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  • Author or Editor: Mohamed Y. Mallem x
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Objective—To investigate the functional expression of β3-adrenoceptors (β3-ARs) in equine digital veins (EDVs) and to examine whether β3-AR relaxation was altered in EDVs incubated with endotoxin.

Sample Population—Forelimbs obtained from 30 horses.

Procedure—Forelimbs were obtained from horses in an abattoir. Equine digital veins were carefully removed from distal portions of the forelimbs. Rings of dissected EDVs were mounted in 5-mL organ baths to record isometric tension in the presence of various β3-AR agonists (SR 58611A, ZD 2079, and ZM 215001).

Results—In intact EDVs, isoprenaline, SR 58611A, ZD 2079, and ZM 215001 induced concentrationdependent relaxation. Isoprenaline and SR 58611Ainduced relaxations were reduced or unaffected by nadolol, respectively. In intact EDVs, SR 58611Ainduced relaxation was significantly reduced in the presence of 2µM ZM 215001 (used as a β3-AR antagonist). In endothelium-denuded EDVs or intact EDVs in the presence of a nitric oxide synthase inhibitor, isoprenaline and SR 58611A-induced relaxations were significantly decreased. The endothelium-independent relaxation to SR 58611A was significantly inhibited in the presence of ZM 215001. In endotoxin-treated EDV, isoprenaline- and SR 58611A-induced relaxations were significantly reduced. In these conditions, cycloheximide (a protein synthesis inhibitor) and ibuprofen (a cyclooxygenase inhibitor) restored the relaxant response to SR 58611A.

Conclusions and Clinical Relevance—β3-Adrenoceptors are functionally expressed in EDVs. Incubation in the presence of endotoxin, used as an in vitro model of laminitis, induced an alteration of β-ARmediated relaxations in EDVs, which could be the consequence of cyclooxygenase induction and subsequent prostanoid production. (Am J Vet Res 2003;64:708–714)

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in American Journal of Veterinary Research


Objective—To investigate the role of superoxide anions in the lipopolysaccharide (LPS)-induced impairment of β-adrenoceptor-mediated equine digital vein (EDV) vasodilation.

Sample Population—EDVs isolated from forelimbs of 24 healthy adult horses.

Procedures—Endothelium-intact or endothelium-denuded EDV rings were incubated with or without LPS (10 μg/mL) of Escherichia coli (O55:B5) for 4 hours. Cumulative concentration-relaxation curves resulting from administration of isoprenaline, a nonselective β-adrenoceptor agonist, or from administration of SR 58611A, a selective β3-adrenoceptor agonist, were recorded in phenylephrine-preconstricted EDVs in the absence or the presence of superoxide dismutase (200 U/mL). Isoprenaline-induced relaxation was also evaluated with or without the cyclooxygenase inhibitors indomethacin (10μM) and NS-398 (10μM).

Results—Isoprenaline and SR 58611A induced concentration-dependent relaxation of EDV rings, which was inhibited by LPS exposure. Superoxide dismutase abolished the inhibitory effect of LPS on the isoprenaline- and SR 58611A-mediated relaxation. Pretreatment of the LPS-treated EDVs with indomethacin or NS-398 restored the isoprenaline-mediated relaxation and abolished the LPS-induced impairment to a similar extent as superoxide dismutase.

Conclusions and Clinical Relevance—Results supported a role of superoxide anions in the LPS-induced impairment of β-adrenoceptor-mediated EDV vasodilation. The LPS-induced oxidative stress in EDVs may contribute to vascular dysfunctions associated with laminitis in horses.

Full access
in American Journal of Veterinary Research