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Orthopaedic Proceedings
Vol. 91-B, Issue SUPP_II | Pages 334 - 334
1 May 2009
Delp M Dominguez J Allen M Prisby R
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Introduction: Bone loss occurs as a consequence of disuse. Using the hindlimb-unloaded (HU) rat, the purpose of this study was to determine whether skeletal unloading and reloading alters regional bone blood flow (microspheres) and PNA vasodilator responsiveness (in vitro).

Results: Femoral bone and marrow perfusion were reduced after 10 minutes, 7 days and 28 days of HU. Further, when the hindlimb skeleton is reloaded for 10 minutes following 14 days HU, bone and marrow perfusion were lower than that in standing control animals (e.g., femoral proximal metaphysis: Control, 20 ± 3 ml/min/100g; HU, 13 ± 3 ml/min/100g). PNA endothelium-dependent vasodilation was attenuated with 14 days of HU (Control, 84 ± 5% maximal relaxation; HU, 55 ± 7% maximal relaxation).

Discussion: The HU-associated changes bone perfusion and endothelium-dependent vasodilation correspond to unloading-induced changes in bone structure. These results support the hypothesis that alterations in bone blood flow and vascular signaling may modulate bone remodeling.


Orthopaedic Proceedings
Vol. 91-B, Issue SUPP_II | Pages 334 - 334
1 May 2009
Dominguez J Prisby R Behnke B Allen M Delp M
Full Access

Introduction: The purpose of this study was to determine whether regional blood flow (microspheres) in the femur is diminished with aging, and whether a reduction in flow is associated with impaired endothelium-dependent vasodilation.

Materials and Methods: Blood flow and PNA endothelium-dependent vasodilation was measured in young (4–6 months old) and aged (24–26 months old) male Fischer-344 rats.

Results: Blood flow in the aged rats was ~25% lower in femoral bone and 45% lower in diaphyseal marrow. Endothelium-dependent vasodilation was lower with old age (young: 83 ± 6% maximal relaxation; aged: 62 ± 5% maximal relaxation) and was mediated through impairment of the NOS signaling pathway, which resulted in a lower nitric oxide bioavailability (young: 168 ± 56 nM nitric oxide; aged: 50 ± 7 nM nitric oxide).

Discussion: Such age-related changes in bone perfusion and nitric oxide signaling could impact clinical bone loss, increase risk of fracture, and impair fracture healing in the elderly.