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.
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
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
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)