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Exogenous Thrombin Delivery Promotes Collateral Capillary Arterialization and Tissue Reperfusion in the Murine Spinotrapezius Muscle Ischemia Model
Author(s) -
BRUCE ANTHONY C.,
PEIRCE SHAYN M.
Publication year - 2012
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2011.00138.x
Subject(s) - thrombin , venule , microcirculation , arteriole , ischemia , skeletal muscle , medicine , degranulation , infiltration (hvac) , microbiology and biotechnology , pathology , chemistry , anatomy , platelet , biology , physics , thermodynamics , receptor
Please cite this paper as : Bruce AC and Peirce SM. Exogenous Thrombin Delivery Promotes Collateral Capillary Arterialization and Tissue Reperfusion in the Murine Spinotrapezius Muscle Ischemia Model. Microcirculation 19: 143–154, 2012. Abstract Objective: We examined the effects of exogenously delivered thrombin on cell recruitment in skeletal muscle and the formation of new collateral arterioles in the microvasculature in response to ligation‐induced ischemia. Methods: Thrombin or vehicle was locally applied to both ligated and nonoperated Balb/c spinotrapezius muscles, which were harvested after three or seven days, imaged using confocal microscopy, and analyzed. Results: Thrombin treatment resulted in accelerated arterialization of collateral capillaries and accelerated tissue reperfusion in ischemic muscles. Uninjured muscle treated with thrombin displayed increased vascular cell adhesion molecule 1 expression on arteriole and venule endothelium, increased expression of smooth muscle α‐actin on capillary‐sized vessels, increased infiltration by CD11b + leukocytes, and mast cell infiltration and degranulation. Conclusions: Exogenous delivery of thrombin enhances microvascular collateral development in response to ischemic insult, and accelerates tissue reperfusion. Elicited responses from multiple cell types probably contribute to these effects.