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)
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.