Introduction: The aim of this study was to investigate fluorescein use in the diagnosis of bladder ruptures in rabbits as an experimental model.Material and Methods: The study was conducted on male New Zealand rabbits divided into a retrograde fluorescein group (n = 8) and an intravenous (IV) fluorescein group (n = 8). Following general anaesthesia, 10 mL of 10% fluorescein dye (sodium fluoresceine powder) was administered via ureterorenoscope to the bladder of the first group, and 0.5 mL of 10% fluorescein was administered intravenously to the second group. Then, the bladder was viewed through the cystoscope by urethral aspect. After experimental bladder perforation, groups were comparatively evaluated by paracentesis and laparotomy.Results: Following IV injection of fluorescein dye, the bladder veins were stained green within 10 s and then fluorescein mixed with urine flowed into bladder lumen. The green fluid flow was observed in the abdominal cavity after the perforation of the bladder in both groups.Conclusion: Fluorescein can be used as a marker in diagnosis of bladder ruptures. If there is no bleeding or intestinal content in the abdominal cavity, although a smoky yellow-green image is observed, bladder rupture can be suspected.

OBJECTIVE To determine the pharmacokinetics of detomidine hydrochloride administered IV (as an injectable formulation) or by the oral-transmucosal (OTM) route (as a gel) and assess sedative effects of the OTM treatment in healthy dogs. ANIMALS 12 healthy adult dogs.PROCEDURES In phase 1, detomidine was administered by IV (0.5 mg/m2) or OTM (1 mg/m2) routes to 6 dogs. After a 24-hour washout period, each dog received the alternate treatment. Blood samples were collected for quantification via liquid chromatography with mass spectrometry and pharmacokinetic analysis. In phase 2, 6 dogs received dexmedetomidine IV (0.125 mg/m2) or detomidine gel by OTM administration (0.5 mg/m2), and sedation was measured by a blinded observer using 2 standardized sedation scales while dogs underwent jugular catheter placement. After a l-week washout period, each dog received the alternate treatment. RESULTS Median maximum concentration, time to maximum concentration, and bioavailability for detomidine gel following OTM administration were 7.03 ng/mL, 1.00 hour, and 34.52%, respectively; harmonic mean elimination half-life was 0.63 hours. All dogs were sedated and became laterally recumbent with phase 1 treatments. In phase 2, median global sedation score following OTM administration of detomidine gel was significantly lower (indicating a lesser degree of sedation) than that following IV dexmedetomidine treatment; however, total sedation score during jugular vein catheterization did not differ between treatments. The gel was subjectively easy to administer, and systemic absorption was sufficient for sedation. CONCLUSIONS AND CLINICAL RELEVANCE Detomidine gel administered by the OTM route provided sedation suitable for a short, minimally invasive procedure in healthy dogs.

OBJECTIVE To determine the effects of acepromazine maleate premedication on cardiovascular function before and after infusion of dobutamine hydrochloride for 30 minutes in isoflurane-anesthetized horses. ANIMALS 6 healthy adult horses. PROCEDURES Each horse was anesthetized once following premedication with acepromazine (0.02 mg/kg, IV) administered 30 minutes prior to anesthetic induction (ACP+ treatment) and once without premedication (ACP– treatment). Anesthesia was induced with IV administration of xylazine hydrochloride (0.8 mg/kg), ketamine hydrochloride (2.2 mg/kg), and diazepam (0.08 mg/kg). Horses were positioned in right lateral recumbency, and anesthesia was maintained via inhalation of isoflurane delivered in oxygen. End-tidal isoflurane concentration was adjusted to achieve a target mean arterial blood pressure of 60 mm Hg (interquartile range [25th to 75th percentile], 57 to 63 mm Hg) for at least 15 minutes. Cardiac index, oxygen delivery index, and femoral arterial blood flow indices were determined 60 minutes after anesthetic induction (baseline). Dobutamine was then infused to achieve a target mean arterial blood pressure of 80 mm Hg (interquartile range, 76 to 80 mm Hg). Data collection was repeated 30 minutes after the start of dobutamine infusion for comparison with baseline values. RESULTS Complete data sets were available from 5 of the 6 horses. Dobutamine administration resulted in significant increases in oxygen delivery and femoral arterial blood flow indices but no significant change in cardiac index for each treatment. However, at baseline or 30 minutes after the start of dobutamine infusion, findings for the ACP+ and ACP– treatments did not differ. CONCLUSIONS AND CLINICAL RELEVANCE In isoflurane-anesthetized horses, dobutamine administration increased oxygen delivery and femoral arterial blood flow indices, but these changes were unaffected by premedication with acepromazine.

OBJECTIVE To determine the pharmacokinetics of meloxicam after single IV and IM injections in red-eared slider turtles (Trachemys scripta elegans). ANIMALS 8 healthy red-eared slider turtles. PROCEDURES Turtles received 1 dose of meloxicam (0.2 mg/kg) IV or IM (4 turtles/route), a 30-day washout period was provided, and then turtles received the same dose by the opposite route. Blood samples were collected at predetermined times for measurement of plasma meloxicam concentration. Pharmacokinetic values for each administration route were determined with a 2-compartment open model approach. RESULTS For IV administration, mean ± SD values of major pharmacokinetic variables were 1.02 ± 0.41 hours for distribution half-life, 9.78 ± 2.23 hours for elimination half-life, 215 ± 32 mL/kg for volume of distribution at steady state, 11.27 ± 1.44 μg•h/mL for area under the plasma concentration versus time curve, and 18.00 ± 2.32 mL/h/kg for total body clearance. For IM administration, mean values were 0.35 ± 0.06 hours for absorption half-life, 0.72 ± 0.06 μg/mL for peak plasma concentration, 1.5 ± 0.0 hours for time to peak concentration, 3.73 ± 2.41 hours for distribution half-life, 13.53 ± 1.95 hours for elimination half-life, 11.33 ± 0.92 μg•h/mL for area under the plasma concentration versus time curve, and 101 ± 6% for bioavailability. No adverse reactions were detected. CONCLUSIONS AND CLINICAL RELEVANCE Long half-life, high bioavailability, and lack of immediate adverse reactions of meloxicam administered IM at 0.2 mg/kg suggested the possibility of safe and effective clinical use in turtles. Additional studies are needed to establish appropriate administration frequency and clinical efficacy.

OBJECTIVE To evaluate effects of simultaneous intra-articular and IV injection of autologous adipose-derived stromal vascular fraction (SVF) and platelet-rich plasma (PRP) to dogs with osteoarthritis of the hip joints. ANIMALS 22 client-owned dogs (12 placebo-treated [control] dogs and 10 treated dogs). PROCEDURES Dogs with osteoarthritis of the hip joints that caused signs of lameness or discomfort were characterized on the basis of results of orthopedic examination, goniometry, lameness score, the Canine Brief Pain Inventory (CBPI), a visual analogue scale, and results obtained by use of a pressure-sensing walkway at week 0 (baseline). Dogs received a simultaneous intraarticular and IV injection of SVF and PRP or a placebo. Dogs were examined again 4, 8, 12, and 24 weeks after injection. RESULTS CBPI scores were significantly lower for the treatment group at week 24, compared with scores for the control group. Mean visual analogue scale score for the treatment group was significantly higher at week 0 than at weeks 4, 8, or 24. Dogs with baseline peak vertical force (PVF) in the lowest 25th percentile were compared, and the treatment group had a significantly higher PVF than did the control group. After the SVF-PRP injection, fewer dogs in the treated group than in the control group had lameness confirmed during examination. CONCLUSIONS AND CLINICAL RELEVANCE For dogs with osteoarthritis of the hip joints treated with SVF and PRP, improvements in CBPI and PVF were evident at some time points, compared with results for the control group.

OBJECTIVE To evaluate the efficacy of IV administration of a product containing hyaluronan, sodium chondroitin sulfate, and N-acetyl-d-glucosamine for prevention or treatment of osteoarthritis in horses. ANIMALS 32 healthy 2- to 5-year-old horses. PROCEDURES The study involved 2 portions. To evaluate prophylactic efficacy of the test product, horses received 5 mL of the product (n = 8) or saline (0.9% NaCl) solution (8; placebo) IV every fifth day, starting on day 0 (when osteoarthritis was induced in the middle carpal joint of 1 forelimb) and ending on day 70. To evaluate treatment efficacy, horses received either the product or placebo (n = 8/treatment) on days 16, 23, 30, 37, and 44 after osteoarthritis induction. Clinical, diagnostic imaging, synovial fluid, gross anatomic, and histologic evaluations and other tests were performed. Results of each study portion were compared between treatment groups. RESULTS Limb flexion and radiographic findings were significantly worse for horses that received the test product in the prophylactic efficacy portion than for placebo-treated horses or product-treated horses in the treatment efficacy portion. In the prophylactic efficacy portion, significantly less articular cartilage erosion was identified in product-treated versus placebo-treated horses. In the treatment efficacy portion, joints of product-treated horses had a greater degree of bone edema identified via MRI than did joints of placebo-treated horses but fewer microscopic articular cartilage abnormalities. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that caution should be used when administering the evaluated product IV to horses, particularly when administering it prophylactically, as it may have no benefit or may even cause harm.

The objective of this study was to investigate the effects of intravenous alfaxalone with and without premedication on intraocular pressure (IOP) in healthy dogs. Thirty-three dogs were randomized to receive 1 of 3 treatments: acepromazine [0.03 mg/kg body weight (BW)] with butorphanol (0.2 mg/kg BW) intramuscularly (IM), followed by intravenous (IV) alfaxalone (1.5 mg/kg BW); dexmedetomidine (0.002 mg/kg BW) with hydromorphone (0.1 mg/kg BW) IM, followed by alfaxalone (1 mg/kg BW) IV; and saline 0.9% (0.02 mL/kg BW) IM, followed by alfaxalone (3 mg/kg BW) IV. Intraocular pressure (IOP) was measured at baseline, 15 min, and 30 min after premedication, after pre-oxygenation, after administration of alfaxalone, and after intubation. After induction and after intubation, the IOP was significantly increased in all groups compared to baseline. While premedication with acepromazine/butorphanol or dexmedetomidine/hydromorphone did not cause a significant increase in IOP, the risk of vomiting and the associated peak in IOP after dexmedetomidine/hydromorphone should be considered when selecting an anesthetic protocol for dogs with poor tolerance for transient increases in IOP.

OBJECTIVE To evaluate antinociceptive effects of IV administration of hydromorphone alone or followed by buprenorphine or butorphanol to cats. ANIMALS 6 healthy adult cats. PROCEDURES In a randomized, blinded crossover design, cats received each of 4 treatments in which 2 IV injections were given 30 minutes apart: 2 of saline (0.9% NaCl) solution (Sal-Sal) or 1 each of hydromorphone HCl and saline solution (H-Sal), hydromorphone and buprenorphine HCl (H-Bupre), or hydromorphone and butorphanol tartrate (H-Butor). Skin temperature and thermal threshold were recorded before (baseline) and for 12 hours after the first injection. Percentage of maximum possible effect (%MPE) and thermal excursion (TE) were compared among treatments and measurement points. RESULTS Compared with baseline values, skin temperature was higher from 0.75 to 2 hours after the first injection for H-Sal; at 0.5, 1, 3, and 4 hours for H-Bupre; from 0.5 to 3 hours for H-Butor; and from 0.5 to 1 hours for Sal-Sal. Thermal excursion was higher than at baseline from 0.25 to 2 hours for H-Sal and H-Bupre and 0.25 to 0.75 hours for H-Butor; %MPE increased from 0.25 to 2 hours for H-Sal, 0.25 to 3 hours for H-Bupre, and 0.25 to 0.75 hours for H-Butor. Results were similar for comparisons with Sal-Sal, except TE was greater for H-Sal versus Sal-Sal and TE and %MPE were greater for H-Bupre versus Sal-Sal from 0.25 to 1 hours after the first injection. CONCLUSIONS AND CLINICAL RELEVANCE Butorphanol administration decreased the duration of antinociception achieved with hydromorphone administration in cats. This opioid interaction and its impact on pain management require additional investigation.

This study investigated the effects of ketamine and lidocaine in combination on the minimum alveolar concentration of sevoflurane (MACSEVO) in alpacas. Eight healthy, intact male, adult alpacas were studied on 2 separate occasions. Anesthesia was induced with SEVO, and baseline MAC (MACB) determination began 45 min after induction. After MACB determination, alpacas were randomly given either an intravenous (IV) loading dose (LD) and infusion of saline or a loading dose [ketamine = 0.5 mg/kg body weight (BW); lidocaine = 2 mg/kg BW] and an infusion of ketamine (25 μg/kg BW per minute) in combination with lidocaine (50 μg/kg BW per minute), and MACSEVO was re-determined (MACT). Quality of recovery, time-to-extubation, and time-to-standing, were also evaluated. Mean MACB was 1.88% ± 0.13% and 1.89% ± 0.14% for the saline and ketamine + lidocaine groups, respectively. Ketamine and lidocaine administration decreased (P < 0.05) MACB by 57% and mean MACT was 0.83% ± 0.10%. Saline administration did not change MACB. Time to determine MACB and MACT was not significantly different between the treatments. The quality of recovery, time-to-extubation, and time-to-standing, were not different between groups. The infusion of ketamine combined with lidocaine significantly decreased MACSEVO by 57% and did not adversely affect time-to-standing or quality of recovery.

The sedative effect of acepromazine combined with 2 doses of tramadol [3 and 5 mg/kg body weight (BW)] was compared with the sedative effect of acepromazine alone in dogs and the effects of each sedative protocol on cardiorespiratory variables were examined. This was a prospective, randomized, blinded, crossover study. Each of 6 dogs received 3 treatments at 1-week intervals. During all anesthetic episodes, dogs received 0.05 mg/kg BW acepromazine. Approximately 25 min later, dogs were given physiological saline (control) or tramadol [3 mg/kg BW (TR3) or 5 mg/kg BW (TR5)]. All drugs were administered intravenously. Variables evaluated included heart rate (HR), respiratory rate (RR), systolic, mean, and diastolic blood pressures (SAP, MAP, and DAP), and sedation [by use of a simple descriptive scale (SDS, range: 0 to 3) and a numeric rating scale (NRS, range: 0 to 10)]. Variables were recorded 25 min after acepromazine and for 80 min after saline or tramadol. Acepromazine administration resulted in mild sedation in most dogs and decreased RR, SAP, MAP, and DAP in all treatments. Tramadol administration did not significantly increase SDS or NRS scores compared to acepromazine alone. The only exception to this rule was observed at 20 min after TR3, when NRS was higher in this group than in the control treatment. Administration of tramadol (TR3 and TR5) decreased HR. Under the conditions of this study, sedation induced by acepromazine with tramadol was similar to that of acepromazine alone. The main adverse effects of the combination were a decrease in blood pressure and HR, without clinical significance.