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Page 6 of 21 Bradshaw et al. Vessel Plus 2023;7:35 https://dx.doi.org/10.20517/2574-1209.2023.121

[116]
Oldenburg et al., 2003 Mouse heart proteins The K channel opener P1075 opened mitoK channels and was cardioprotective via this action
ATP ATP
[120]
Dzeja et al., 2003 Rat heart mitochondria; rat heart, Langendorff Production of ROS and degradation of nucleotides were reduced by diazoxide, resulting in cellular protection
[127]
Uchiyama et al., 2003 Rat heart, Langendorff Pharmacological preconditioning involved protein kinase C, and this involves adenosine, mitoK activation, and nitric oxide
ATP
[100]
Rousou et al., 2004 Rabbit heart, Langendorff Diazoxide added to cardioplegia was cardioprotective via preservation of mitochondrial physiology
[86]
Wakahara et al., 2004 Rat heart, Langendorff The mitoK ATP channel blocker and antioxidant abolished postischemic recovery of contractile function by diazoxide but not by
IPC
[111]
Ardehali et al., 2004 Rat liver mitochondria The mitoK channel composition includes SDH as a component
ATP
[125]
Eaton et al., 2005 Rat heart, Langendorff IPC and diazoxide appeared to have protective effects via a mechanism involving reactive oxygen species generation before
ischemia onset
[77]
Mizutani et al., 2005 Rabbit myocytes Cellular swelling was detrimental for cardiac contractility, and diazoxide attenuated swelling
[122]
Busija et al., 2005 Piglet mitochondria ROS production was increased by diazoxide, and this was likely via inhibition of SDH
[76]
Deja et al., 2006 Human atrial trabeculae Diazoxide given throughout an ischemic episode led to maximal protection, suggesting diazoxide could be a helpful additive to
cardioplegia
Yonemochi et al., Rat myocytes The mitoK ATP channels acted as a trigger and mediator of cardioprotection through ΔΨm loss
[130]
2006
[61]
Prasad et al., 2006 Mouse heart, Langendorff The sarcolemmal K channel appeared necessary for exaggerated swelling and reduced contractility after cardioplegia
ATP
[82]
Mizutani et al., 2006 Rabbit myocytes Diazoxide abolished the swelling and reduced contractility caused by St. Thomas’ cardioplegia
[128]
Kim et al., 2006 Rat myocytes Diazoxide cardioprotection appeared to occur via protein kinase C pathway
[106]
Al-Dadah et al., 2007 Rabbit myocytes The attenuation of both swelling and reduced contractility by diazoxide was unchanged by adding K blockers
ATP
[44]
Flagg et al., 2008 Mouse myocytes Atrial and ventricular K channels have fundamentally different structures, including a difference in SUR1
ATP
[110]
Wojtovich et al., 2008 Rat heart, Langendorff; rat mitochondria MitoK activation in IPC may involve complex II inhibition by malonate
ATP
[138]
Deja et al, 2009 Humans Adding diazoxide to cardioplegia improved myocardial protection
[41]
Sellitto et al., 2010 Mouse myocytes Diazoxide did not open the ventricular sarcolemmal K channel. The mechanism involved a pathway involving SUR1
ATP
[108]
Zhang et al., 2011 Mouse myocytes HMR 1098, a K channel blocker, is nonspecific. Methods such as genetic deletion are needed to confirm channel subunit
ATP
involvement in cardioprotection
[107]
Maffit et al., 2012 Human myocytes Diazoxide lessened swelling with or without inhibition of K channel
ATP
[60]
Anastacio et al., 2013 Mouse mitochondria The benefit of diazoxide during stress involves inhibition of SDH and possibly opening of mitoK
ATP
[103]
Anastacio et al., 2013 Mouse mitochondria Inhibition of mitoK channels with 5-HD reduced mitochondrial volume during stress, indicating a role for mitoK channel
ATP ATP
with diazoxide
[124]
Anastacio et al., 2013 Mouse mitochondria The cardioprotection of diazoxide was independent of the SUR1 subunit of the K ATP channel, though it may occur via inhibition of
the SDH enzyme complex
[117]
Garlid et al., 2013 Rat heart mitochondria The mitochondrial ROS involved in cardioprotection by IPC and diazoxide appeared to be hydroxyl radical (HO·)
[73]
Janjua et al., 2014 Mouse ventricular myocytes, human atrial myocytes Diazoxide was only cardioprotective if administered at the onset of stress and not if administered after onset of stress
[62]
Henn et al., 2015 Mouse ventricular mitochondria The subunits Kir1.1, Kir3.1, and Kir3.4 all could possibly be involved in cardioprotection caused by diazoxide
[63]
Henn et al., 2015 Mouse myocytes The Kir6.1 subunit improved myocyte tolerance to stress, but the mechanism was unknown
[65]
Henn et al., 2016 Mouse myocytes The negative effects of cardioplegia were decreased in Kir6.1GOF myocytes