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Post‐Occlusive Reactive Hyperemia: Effects on Skeletal Muscle Capillary Hemodynamics
Author(s) -
Wright J,
Ferguson S,
Holdsworth C,
Colburn T,
Fees A,
Barstow T,
Musch T,
Poole D
Publication year - 2015
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.29.1_supplement.994.7
Subject(s) - reactive hyperemia , hemodynamics , medicine , cardiology , brachial artery , blood flow , occlusion , ischemia , microcirculation , chemistry , blood pressure
Post‐occlusive reactive hyperemia (PORH) is the commonly accepted non‐invasive diagnostic test used for evaluating endothelial function in humans. In contrast to conduit brachial artery blood flow, little is known regarding capillary hemodynamics during PORH. An understanding of microcirculatory behavior post occlusion is fundamental to interpreting the PORH response. Based on previous results found in humans we tested the hypothesis that mechanically induced ischemia of the spinotrapezius muscle would increase the percentage of capillaries supporting red blood cell (RBC) flux during reperfusion. Capillary hemodynamics were measured via intravital microscopy in young male Sprague‐Dawley rats at baseline (BL), during mechanical feed artery occlusion (OCC, 1 min and 5 min) and subsequent reperfusion. Mean arterial pressure and heart rate were not altered (both P > 0.05). As expected, the percentage of capillaries supporting RBC flux was reduced during 1 min OCC (BL: 90 ± 3, OCC: 2 ± 2%, P < 0.05) and 5 min OCC (BL: 87 ± 3, OCC: 0 ± 0%, P <0.05). At 30 s reperfusion the percentage of capillaries supporting RBC flux decreased relative to BL following 1 min OCC (BL: 90 ± 3%, reperfusion: 85 ± 3%, P < 0.05) and 5 min OCC (BL: 87 ± 3, reperfusion: 29 ± 3%, P < 0.05). Thus during reperfusion the percentage of capillaries supporting RBC flux neither exceeded nor even returned to BL levels up to 5 min post OCC thereby demonstrating impaired capillary function and thus blood‐myocyte O 2 and substrate flux. Consequently, the PORH state in the spinotrapezius muscle of the rat differs markedly from physiological contraction‐induced hyperemia found in humans. Grants: NIH HL‐108328 NIH T32OD011169