Table 1. Microvascular obstruction triggers: analysis of experimental data.
Hypothetical trigger | Species | Experimental model | Effect | Ref. |
Endothelial cell injury | Dog | CAO in vivo | Ultrastructural damage of cardiomyocytes, microvascular injury | [22] |
Rat | Isolated heart | Decreased capillary lumen, endothelial edema |
[24] |
|
Guinea pig | Isolated heart | Glycocalyx injury, endothelial cell dysfunction | [25–26] | |
Microembolization and microthrombi | Dog | CAO and reperfusion in vivo | Insignificant decrease in CBF | [27] |
Rabbit | Isolated heart | MVO occurred without thrombosis, platelets and leukocytes | [32] | |
Rat | Isolated heart | No-reflow area formation | [33] | |
Rat | Isolated heart | CBF decreased in LV outer layers | [34–35] | |
Leukocyte invasion | Rat | Isolated heart | Decrease in the number of perfused capillaries (approximately 62%) | [81] |
Rabbit | CAO and reperfusion in vivo | CY1503 did not reduce infarct size or no-reflow |
[82] |
|
Rat | Isolated heart | Platelets and neutrophils injured coronary arteries in reperfusion | [83] | |
Dog | CAO and reperfusion in vivo | R15.7 reduced infarct size and the no-reflow area | [53] | |
Human | HUVEC, Hypoxia/reoxygenation | Induction of adhesion of neutrophils, ZM-241385 abolished adhesion |
[66] |
|
Rat | CAO and reperfusion in vivo | Correlation of MPO with no reflow area | [84] | |
Platelet aggregation | Rabbit | CAO and reperfusion in vivo | Platelets were involved in the pathogenesis of MVO in animals with hypercholesterolemia | [37] |
Minipig | CAO and reperfusion in vivo | Tirofiban reduced the MVO area. A Combination of clopidogrel + aspirin had no effect on the MVO area | [39] | |
Rat | Isolated heart | An increase in CPP |
[40] |
|
Rat | Isolated heart | Platelets reduced infarct size, activated ERK1/2 |
[41] |
|
Coronary artery dysfunction | Dog | CAO and reperfusion in vivo | Decreased acetylcholine-induced vasodilation. Verapamil reduced impaired vascular relaxation. |
[42] |
Dog | CAO and reperfusion in vivo | Disruption of endothelium-dependent vasodilation of the infarcted coronary artery | [43] | |
Cat | CAO and reperfusion in vivo | Decrease in vasodilation caused by acetylcholine. A23187-induced vasodilation was reduced by reperfusion. SOD improved acetylcholine-induced vascular relaxation | [44] | |
Pig | Isolated intramyocardial ring of arteries | Reduced vasodilation triggered by bradykinin | [46] | |
Pericytes | Rat | CAO and reperfusion in vivo | I/R blocked blood flow in 40% of capillaries | [47] |
Mouse | CAO and reperfusion in vivo | GPR39 knockout reduced the no-reflow area, VC43 also reduced MVO | [48] |