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Abstract
OBJECTIVE
To determine the effects of dexmedetomidine, doxapram, and dexmedetomidine plus doxapram on ventilation (
e), breath frequency, and tidal volume (Vt) in ball pythons (Python regius) and of doxapram on the thermal antinociceptive efficacy of dexmedetomidine.
ANIMALS
14 ball pythons.
PROCEDURES
Respiratory effects of dexmedetomidine and doxapram were assessed with whole-body, closed-chamber plethysmography, which allowed for estimates of
e and Vt. In the first experiment of this study with a complete crossover design, snakes were injected, SC, with saline (0.9% NaCl) solution, dexmedetomidine (0.1 mg/kg), doxapram (10 mg/kg), or dexmedetomidine and doxapram, and breath frequency,
e, and Vt were measured before and every 30 minutes thereafter, through 240 minutes. In the second experiment, antinociceptive efficacy of saline solution, dexmedetomidine, and dexmedetomidine plus doxapram was assessed by measuring thermal withdrawal latencies before and 60 minutes after SC injection.
RESULTS
Dexmedetomidine significantly decreased breath frequency and increased Vt but did not affect
e at all time points, compared with baseline. Doxapram significantly increased
e, breath frequency, and Vt at 60 minutes after injection, compared with saline solution. The combination of dexmedetomidine and doxapram, compared with dexmedetomidine alone, significantly increased
e at 30 and 60 minutes after injection and did not affect breath frequency and Vt at all time points. Thermal withdrawal latencies significantly increased when snakes received dexmedetomidine or dexmedetomidine plus doxapram, versus saline solution.
CONCLUSIONS AND CLINICAL RELEVANCE
Concurrent administration of doxapram may mitigate the dexmedetomidine-induced reduction of breathing frequency without disrupting thermal antinociceptive efficacy in ball pythons.
Abstract
Objective—To determine the effects of μ-, δ-, and κ-opioid receptor (MOR, DOR, and KOR, respectively) activation on thermal antinociception in red-eared slider turtles Trachemys scripta.
Animals—51 adult turtles.
Procedures—Infrared heat stimuli were applied to the plantar surface of turtle hind limbs. Thermal hind limb withdrawal latencies (HLWLs) were measured before (baseline) and at intervals after SC administration of various doses of saline (0.9% NaCl) solution (SS), MOR, DOR, or KOR agonists (3 to 13 turtles/treatment). Treatment with a DOR antagonist SC prior to DOR agonist administration was also evaluated.
Results—Treatment with an MOR agonist ([D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin acetate salt [DAMGO; 1.3 or 6.6 mg/kg]) increased HLWLs (from baseline) at 2 to 8 hours after injection; at the higher dose, the maximum mean increase was 5.6 seconds at 4 hours. Treatment with a DOR agonist ([D-Ala2, D-Leu5]-enkephalin acetate salt [DADLE; 25 mg/kg]) increased mean HLWL by 11.3 seconds at 4 hours; however, treatment with DADLE (5.8 mg/kg) or with another DOR agonist ([D-Pen2,5]-enkephalin hydrate [DPDPE; 1.2 or 6.3 mg/kg]) did not alter HLWL, compared with SS effects. Administration of a DOR antagonist (naltrindole hydrochloride; 10 mg/kg) prior to DADLE administration (25 mg/kg) increased mean HLWL by 2.7 seconds at 4 hours. One KOR agonist, U50488 ([−]-trans-[1S,2S]-U50488 hydrochloride hydrate; 6.7 mg/kg) decreased HLWL steadily from 2 to 24 hours (less than baseline value); another KOR agonist, U69593 ([+]-[5α,7α,8β]-N-Methyl-N-[7-{1-pyrrolidinyl}-1-oxaspiro{4.5}dec-8-yl]-benzene-acet-amide; 6.7 or 26 mg/kg) did not alter HLWLs, compared with SS effects.
Conclusions and Clinical Relevance—Opioid-dependent thermal antinociception in turtles appeared to be attributable mainly to MOR activation with a relatively minor contribution of DOR activation.
Abstract
Objective—To determine the dose- and time-dependent changes in analgesia and respiration caused by tramadol administration in red-eared slider turtles (Trachemys scripta).
Design—Crossover study.
Animals—30 adult male and female red-eared slider turtles.
Procedures—11 turtles received tramadol at various doses (1, 5, 10, or 25 mg/kg [0.45, 2.27, 4.54, or 11.36 mg/lb], PO; 10 or 25 mg/kg, SC) or a control treatment administered similarly. Degree of analgesia was assessed through measurement of hind limb thermal withdrawal latencies (TWDLs) at 0, 3, 6, 12, 24, 48, 72, and 96 hours after tramadol administration. Nineteen other freely swimming turtles received tramadol PO (5, 10, or 25 mg/kg), and ventilation (VE), breath frequency, tidal volume (VT), and expiratory breath duration were measured.
Results—The highest tramadol doses (10 and 25 mg/kg, PO) yielded greater mean TWDLs 6 to 96 hours after administration than the control treatment did, whereas tramadol administered at 5 mg/kg, PO, yielded greater mean TWDLs at 12 and 24 hours. The lowest tramadol dose (1 mg/kg, PO) failed to result in analgesia. Tramadol administered SC resulted in lower TWDLs, slower onset, and shorter duration of action, compared with PO administration. Tramadol at 10 and 25 mg/kg, PO, reduced the VE at 12 hours by 51% and 67%, respectively, and at 24 through 72 hours by 55% to 62% and 61 % to 70%, respectively. However, tramadol at 5 mg/kg, PO, had no effect on the VE.
Conclusions and Clinical Relevance—Tramadol administered PO at 5 to 10 mg/kg provided thermal analgesia with less respiratory depression than that reported for morphine in red-eared slider turtles.
Abstract
Objective—To test the hypothesis that administration of butorphanol or morphine induces antinociception in bearded dragons and corn snakes.
Design—Prospective crossover study.
Animals—12 juvenile and adult bearded dragons and 13 corn snakes.
Procedures—Infrared heat stimuli were applied to the plantar surface of bearded dragon hind limbs or the ventral surface of corn snake tails. Thermal withdrawal latencies (TWDLs) were measured before (baseline) and after SC administration of physiologic saline (0.9% NaCl) solution (equivalent volume to opioid volumes), butorphanol tartrate (2 or 20 mg/kg [0.91 or 9.1 mg/lb]), or morphine sulfate (1, 5, 10, 20, or 40 mg/kg [0.45, 2.27, 4.5, 9.1, or 18.2 mg/lb]).
Results—For bearded dragons, butorphanol (2 or 20 mg/kg) did not alter hind limb TWDLs at 2 to 24 hours after administration. However, at 8 hours after administration, morphine (10 and 20 mg/kg) significantly increased hind limb TWDLs from baseline values (mean ± SEM maximum increase, 2.7 ± 0.4 seconds and 2.8 ± 0.9 seconds, respectively). For corn snakes, butorphanol (20 mg/kg) significantly increased tail TWDLs at 8 hours after administration (maximum increase from baseline value, 3.0 ± 0.8 seconds); the low dose had no effect. Morphine injections did not increase tail TWDLs at 2 to 24 hours after administration.
Conclusions and Clinical Relevance—Compared with doses used in most mammalian species, high doses of morphine (but not butorphanol) induced analgesia in bearded dragons, whereas high doses of butorphanol (but not morphine) induced analgesia in corn snakes.
Abstract
OBJECTIVE To determine antinociceptive efficacy, behavioral patterns, and respiratory effects associated with dexmedetomidine administration in ball pythons (Python regius).
ANIMALS 12 ball pythons.
PROCEDURES Antinociception was assessed by applying an infrared heat stimulus to the cranioventral surface of snakes during 2 experiments. Thermal withdrawal latency was measured at 0, 2, and 24 hours after SC injections of dexmedetomidine (0.1 or 0.2 mg/kg) or saline (0.9% NaCl) solution and at 0 to 60 minutes after injection of dexmedetomidine (0.1 mg/kg) or saline solution. Behaviors were recorded at 0, 2, and 24 hours after administration of dexmedetomidine (0.1 mg/kg) or saline solution. Tongue flicking, head flinch to the approach of an observer's hand, movement, and righting reflex were scored. Respiratory frequency was measured by use of plethysmography to detect breathing-related movements after injection of dexmedetomidine (0.1 mg/kg) or saline solution.
RESULTS Mean baseline withdrawal latency was 5 to 7 seconds; saline solution did not alter withdrawal latency. Dexmedetomidine increased withdrawal latency by 18 seconds (0.2 mg/kg) and 13 seconds (0.1 mg/kg) above baseline values at 2 hours. Increased withdrawal latency was detected within 15 minutes after dexmedetomidine administration. At 2 hours after injection, there were few differences in behavioral scores. Dexmedetomidine injection depressed respiratory frequency by 55% to 70%, compared with results for saline solution, but snakes continued to breathe without prolonged apnea.
CONCLUSIONS AND CLINICAL RELEVANCE Dexmedetomidine increased noxious thermal withdrawal latency without causing excessive sedation. Therefore, dexmedetomidine may be a useful analgesic drug in ball pythons and other snake species.
Abstract
Objective—To determine cytologic and microbiologic findings in bronchoalveolar lavage (BAL) fluid and SpO 2 values obtained during BAL in healthy rabbits.
Animals—9 rabbits.
Procedures—Bronchoscopic BAL of left and right caudal lobar bronchi (LB2 and RB4) was performed with 3 mL of sterile saline (0.9% NaCl) solution; SpO 2 was measured before, during, and after BAL. Percentage fluid recovered, total leukocyte counts, and differential cell counts were determined. Aerobic and anaerobic bacterial, mycoplasmal, and fungal cultures were performed from combined LB2 and RB4 samples.
Results—Mean ± SD percentage fluid volumes recovered from LB2 and RB4 were 53 ± 13% and 63 ± 13%, respectively. Mean ± SD total leukocyte counts from LB2 and RB4 were 422 ± 199 cells/μL and 378 ± 97 cells/μL, respectively. Macrophages were most frequently identified. There were no significant differences in volumes retrieved, total leukocyte counts, or differential cell percentages between LB2 and RB4. Microbial culture results were negative for 3 rabbits and positive for mixed aerobic and anaerobic bacterial growth in 6 and 2 rabbits, respectively. The SpO 2 was ≥ 95% in 7 of 9 rabbits after anesthetic induction, < 95% in 5 of 6 rabbits 1 minute after BAL, and ≥ 95% in 5 of 9 rabbits and > 90% in 4 of 9 rabbits 3 minutes after BAL.
Conclusions and Clinical Relevance—Bronchoscopic BAL with 3 mL of saline solution provided adequate fluid recovery for microbiologic and cytologic examination from the caudal lung lobes. Transient low SpO 2 was detected immediately after BAL.
Abstract
Objective—To test the hypothesis that butorphanol or morphine induces antinociception with minimal respiratory depression in conscious red-eared slider turtles.
Design—Prospective crossover study.
Animals—37 adult male and female red-eared slider turtles (Trachemys scripta).
Procedures—Antinociception (n = 27 turtles) and respiratory (10 turtles) experiments were performed. Infrared heat stimuli were applied to the plantar surface of turtle limbs. Thermal withdrawal latencies were measured before and at intervals after SC administration of physiologic saline (0.9% NaCl) solution, butorphanol tartrate (2.8 or 28 mg/kg [1.27 or 12.7 mg/lb]), or morphine sulfate (1.5 or 6.5 mg/kg [0.68 or 2.95 mg/lb]). Ventilation was assessed in freely swimming turtles before and after SC administration of saline solution, butorphanol (28 mg/kg), or morphine (1.5 mg/kg).
Results—For as long as 24 hours after injection of saline solution or either dose of butorphanol, thermal withdrawal latencies among turtles did not differ. Low- and high-dose morphine injections increased latencies significantly by 8 hours. Ventilation was not altered by saline solution administration, was temporarily depressed by 56% to 60% for 1 to 2 hours by butorphanol (28 mg/kg) administration, and was significantly depressed by a maximum of 83 ± 9% at 3 hours after morphine (1.5 mg/kg) injection. Butorphanol and morphine depressed ventilation by decreasing breathing frequency.
Conclusions and Clinical Relevance—Although widely used in reptile species, butorphanol may not provide adequate antinociception for invasive procedures and caused short-term respiratory depression in red-eared slider turtles. In contrast, morphine apparently provided antinociception but caused long-lasting respiratory depression.
Abstract
Objective—To examine acid-base and hormonal abnormalities in dogs with diabetes mellitus.
Design—Cross-sectional study.
Animals—48 dogs with diabetes mellitus and 17 healthy dogs.
Procedures—Blood was collected and serum ketone, glucose, lactate, electrolytes, insulin, glucagon, cortisol, epinephrine, norepinephrine, nonesterified fatty acid, and triglyceride concentrations were measured. Indicators of acid-base status were calculated and compared between groups.
Results—Serum ketone and glucose concentrations were significantly higher in diabetic than in healthy dogs, but there was no difference in venous blood pH or base excess between groups. Anion gap and strong ion difference were significantly higher and strong ion gap and serum bicarbonate concentration were significantly lower in the diabetic dogs. There were significant linear relationships between measures of acid-base status and serum ketone concentration, but not between measures of acid-base status and serum lactate concentration. Serum insulin concentration did not differ significantly between groups, but diabetic dogs had a wider range of values. All diabetic dogs with a serum ketone concentration > 1,000 μmol/L had a serum insulin concentration < 5 μU/mL. There were strong relationships between serum ketone concentration and serum glucagon-insulin ratio, serum cortisol concentration, and plasma norepinephrine concentration. Serum β-hydroxybutyrate concentration, expressed as a percentage of serum ketone concentration, decreased as serum ketone concentration increased.
Conclusions and Clinical Relevance—Results suggested that ketosis in diabetic dogs was related to the glucagon-insulin ratio with only low concentrations of insulin required to prevent ketosis. Acidosis in ketotic dogs was attributable largely to high serum ketone concentrations.
Abstract
Case Description—3 adult (24- to 43-year-old) Atlantic bottlenose dolphins (Tursiops truncatus) with chronic episodic malaise and inappetence associated with high serum aminotransferase (alanine aminotransferase and aspartate aminotransferase) activities, high serum iron concentration, and serum transferrin saturation > 80% were evaluated.
Clinical Findings—Results of histologic examination of liver biopsy specimens revealed hemosiderosis in all 3 dolphins. Except for chronic lymphocytosis in 1 dolphin, results of extensive diagnostic testing revealed no other abnormalities. For each dolphin, a diagnosis of iron overload of unknown origin was made.
Treatment and Outcome—Phlebotomy treatment was implemented to reduce body stores of iron. Each phlebotomy procedure removed 7% to 17% (1 to 3 L) of estimated blood volume. Treatment consisted of an induction phase of weekly phlebotomy procedures for 22 to 30 weeks, which was complete when serum iron concentration and aminotransferase activities were within reference ranges and serum transferrin saturation was ≤ 20% or Hct was ≤ 30%. Total amount of iron removed from each dolphin was 53 to 111 mg/kg (24.1 to 50.5 mg/lb) of body weight. One dolphin required maintenance procedures at 8- to 12-week intervals when high serum iron concentration was detected.
Clinical Relevance—Although the cause of the iron overload and high serum aminotransferase activities remained unknown, phlebotomy treatment successfully resolved the clinicopathologic abnormalities, supporting a role of iron overload in the hepatopathy of the 3 dolphins.
