Microcirculation (2010) 17, 333–347. doi: 10.1111/j.1549‐8719.2010.00034.x

Objective:  Chronic and acute ischemic diseases—peripheral artery disease, coronary artery disease, stroke—result in tissue damage unless blood flow is maintained or restored in a timely manner. Mice of different strains recover from arteriolar ligation (by increasing collateral blood flow) at different speeds. We quantify the spatio‐temporal patterns of microvascular network remodeling following arteriolar ligation in different mouse strains to better understand inter‐individual variability.

Methods:  Whole‐muscle spinotrapezius microvascular networks of mouse strains C57Bl/6, Balb/c and CD1 were imaged using confocal microscopy following ligation of feeding arterioles.

Results:  Baseline arteriolar structures of C57Bl/6 and Balb/c mice feature heavily ramified arcades and unconnected dendritic trees, respectively. This network angioarchitecture identifies ischemia‐protected and ischemia‐vulnerable tissues; unlike C57Bl/6, downstream capillary perfusion in Balb/c spinotrapezius is lost following ligation. Perfusion recovery requires arterialization (expansion and investment of mural cells) of a subset of capillaries forming a new low‐resistance collateral pathway between arteriolar trees. Outbred CD1 exhibit either Balb/c‐like or C57Bl/6‐like spinotrapezius angioarchitecture, predictive of response to arteriolar ligation.

Conclusions:  This collateral capillary arterialization process may explain the reported longer time required for blood flow recovery in Balb/c hindlimb ischemia, as low‐resistance blood flow pathways along capillary conduits must be formed (“arterialization”) before reperfusion.