Table 1. Microvascular obstruction triggers: analysis of experimental data (continued).

Hypothetical trigger	Species	Experimental model	Effect	Ref.
CAO: coronary artery occlusion; CBF: coronary blood flow; CPP: coronary perfusion pressure; ERK1/2: extracellular signal-regulated kinase 1/2; HINT2: histidine triad nucleotide-binding 2; HUVEC: human umbilical vein endothelial cells; LV: left ventricle; MPO: marker of neutrophil myeloperoxidase; MVO: microvascular obstruction; NLRP3: (NOD)-like receptor pyrin domain containing 3; ROS: reactive oxygen species; SOD: superoxide dismutase; tBHP: tert-butyl hydroperoxid.
ROS, Ca2+ overload	Rat	Isolated heart	Acetylcholine-induced vasodilation decreased after reperfusion following tBHP administration	[51]
	Rabbit	CAO and reperfusion in vivo	Gallopamil and SOD reduced the no-reflow area	[52]
	Dog	CAO and reperfusion in vivo	CBF decreased after three hours of reperfusion. Clentiazem reduced the no-reflow zone and reduced infarct size	[54]
	Rabbit	CAO and reperfusion in vivo	Verapamil had no effect on the no-reflow area and infarct size	[55]
	Rat	CAO and reperfusion in vivo	Verapamil reduced infarct size	[56]
	Pig	CAO and reperfusion in vivo	Diltiazem and verapamil reduced the no-reflow area but did not affect infarct size	[57]
	Mouse	CAO and reperfusion in vivo	HINT2 overexpression promoted a decrease in the no-reflow area	[58]
	Minipig	CAO and reperfusion in vivo	Fosinopril and valsartan reduced the MVO area	[64]