Literature DB >> 28174322

Four-Dimensional Microvascular Analysis Reveals That Regenerative Angiogenesis in Ischemic Muscle Produces a Flawed Microcirculation.

John-Michael Arpino1, Zengxuan Nong1, Fuyan Li1, Hao Yin1, Nour Ghonaim1, Stephanie Milkovich1, Brittany Balint1, Caroline O'Neil1, Graham M Fraser1, Daniel Goldman1, Christopher G Ellis1, J Geoffrey Pickering2.   

Abstract

RATIONALE: Angiogenesis occurs after ischemic injury to skeletal muscle, and enhancing this response has been a therapeutic goal. However, to appropriately deliver oxygen, a precisely organized and exquisitely responsive microcirculation must form. Whether these network attributes exist in a regenerated microcirculation is unknown, and methodologies for answering this have been lacking.
OBJECTIVE: To develop 4-dimensional methodologies for elucidating microarchitecture and function of the reconstructed microcirculation in skeletal muscle. METHODS AND
RESULTS: We established a model of complete microcirculatory regeneration after ischemia-induced obliteration in the mouse extensor digitorum longus muscle. Dynamic imaging of red blood cells revealed the regeneration of an extensive network of flowing neo-microvessels, which after 14 days structurally resembled that of uninjured muscle. However, the skeletal muscle remained hypoxic. Red blood cell transit analysis revealed slow and stalled flow in the regenerated capillaries and extensive arteriolar-venular shunting. Furthermore, spatial heterogeneity in capillary red cell transit was highly constrained, and red blood cell oxygen saturation was low and inappropriately variable. These abnormalities persisted to 120 days after injury. To determine whether the regenerated microcirculation could regulate flow, the muscle was subjected to local hypoxia using an oxygen-permeable membrane. Hypoxia promptly increased red cell velocity and flux in control capillaries, but in neocapillaries, the response was blunted. Three-dimensional confocal imaging revealed that neoarterioles were aberrantly covered by smooth muscle cells, with increased interprocess spacing and haphazard actin microfilament bundles.
CONCLUSIONS: Despite robust neovascularization, the microcirculation formed by regenerative angiogenesis in skeletal muscle is profoundly flawed in both structure and function, with no evidence for normalizing over time. This network-level dysfunction must be recognized and overcome to advance regenerative approaches for ischemic disease.
© 2017 American Heart Association, Inc.

Entities:  

Keywords:  angiogenesis; erythrocyte; microcirculation; microvascular dysfunction; smooth muscle

Mesh:

Substances:

Year:  2017        PMID: 28174322     DOI: 10.1161/CIRCRESAHA.116.310535

Source DB:  PubMed          Journal:  Circ Res        ISSN: 0009-7330            Impact factor:   17.367


  19 in total

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