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Impact of a single session of intermittent pneumatic leg compressions on skeletal muscle and isolated collateral artery gene expression in rats
Author(s) -
Roseguini Bruno T.,
ArceEsquivel Arturo A.,
Newcomer Sean C.,
Laughlin M. H.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1092.23
Subject(s) - medicine , hindlimb , arteriogenesis , skeletal muscle , cardiology , femoral artery , intermittent claudication , cxcl1 , artery , isometric exercise , collateral circulation , endocrinology , ischemia , anatomy , chemokine , inflammation , vascular disease , arterial disease
Intermittent pneumatic leg compressions (IPC) have proven to be an effective approach to treat patients with intermittent claudication but the mechanistic basis behind the clinical benefits remains elusive. In the present study we examined the impact of a single session of IPC (150 min) on skeletal muscle (tibialis anterior) and isolated collateral artery (perforating artery) expression of genes involved in vascular remodeling in rats that had undergone bilateral ligation of the femoral artery. We also compared the effects of two compression frequencies (12 vs. 3 cycles/min) on the expression of these factors. In ligated rats high frequency IPC evoked an increase in MCP‐1 (p<0.01) and CXCL1 mRNA (p<0.01) in the muscle accompanied by an increase in immunostaining of MCP‐1 and VEGF. Further, collateral arteries from these animals showed an increased expression of MCP‐1 (~2 fold, p=0.02). These effects were mostly evident in the group exposed to high frequency protocol (12 cycles/min). In contrast, in sham‐operated animals high frequency IPC evoked a modest up‐regulation of VEGF (p=0.01), MCP‐1 (p=0.02) and CXCL1 (p=0.03) mRNA in the muscle without concomitant changes in protein levels. In conclusion, high‐frequency IPC acutely up‐regulates the expression of factors involved in vascular remodeling in the compressed muscle and collateral arteries in a model of hindlimb ischemia. Support: NIH RR‐18276, HL‐36088