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Influence of Alpha‐Adrenergic Receptor (αAR) Inhibition on Collateral Blood Flow (BF) and Conductance (C) to the Calf Muscle Following Acute Femoral Artery Occlusion
Publication year - 2008
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.22.1_supplement.745.4
Subject(s) - medicine , cardiology , hindlimb , perfusion , ischemia , femoral artery , constriction , collateral circulation , antagonist , endocrinology , anesthesia , chemistry , receptor
Following arterial occlusion (OCC), collateral‐dependent BF is reliant upon the caliber and vascular control of the inherent collateral circuit. The objective of this study was to examine whether αAR activation contributes to C of the nascent collateral circuit following acute OCC of the femoral artery (FA) in male rats (n=20). BF was measured using μspheres during treadmill exercise at an intensity requiring maximal collateral BF, before and after delivery of a nonselective α‐antagonist (phentolamine: PHEN) that lowered MAP 40–50 mmHg. MAP (caudal a.) and perfusion pressure below the OCC (distal FA) were monitored. PHEN increased BF and C in non‐ischemic muscles, showing release of αAR activation. PHEN also increased BF (9.6±0.90 to 20.5±2.05 ml/min/100g) and C in the ischemic muscles, due primarily to a decrease in collateral resistance (~70%). Thus, collateral BF is reduced by αAR activation during exercise following acute‐onset hindlimb ischemia. Interestingly, the peak C of the OCC calf muscle sections were only ~half of that observed in the non‐ischemic hindlimb, despite being frankly ischemic (i.e., BF only ~10% of normal). This suggests, that even after removal of αAR constriction, the dilatory capacity of the collateral circuit is still attenuated; this may be related to reduced dilatory capacity due to decreased vascular transmural pressure caused by FA OCC. Support: HL 37387‐17