|First Author, Year (Ref. #)||Experimental AMI Model||Cardioprotective Agents or Interventions||Cardioprotective Effect||Signaling Pathways|
|Schwiebert et al., 2010 (58)||In vivo rat||Xenon (20%) at reperfusion|
Hypothermia (34°C) at reperfusion
|Additive effects on reducing MI size||Not investigated|
|Alburquerque-Béjar et al., 2015 (8)||In vivo pig||RIPerC|
GIK or exenatide at reperfusion
|Additive effects of RIPerC with either insulin or exenatide||RIPerC—less oxidative stress and reduced eNOS uncoupling|
GIK and exenatide—shift to glycolysis
|Sun et al., 2016 (59)||In vivo mice||NaHS (H2S donor) at reperfusion|
SNAP (NO donor) at reperfusion
|Additive effects on reducing MI size||NaHS—S-sulfhydration|
Experimental studies illustrating the potential for additive cardioprotective effects with 2 or more agents or interventions given acutely in combination during ischemia or shortly after reperfusion. Only those agents given in the short term in combination during ischemia or shortly after reperfusion, and demonstrating a reduction in infarct size that is additive are shown.
AMI = acute myocardial infarction; eNOS = endothelial nitric oxide synthase; GIK = glucose/insulin/potassium; MI = myocardial infarction; NaHS = Sodium hydrosulfide; NO = nitric oxide; RIPerC = remote limb ischemic per-conditioning during cardiac ischemia; SNAP = S-nitroso-N-acetylpenicillamine.