide are able to alter K+ fluxes in mutant mitochondria, indicating lack of mitochondrial KATP activity
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homeostasis/metabolism
• following ischemia-reperfusion, hearts of untreated mice exhibit a slightly higher % of lactate dehydrogenase (LDH) release than those of wild-type controls, indicating more heart injury
• hearts are resistant to diazoxide-induced cardioprotection from reperfusion damage, showing a significantly higher % of LDH release and infarct size than similarly treated wild-type hearts
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