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. 2019 May 7;115(13):1918–1932. doi: 10.1093/cvr/cvz118

Figure 6.

Figure 6

Myocardial endothelial cells are more susceptible than myocytes to oxidative stress following acute IRI but this injury can be reduced by HSPCs. (A) Flow cytometric gating strategy used for identifying oxidatively damaged (8-OHdG+) ECs (CD31+; left) and myocytes (cTnT+; right) in digested whole hearts. (B) Percentage of each cell type obtained from a total of 30 000 events. A greater yield of myocytes is obtained (n = 5; IR+HSPC groups n = 4). (C) Endothelial ICAM-1 expression increases during ischaemia and further during reperfusion. This is reduced by HSPCs injected at the onset of reperfusion (*P < 0.05, **P < 0.01 vs. sham; +P < 0.05 vs. IR; Sidak; n = 3). (D) Endothelial VCAM-1 expression does not increase during ischaemia but non-significantly increases during reperfusion. This is also reduced following HSPC administration (Sidak; n = 3). (E) IRI, but not ischaemia alone, results in a significant endothelial oxidative damage which is reduced with HSPCs (**P < 0.01 vs. sham; #P < 0.05 vs. IR; Sidak; sham and ischaemia groups n = 5; IR and IR+HSPC groups n = 4). (F) Oxidative damage in myocytes also increases but not to levels seen in endothelium (Sidak; n = 5; IR+HSPC group n = 4).