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Endogenous norepinephrine regulates blood flow to the intact rat tibia
Author(s) -
Feitelson J. B. A.,
Kulenovic E.,
Beck D. J.,
Harris P. D.,
Passmore J. C.,
Malkani A. L.,
Fleming J. T.
Publication year - 2002
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/s0736-0266(01)00121-8
Subject(s) - phentolamine , phenoxybenzamine , norepinephrine , medicine , endocrinology , blood flow , vascular resistance , blood pressure , chemistry , receptor , dopamine
The goal of our study was to determine if endogenous norepinephrine (NE) has a role in the regulation of basal blood flow to intact bone. The experimental plan was to measure bone blood flow before and after pharmacological blockade of alpha‐adrenergic receptors. A significant increase in blood flow after receptor blockade would suggest that endogenous norepinephrine exerts a tonic constrictor effect on the vessels supplying blood to the bone. Mature, male rats were anesthetized with Inactin. Arterial blood pressure and left tibia blood flow (laser Doppler flowmetry) were measured. A cannula was inserted into the right iliac artery and advanced to the aortic bifurcation to deliver drugs into the left hindlimb circulation, including the left tibia vasculature. Bolus injection of norepinephrine caused a dose‐dependent decrease in bone blood flow (30–40%). Blockade of alpha‐adrenergic receptors with phentolamine or phenoxybenzamine attenuated by more than 50% the norepinephrine‐induced decrease in bone blood flow. In separate rats that had not received exogenous norepinephrine, injection of phentolamine alone decreased bone vascular resistance by 34 ± 3%. Similarly, phenoxybenzamine decreased resistance by 25 ± 4%. These results are consistent with the conclusion that alpha‐adrenergic receptors mediate a significant constriction of blood vessels which participate in the partial control of basal blood flow to the intact rat tibia. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.

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