Figure 1. Mice lack native coronary collaterals.

A–E, Three months-old C57BL/6 (B6) mice received acute ligation of the distal left anterior descending artery (LADX), followed by coronary infusion at 100 mmHg of papavarine and nitroprusside in PBS for maximal dilation, then 4% paraformaldehyde (PFA); Microfil^R was then infused at a viscosity and pressure that fills all pre-capillary vessels. Panel A is before and B–E are after optical clearing with methyl salicylate. Absence of Microfil^R in the LAD artery tree below the ligation (infarct zone, IFZ), including in C where capillaries and some venules were also filled by using a higher pressure, indicates absence of native collaterals is not from failure to fill the smallest-diameter vessels. D, RCA, right coronary artery. E, Higher magnification of panel D from endocardial side. Data are representative of ≥ 10 B6 adults. The same lack of collaterals was obtained in: adult BALB/c, A/J, C57BLKS (BLKS), SJL, CBA, DBA/2, C3H-He and CD1 strains (≥ 5 of each strain); after transection of the LAD below the ligation to create a minimum-resistance pathway; after endothelial staining using ephrin-B2^LacZ/+ B6 mice or infusion of the coronary circulation with isolectin-B4-Alex568; and during perfusion with Evans blue-PBS (see Online Figures 1–5) (≥ 3 mice per last 4 procedures).