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  • Author or Editor: Freddy Gautier x
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Objective—To investigate renal function in clinically normal dogs when awake and during anesthesia with medetomidine; xylazine, ketamine, and halothane (XKH) combination; or propofol.

Animals—10 adult female Beagles.

Procedures—At intervals of 15 days, dogs were administered medetomidine (0.05 mg/kg, IV); XKH combination (xylazine [1 mg/kg, IV], ketamine [5 mg/kg, IV], and halothane [1% end-tidal concentration]); or propofol (6 mg/kg, IV) to induce anesthesia or no treatment. Glomerular filtration rate was assessed on the basis of renal uptake (RU; determined via renal scintigraphy) and plasma clearance (CL) of technetium 99m-labeled diethylenetriamine peentaacetic acid (99mTc-DTPA).

Results—In awake dogs, mean ± SEM RU was 9.7 ± 0.4% and CL was 3.86 ± 0.23 mL/min/ kg. Renal uptake and CL of 99mTc-DTPA were not significantly modified by administration of XKH (RU, 11.4 ± 0.9%; CL, 4.6 ± 0.32 mL/min/kg) or propofol (RU, 9.7 ± 0.3%; CL, 3.78 ± 0.37 mL/min/kg). Half-life elimination time of plasma 99mTc-DTPA decreased significantly in XKH-anesthetized dogs, compared with the value in awake dogs (14.4 minutes and 28.9 minutes, respectively). However, glomerular filtration rate was significantly decreased by administration of medetomidine (RU, 3.9 ± 0.1%), and the time to maximum kidney activity was significantly increased (867 ± 56 seconds vs 181 ± 11 seconds without anesthesia).

Conclusions and Clinical Relevance—Results indicated that anesthesia with propofol or an XKH combination did not alter renal function in healthy Beagles, but anesthesia with medetomidine decreased early RU of 99mTc-DTPA.

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in American Journal of Veterinary Research


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