Influence of a novel scaffold composed of polyurethane, hydroxyapatite, and decellularized bone particles on the healing of fourth metacarpal defects in mares.

OBJECTIVE: To determine the effect of a novel scaffold, designed for use in bone regeneration, on healing of splint bone segmental defects in mares. STUDY DESIGN: In vivo experimental study. SAMPLE POPULATION: Five adult mares (4-10 years old; mean weight, 437.7 kg ± 29 kg). METHODS: Bilateral 2-cm full-thickness defects were created in the fourth metacarpal bones (MCIV) of each horse. Each defect was randomly assigned to either a novel scaffold treatment (n = 5) or an untreated control (n = 5). The scaffold was composed of polyurethane, hydroxyapatite, and decellularized bone particles. Bone healing was assessed for a period of 60 days by thermography, ultrasonography, radiography, and computed tomography (CT). Biopsies of each defect were performed 60 days after surgery for histological evaluation. RESULTS: On the basis of radiographic analysis, scaffold-treated defects had greater filling (67.42% ± 26.7%) compared with untreated defects (35.88% ± 32.7%; P = .006). After 60 days, CT revealed that the density of the defects treated with the scaffolds (807.80 ± 129.6 Hounsfield units [HU]) was greater than density of the untreated defects (464.80 ± 81.3 HU; P = .004). Evaluation of histology slides provided evidence of bone formation within an average of 9.43% ± 3.7% of the cross-sectional area of scaffolds in contrast to unfilled defects in which connective tissue was predominant throughout the biopsy specimens. CONCLUSION: The novel scaffold was biocompatible and supported bone formation within the MCIV segmental defects. CLINICAL SIGNIFICANCE: This novel scaffold offers an effective option for filling bone voids in horses when support of bone healing is indicated.

Sedative effects and pharmacokinetics of detomidine when administered intravenously and intravaginally as a gel in alpacas.

OBJECTIVES: To evaluate the sedative effects and pharmacokinetics of detomidine gel administered intravaginally to alpacas in comparison with intravenously (IV) administered detomidine. STUDY DESIGN: Randomized, crossover, blinded experiment. ANIMALS: A group of six healthy adult female Huacaya alpacas (70.3 ± 7.9 kg). METHODS: Alpacas were studied on two occasions separated by ≥5 days. Treatments were IV detomidine hydrochloride (70 µg kg-1; treatment DET-IV) or detomidine gel (200 µg kg-1; treatment DET-VAG) administered intravaginally. Sedation and heart rate (HR) were evaluated at intervals for 240 minutes. Venous blood was collected at intervals for 360 minutes after treatment for analysis of detomidine, carboxydetomidine and hydroxydetomidine using liquid chromatography-tandem mass spectrometry. Measured variables were compared between treatments and over time using mixed model analysis. Data are presented as the mean ± standard error of the mean, and a p value of <0.05 was considered significant. RESULTS: Onset of sedation was faster in treatment DET-IV (1.6 ± 0.2 minutes) than in treatment DET-VAG (13.0 ± 2.5 minutes). Time to maximum sedation was shorter in treatment DET-IV (8.3 ± 1.3 minutes) than in treatment DET-VAG (25 ± 4 minutes). Duration of sedation was not different between treatments. There was a significant linear relationship between sedation score and plasma detomidine concentration. HR was less than baseline for 60 and 125 minutes for treatments DET-IV and DET-VAG, respectively. The maximal decrease in HR occurred at 15 minutes for both treatments. The mean maximum plasma concentration of detomidine, time to maximum concentration and bioavailability for treatment DET-VAG were 39.6 ng mL-1, 19.9 minutes and 20%, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine administration at the doses studied resulted in moderate sedation when administered IV or intravaginally to alpacas.

Evaluation of the sedative effects and pharmacokinetics of detomidine gel administered intravaginally to horses.

OBJECTIVES: To determine the sedative effects and pharmacokinetic profile of detomidine when administered intravaginally as a gel formulation to horses. STUDY DESIGN: Randomized, crossover, masked experimental design. ANIMALS: A group of six healthy adult mares (494 ± 56 kg). METHODS: Mares were studied on two occasions and were administered either detomidine hydrochloride (10 µg kg-1) intravenously (treatment IV) or detomidine gel (40 µg kg-1) intravaginally (treatment IVG), separated by 1 week. Sedation, ataxia, muzzle-floor distance and heart rate (HR) were evaluated every 15 minutes for 240 minutes. Venous blood samples were collected at 15, 30, 45, 60, 90, 120, 150, 180, 240, 300 and 360 minutes postadministration and were analyzed for detomidine and metabolites using liquid chromatography-tandem mass spectrometry. Measured variables were compared over time and between treatments using mixed model analysis. Correlation between drug plasma concentrations and muzzle-floor distance, and sedation and ataxia scores was determined using the Spearman correlation coefficient. Data are presented as mean ± standard error of the mean and p value was set at <0.05. RESULTS: Sedation was shorter with IV (119 ± 16 minutes) than with IVG (188 ± 22 minutes). Ataxia scores remained greater than baseline for 90 and 135 minutes for treatments IV and IVG, respectively. HR was lower than baseline for 45 and 30 minutes for IV and IVG, respectively, but did not differ between treatments. The mean maximum plasma concentration of detomidine, time to maximum concentration and bioavailability for treatment IVG was 8.57 ng mL-1, 0.37 hour and 25%, respectively. There was a significant correlation (r = 0.68) between plasma detomidine concentrations and sedation score. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine gel administered intravaginally resulted in clinically important sedation and is a viable method for detomidine gel delivery in mares.

Effect of fentanyl on the induction dose and minimum infusion rate of alfaxalone preventing movement in dogs.

OBJECTIVE: To determine the effect of fentanyl on the induction dose and minimum infusion rate of alfaxalone required to prevent movement in response to a noxious stimulus (MIRNM) in dogs. STUDY DESIGN: Experimental crossover design. ANIMALS: A group of six healthy, adult, intact female mixed-breed dogs, weighing 19.7 ± 1.3 kg. METHODS: Dogs were randomly administered one of three treatments at weekly intervals: premedication with 0.9% saline (treatment A), fentanyl 5 µg kg-1 (treatment ALF) or fentanyl 10 µg kg-1 (treatment AHF), administered intravenously over 5 minutes. Anesthesia was induced 5 minutes later with incremental doses of alfaxalone to achieve intubation and was maintained for 90 minutes in A with alfaxalone (0.12 mg kg-1 minute-1), in ALF with alfaxalone (0.09 mg kg-1 minute-1) and fentanyl (0.1 µg kg-1 minute-1) and in AHF with alfaxalone (0.06 mg kg-1 minute-1) and fentanyl (0.2 µg kg-1 minute-1). The alfaxalone infusion was increased or decreased by 0.006 mg kg-1 minute-1 based on positive or negative response to antebrachium stimulation (50 V, 50 Hz, 10 ms). Data were analyzed using a mixed-model anova and presented as least squares means ± standard error. RESULTS: Alfaxalone induction doses were 3.50 ± 0.13 (A), 2.17 ± 0.10 (ALF) and 1.67 ± 0.10 mg kg-1 (AHF) and differed among treatments (p < 0.05). Alfaxalone MIRNM was 0.17 ± 0.01 (A), 0.10 ± 0.01 (ALF) and 0.07 ± 0.01 mg kg-1 minute-1 (AHF) and differed among treatments. ALF and AHF decreased the MIRNM by 44 ± 8% and 62 ± 5%, respectively (p < 0.05). Plasma alfaxalone concentrations at MIRNM were 5.82 ± 0.48 (A), 4.40 ± 0.34 (ALF) and 2.28 ± 0.09 µg mL-1 (AHF). CONCLUSIONS AND CLINICAL RELEVANCE: Fentanyl, at the doses studied, significantly decreased the alfaxalone induction dose and MIRNM.

Effect of fentanyl on the induction dose and minimum infusion rate of propofol preventing movement in dogs.

OBJECTIVE: To determine the effect of fentanyl on the induction dose of propofol and minimum infusion rate required to prevent movement in response to noxious stimulation (MIRNM) in dogs. STUDY DESIGN: Crossover experimental design. ANIMALS: Six healthy, adult intact male Beagle dogs, mean±standard deviation 12.6±0.4 kg. METHODS: Dogs were administered 0.9% saline (treatment P), fentanyl (5 µg kg-1) (treatment PLDF) or fentanyl (10 µg kg-1) (treatment PHDF) intravenously over 5 minutes. Five minutes later, anesthesia was induced with propofol (2 mg kg-1, followed by 1 mg kg-1 every 15 seconds to achieve intubation) and maintained for 90 minutes by constant rate infusions (CRIs) of propofol alone or with fentanyl: P, propofol (0.5 mg kg-1 minute-1); PLDF, propofol (0.35 mg kg-1 minute-1) and fentanyl (0.1 µg kg-1 minute-1); PHDF, propofol (0.3 mg kg-1 minute-1) and fentanyl (0.2 µg kg-1 minute-1). Propofol CRI was increased or decreased based on the response to stimulation (50 V, 50 Hz, 10 mA), with 20 minutes between adjustments. Data were analyzed using a mixed-model anova and presented as mean±standard error. RESULTS: ropofol induction doses were 6.16±0.31, 3.67±0.21 and 3.33±0.42 mg kg-1 for P, PLDF and PHDF, respectively. Doses for PLDF and PHDF were significantly decreased from P (p<0.05) but not different between treatments. Propofol MIRNM was 0.60±0.04, 0.29±0.02 and 0.22±0.02 mg kg-1 minute-1 for P, PLDF and PHDF, respectively. MIRNM in PLDF and PHDF was significantly decreased from P. MIRNM in PLDF and PHDF were not different, but their respective percent decreases of 51±3 and 63±2% differed (p=0.035). CONCLUSIONS AND CLINICAL RELEVANCE: Fentanyl, at the doses studied, caused statistically significant and clinically important decreases in the propofol induction dose and MIRNM.

Effect of dexmedetomidine on the minimum infusion rate of propofol preventing movement in dogs.

OBJECTIVE: To determine the effect of dexmedetomidine on induction dose and minimum infusion rate of propofol preventing movement (MIRNM). STUDY DESIGN: Randomized crossover, unmasked, experimental design. ANIMALS: Three male and three female healthy Beagle dogs weighing 10.2 ± 2.8 kg. METHODS: Dogs were studied on three occasions at weekly intervals. Premedications were 0.9% saline (treatment P) or dexmedetomidine (1 µg kg-1, treatment PLD; 2 µg kg-1, treatment PHD) intravenously. Anesthesia was induced with propofol (2 mg kg-1 and then 1 mg kg-1 every 15 seconds) until intubation. Anesthesia was maintained for 90 minutes in P with propofol (0.5 mg kg-1 minute-1) and saline, in PLD with propofol (0.35 mg kg-1 minute-1) and dexmedetomidine (1 µg kg-1 hour-1), and in PHD with propofol (0.3 mg kg-1 minute-1) and dexmedetomidine (2 µg kg-1 hour-1). The stimulus (50 V, 50 Hz, 10 ms) was applied to the antebrachium, and propofol infusion was increased or decreased by 0.025 mg kg-1 minute-1 based on a positive or negative response, respectively. Data were analyzed using a mixed-model anova and presented as mean ± standard error. RESULTS: Propofol induction doses were 8.68 ± 0.57 (P), 6.13 ± 0.67 (PLD) and 4.78 ± 0.39 (PHD) mg kg-1 and differed among treatments (p < 0.05). Propofol MIRNM values were 0.68 ± 0.13, 0.49 ± 0.16 and 0.26 ± 0.05 mg kg-1 minute-1 for P, PLD and PHD, respectively. Propofol MIRNM decreased 59% in PHD (p < 0.05). Plasma propofol concentrations were 14.04 ± 2.30 (P), 11.30 ± 4.30 (PLD) and 7.96 ± 0.72 (PHD) µg mL-1 and dexmedetomidine concentrations were 0.68 ± 0.12 (PLD) and 0.89 ± 0.08 (PHD) ng mL-1 at MIRNM determination. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine (1 and 2 µg kg-1) decreased propofol induction dose. Dexmedetomidine (2 µg kg-1 hour-1) resulted in a significant decrease in propofol MIRNM.

Antinociceptive and selected physiological effects of morphine and xylazine on tiletamine-zolazepam anesthesia in llamas.

OBJECTIVE: Evaluate antinociception, anesthesia, and recovery in llamas given tiletamine-zolazepam (TZ) with either morphine, xylazine, morphine and xylazine, or saline. STUDY DESIGN: Randomized crossover experimental study. ANIMALS: Six healthy, adult intact male llamas. METHODS: Llamas were given each of four treatments intramuscularly with a 1-week washout: TZ (2 mg kg(-1) ) combined with either morphine (0.5 mg kg(-1) ; M), xylazine (0.15 mg kg(-1) ; X), morphine (0.5 mg kg(-1) ) and xylazine (0.15mg kg(-1) ) (MX), or saline (C). Llamas breathed room air during the experiment. Characteristics of anesthesia, recovery, and selected cardiopulmonary variables were recorded. Antinociception was assessed by clamping a claw at 5-minute intervals. Data were analyzed using a mixed-model anova and Tukey-Kramer test, and are expressed as least squares mean ± SEM. Significance was set at p < 0.05. RESULTS: No llama in the control group demonstrated antinociception. Antinociception was longest with treatment MX, followed by treatments X and M, respectively. Heart rates in llamas given treatments X and MX were significantly lower than with other treatments. The respiratory rate in llamas given treatment C was greater (p < 0.05) than for all other treatments, however, the respiratory rate was not significantly different among treatments X, M and MX. The PaO2 for llamas given MX remained <60 mmHg throughout the 20 minute period of blood gas analysis. Mean arterial blood pressure in llamas in treatment MX was less than for treatments M or C. CONCLUSION AND CLINICAL RELEVANCE: The combination of morphine (0.5 mg kg(-1) ) and xylazine (0.15 mg kg(-1) ) increased the duration of antinociception compared with xylazine alone, in TZ-anesthetized llamas. Treatments X, M and MX were associated with hypoxemia (PaO2 < 60 mmHg).

The effect of fentanyl on the end-tidal sevoflurane concentration needed to prevent motor movement in dogs.

OBJECTIVE: The objectives of this study were to determine the effects of fentanyl on the end-tidal concentration of sevoflurane needed to prevent motor movement (MACNM ) in response to noxious stimulation, and to evaluate if acute tolerance develops. STUDY DESIGN: Randomized cross-over experimental study. ANIMALS: Six healthy, adult (2-3 years old), intact male, mixed-breed dogs weighing 16.2 ± 1.1 kg. METHODS: Six dogs were randomly assigned to receive one of three separate treatments over a 3 week period. After baseline sevoflurane MACNM (MACNM-B) determination, fentanyl treatments (T) were administered as a loading dose (Ld) and constant rate infusion (CRI) as follows: T1-Ld of 7.5 µg kg(-1) and CRI at 3 µg kg(-1) hour(-1); T2-Ld of 15 µg kg(-1) and CRI at 6.0 µg kg (-1) hour(-1); T3-Ld of 30 µg kg(-1) and CRI at 12 µg kg(-1) hour(-1). The MACNM was defined as the minimum end-tidal sevoflurane concentration preventing motor movement. The first post-treatment MACNM (MACNM-I) determination was initiated 90 minutes after the start of the CRI, and a second MACNM (MACNM - II) determination was initiated 3 hours after MACNM-I was established. RESULTS: The overall least square mean MACNM-B for all groups was 2.66%. All treatments decreased (p < 0.05) MACNM, and the decrease from baseline was 22%, 35% and 41% for T1, T2 and T3, respectively. Percentage change in T1 differed (p < 0.05) from T2 and T3; however, T2 did not differ from T3. MACNM-I was not significantly different from MACNM-II within treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Fentanyl doses in the range of 3-12 µg kg(-1) hour(-1) significantly decreased the sevoflurane MACNM. Clinically significant tolerance to fentanyl did not occur under the study conditions.

The effect of midazolam on the end-tidal concentration of isoflurane necessary to prevent movement in dogs.

OBJECTIVE: To determine the possible additive effect of midazolam, a GABA(A) agonist, on the end-tidal concentration of isoflurane that prevents movement (MAC(NM) ) in response to noxious stimulation. STUDY DESIGN: Randomized cross-over experimental study. ANIMALS: Six healthy, adult intact male, mixed-breed dogs. METHODS: After baseline isoflurane MAC(NM) (MAC(NM-B) ) determination, midazolam was administered as a low (LDS), medium (MDS) or high (HDS) dose series of midazolam. Each series consisted of two dose levels, low and high. The LDS was a loading dose (Ld) of 0.2 mg kg(-1) and constant rate infusion (CRI) (2.5 µg kg(-1) minute(-1)) (LDL), followed by an Ld (0.4 mg kg(-1)) and CRI (5 µg kg(-1) minute(-1)) (LDH). The MDS was an Ld (0.8 mg kg(-1)) and CRI (10 µg kg(-1) minute(-1)) (MDL) followed by an Ld (1.6 mg kg(-1)) and CRI (20 µg kg(-1) minute(-1)) (MDH). The HDS was an Ld (3.2 mg kg(-1)) and CRI (40 µg kg(-1) minute(-1)) (HDL) followed by an Ld (6.4 mg kg(-1)) and CRI (80 µg kg(-1) minute(-1)) (HDH). MAC(NM) was re-determined after each dose in each series (MAC(NM-T)). RESULTS: The median MAC(NM-B) was 1.42. MAC(NM-B) did not differ among groups (p > 0.05). Percentage reduction in MAC(NM) was significantly less in the LDS (11 ± 5%) compared with MDS (30 ± 5%) and HDS (32 ± 5%). There was a weak correlation between the plasma midazolam concentration and percentage MAC(NM) reduction (r = 0.36). CONCLUSION AND CLINICAL RELEVANCE: Midazolam doses in the range of 10-80 µg kg(-1) minute(-1) significantly reduced the isoflurane MAC(NM) . However, doses greater than 10 µg kg(-1) minute(-1) did not further decrease MAC(NM) indicating a ceiling effect.

Dexmedetomidine prolongs the duration of action of mepivacaine on anesthesia of the palmar digital nerves of horses.

OBJECTIVE: To determine whether palmar digital nerve (PDN) blockade in horses with a combination of dexmedetomidine and mepivacaine would block the response to mechanical force applied to the digit longer than would anesthetizing these nerves with mepivacaine alone or dexmedetomidine alone. ANIMALS: 8 mares with no signs of lameness. PROCEDURES: In a randomized, crossover, blinded, experimental study, both PDNs of the same forelimb of each horse were anesthetized by perineural injection with either 30 mg mepivacaine alone, 250 µg of dexmedetomidine alone, or 30 mg mepivacaine combined with 250 µg of dexmedetomidine. Each horse received each treatment, and treatments were administered ≥ 2 weeks apart. The mechanical nociceptive threshold was measured at a region between the heel bulbs with the use of a digital force gauge before (baseline) and at 15-minute intervals after treatment. RESULTS: The mean duration of sensory blockade of the digit was 2-fold longer when a combination of mepivacaine and dexmedetomidine was administered (371 minutes), compared with when mepivacaine alone was administered (186 minutes). Treatment with dexmedetomidine alone did not change the mechanical nociceptive threshold substantially from baseline and resulted in no clinical signs of sedation. CLINICAL RELEVANCE: Results indicated that relief from digital pain provided by perineural treatment with mepivacaine for PDN blockade can be extended by adding dexmedetomidine to the injectate.

Local anesthetics as pain therapy in horses.

This article describes the rationale behind the use of systemically administered lidocaine as an analgesic. The analgesic efficacy of intravenously administered lidocaine is well documented by studies in human patients and laboratory animals. The mechanism by which systemically administered lidocaine produces analgesia is uncertain but is thought to include action at sodium, calcium, and potassium channels and the N-methyl-D-aspartate acid receptor. In addition, the anti-inflammatory actions of lidocaine are important in producing analgesia because inflammatory mediators augment neuronal excitability. The available studies of systemically administered lidocaine in horses provide evidence for the analgesic and anesthetic effects of intravenous lidocaine in this species.

Efficacy and duration of effect for liposomal bupivacaine when administered perineurally to the palmar digital nerves of horses.

OBJECTIVE: To determine the efficacy and duration of effect for liposomal bupivacaine following perineural administration to the medial and lateral palmar digital nerves of horses. ANIMALS: 9 nonlame mares. PROCEDURES: For each horse, 2 mL of liposomal bupivacaine (13.3 mg/mL; total dose, 53.2 mg or approx 0.11 mg/kg) or sterile saline (0.9% NaCl) solution was injected adjacent to the medial and lateral palmar digital nerves at the level of the distal aspect of the proximal sesamoid bones of a randomly selected forelimb. Twenty-one days later, the opposite treatment was administered in the contralateral forelimb. A digital algometer was used to measure the mechanical nociceptive threshold (MNT) immediately before and at predetermined times for 48 hours after injection of each treatment. The mean MNT was compared between the 2 treatments at each measurement time. RESULTS: The mean MNT for the liposomal bupivacaine-treated limbs was significantly greater (ie, the limb was less sensitive) than that for the saline-treated limbs between 30 minutes and 4 hours after treatment injection. Following liposomal bupivacaine administration, 1 horse developed mild swelling at the injection sites that resolved without treatment within 24 hours. No other adverse effects were observed. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that liposomal bupivacaine is another option for perineural anesthesia in horses. Further research is necessary to determine the optimal dose and better elucidate the duration of effect for the drug when used for palmar digital nerve blocks in horses.

Effects of tramadol on the minimum alveolar concentration of sevoflurane in dogs.

OBJECTIVE: To evaluate the effect of tramadol on sevoflurane minimum alveolar concentration (MAC(SEVO)) in dogs. It was hypothesized that tramadol would dose-dependently decrease MAC(SEVO). STUDY DESIGN: Randomized crossover experimental study. ANIMALS: Six healthy, adult female mixed-breed dogs (24.2 +/- 2.6 kg). METHODS: Each dog was studied on two occasions with a 7-day washout period. Anesthesia was induced using sevoflurane delivered via a mask. Baseline MAC (MAC(B)) was determined starting 45 minutes after tracheal intubation. A noxious stimulus (50 V, 50 Hz, 10 ms) was applied subcutaneously over the mid-humeral area. If purposeful movement occurred, the end-tidal sevoflurane was increased by 0.1%; otherwise, it was decreased by 0.1%, and the stimulus was re-applied after a 20-minute equilibration. After MAC(B) determination, dogs randomly received a tramadol loading dose of either 1.5 mg kg(-1) followed by a continuous rate infusion (CRI) of 1.3 mg kg(-1 )hour(-1) (T1) or 3 mg kg(-1) followed by a 2.6 mg kg(-1 )hour(-1) CRI (T2). Post-treatment MAC determination (MAC(T)) began 45 minutes after starting the CRI. Data were analyzed using a mixed model anova to determine the effect of treatment on percentage change in baseline MAC(SEVO) (p < 0.05). RESULTS: The MAC(B) values were 1.80 +/- 0.3 and 1.75 +/- 0.2 for T1 and T2, respectively, and did not differ significantly. MAC(T) decreased by 26 +/- 8% for T1 and 36 +/- 12% for T2. However, there was no statistically significant difference in the decrease between the two treatments. CONCLUSION AND CLINICAL RELEVANCE: Tramadol significantly reduced MAC(SEVO) but this was not dose dependent at the doses studied.

Postoperative ileus: pathogenesis and treatment.

Surgical manipulation of the intestines activates intestinal macrophages that release cytokines and nitric oxide, which results in inhibition of intestinal motility. Subsequent infiltration of circulating leukocytes into the intestinal wall contributes to cytokine and nitric oxide release and exacerbates ileus. Other factors contributing to ileus are endotoxemia; edema of the intestine wall subsequent to excessive fluid therapy; hypocalcemia; and long abdominal incisions. Because treatment of ileus with prokinetic drugs has not proven to be very effective, efforts should be directed at reducing its severity. Strategies which reduce the severity of ileus include pretreatment with a nonsteroidal anti-inflammatory drug, minimizing the length of the abdominal incision, reducing intestinal manipulation, intraoperative lidocaine infusion, correction of hypocalcemia, limiting the volume of intravenous fluids to prevent intestinal edema, and administration of alpha(2) antagonists.

Effects of intravenous lidocaine, ketamine, and the combination on the minimum alveolar concentration of sevoflurane in dogs.

OBJECTIVE: To evaluate the effects of intravenous lidocaine (L) and ketamine (K) alone and their combination (LK) on the minimum alveolar concentration (MAC) of sevoflurane (SEVO) in dogs. STUDY DESIGN: Prospective randomized, Latin-square experimental study. ANIMALS: Six, healthy, adult Beagles, 2 males, 4 females, weighing 7.8 - 12.8 kg. METHODS: Anesthesia was induced with SEVO in oxygen delivered by face mask. The tracheas were intubated and the lungs ventilated to maintain normocapnia. Baseline minimum alveolar concentration of SEVO (MAC(B)) was determined in duplicate for each dog using an electrical stimulus and then the treatment was initiated. Each dog received each of the following treatments, intravenously as a loading dose (LD) followed by a constant rate infusion (CRI): lidocaine (LD 2 mg kg(-1), CRI 50 microg kg(-1)minute(-1)), lidocaine (LD 2 mg kg(-1), CRI 100 microg kg(-1) minute(-1)), lidocaine (LD 2 mg kg(-1), CRI 200 microg kg(-1) minute(-1)), ketamine (LD 3 mg kg(-1), CRI 50 microg kg(-1) minute(-1)), ketamine (LD 3 mgkg(-1), CRI 100 microg kg(-1) minute(-1)), or lidocaine (LD 2 mg kg(-1), CRI 100 microg kg(-1) minute(-1)) + ketamine (LD 3 mg kg(-1), CRI 100 microg kg(-1) minute(-1)) in combination. Post-treatment MAC (MAC(T)) determination started 30 minutes after initiation of treatment. RESULTS: Least squares mean +/- SEM MAC(B) of all groups was 1.9 +/- 0.2%. Lidocaine infusions of 50, 100, and 200 microg kg(-1) minute(-1) significantly reduced MAC(B) by 22.6%, 29.0%, and 39.6%, respectively. Ketamine infusions of 50 and 100 microg kg(-1) minute(-1) significantly reduced MAC(B) by 40.0% and 44.7%, respectively. The combination of K and L significantly reduced MAC(B) by 62.8%. CONCLUSIONS AND CLINICAL RELEVANCE: Lidocaine and K, alone and in combination, decrease SEVO MAC in dogs. Their use, at the doses studied, provides a clinically important reduction in the concentration of SEVO during anesthesia in dogs.

Effects of stacked wedge pads and chains applied to the forefeet of Tennessee Walking Horses for a five-day period on behavioral and biochemical indicators of pain, stress, and inflammation.

OBJECTIVE To determine the effects of stacked wedge pads and chains applied to the forefeet of Tennessee Walking Horses on behavioral and biochemical indicators of pain, stress, and inflamation. ANIMALS 20 Tennessee Walking Horses. PROCEDURES Horses were randomly assigned to 2 treatment groups: keg shoes (control; n = 10) or stacked wedge pads and exercise with chains (10). Ten days before treatment application, an accelerometer was attached at the left metatarsus of each horse to record daily activity. Horses were exercised for 20 minutes daily, beginning on day -7. On day 0, exercise ceased, the forefeet were trimmed, and the assigned treatment was applied. From days 1 through 5, horses were exercised as before. Blood samples for measurement of plasma cortisol, substance P, and fibrinogen concentrations were collected on days -5, 1, and 5 before and after exercise and every 30 minutes thereafter for 6 hours. RESULTS No significant differences in plasma concentrations of cortisol, substance P, and fibrinogen were detected between groups. Although lying behaviors changed after shoes were applied, these behaviors did not differ significantly between groups. Shoeing appeared to have altered behavior to a greater extent than did the type of treatment applied. CONCLUSIONS AND CLINICAL RELEVANCE Application of stacked wedge pads and chains to the forefeet of horses for a 5-day period as performed in this study evoked no acute or subacute stress or nociceptive response as measured. Although these findings should not be extrapolated to the long-term use of such devices in Tennessee Walking Horses performing the running walk, the data should be considered when making evidence-based decisions relating to animal welfare and the use of stacked wedge pads and chains.

Pharmacokinetics and pharmacodynamics of midazolam following intravenous and intramuscular administration to sheep.

OBJECTIVE To determine the pharmacokinetic and pharmacodynamic effects of midazolam following IV and IM administration in sheep. ANIMALS 8 healthy adult rams. PROCEDURES Sheep were administered midazolam (0.5 mg/kg) by the IV route and then by the IM route 7 days later in a crossover study. Physiologic and behavioral variables were assessed and blood samples collected for determination of plasma midazolam and 1-hydroxymidazolam (primary midazolam metabolite) concentrations immediately before (baseline) and at predetermined times for 1,440 minutes after midazolam administration. Pharmacokinetic parameters were calculated by compartmental and noncompartmental methods. RESULTS Following IV administration, midazolam was rapidly and extensively distributed and rapidly eliminated; mean ± SD apparent volume of distribution, elimination half-life, clearance, and area under the concentration-time curve were 838 ± 330 mL/kg, 0.79 ± 0.44 hours, 1,272 ± 310 mL/h/kg, and 423 ± 143 h·ng/mL, respectively. Following IM administration, midazolam was rapidly absorbed and bioavailability was high; mean ± SD maximum plasma concentration, time to maximum plasma concentration, area under the concentration-time curve, and bioavailability were 820 ± 268 ng/mL, 0.46 ± 0.26 hours, 1,396 ± 463 h·ng/mL, and 352 ± 148%, respectively. Respiratory rate was transiently decreased from baseline for 15 minutes after IV administration. Times to peak sedation and ataxia after IV administration were less than those after IM administration. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated midazolam was a suitable short-duration sedative for sheep, and IM administration may be a viable alternative when IV administration is not possible.

Effect of fentanyl and lidocaine on the end-tidal sevoflurane concentration preventing motor movement in dogs.

OBJECTIVE To determine effects of fentanyl, lidocaine, and a fentanyl-lidocaine combination on the minimum alveolar concentration of sevoflurane preventing motor movement (MACNM) in dogs. ANIMALS 6 adult Beagles. PROCEDURES Dogs were anesthetized with sevoflurane in oxygen 3 times (1-week intervals). Baseline MACNM (MACNM-B) was determined starting 45 minutes after induction of anesthesia. Dogs then received 1 of 3 treatments IV: fentanyl (loading dose, 15 µg/kg; constant rate infusion [CRI], 6 µg/kg/h), lidocaine (loading dose, 2 mg/kg; CRI, 6 mg/kg/h), and the fentanyl-lidocaine combination at the same doses. Determination of treatment MACNM (MACNM-T) was initiated 90 minutes after start of the CRI. Venous blood samples were collected at the time of each treatment MACNM measurement for determination of plasma concentrations of fentanyl and lidocaine. RESULTS Mean ± SEM overall MACNM-B for the 3 treatments was 2.70 ± 0.27 vol%. The MACNM decreased from MACNM-B to MACNM-T by 39%, 21%, and 55% for fentanyl, lidocaine, and the fentanyl-lidocaine combination, respectively. This decrease differed significantly among treatments. Plasma fentanyl concentration was 3.25 and 2.94 ng/mL for fentanyl and the fentanyl-lidocaine combination, respectively. Plasma lidocaine concentration was 2,570 and 2,417 ng/mL for lidocaine and the fentanyl-lidocaine combination, respectively. Plasma fentanyl and lidocaine concentrations did not differ significantly between fentanyl and the fentanyl-lidocaine combination or between lidocaine and the fentanyl-lidocaine combination. CONCLUSIONS AND CLINICAL RELEVANCE CRIs of fentanyl, lidocaine, and the fentanyl-lidocaine combination at the doses used were associated with clinically important and significant decreases in the MACNM of sevoflurane in dogs.

Assessment of agreement among diplomates of the American College of Veterinary Anesthesia and Analgesia for scoring the recovery of horses from anesthesia by use of subjective grading scales and development of a system for evaluation of the recovery of horses from anesthesia by use of accelerometry.

OBJECTIVE To evaluate agreement among diplomates of the American College of Veterinary Anesthesia and Analgesia for scores determined by use of a simple descriptive scale (SDS) or a composite grading scale (CGS) for quality of recovery of horses from anesthesia and to investigate use of 3-axis accelerometry (3AA) for objective evaluation of recovery. ANIMALS 12 healthy adult horses. PROCEDURES Horses were fitted with a 3AA device and then were anesthetized. Eight diplomates evaluated recovery by use of an SDS, and 7 other diplomates evaluated recovery by use of a CGS. Agreement was tested with κ and AC1 statistics for the SDS and an ANOVA for the CGS. A library of mathematical models was used to map 3AA data against CGS scores. RESULTS Agreement among diplomates using the SDS was slight (κ = 0.19; AC1 = 0.22). The CGS scores differed significantly among diplomates. Best fit of 3AA data against CGS scores yielded the following equation: RS = 9.998 × SG0.633 × ∑UG0.174, where RS is a horse's recovery score determined with 3AA, SG is acceleration of the successful attempt to stand, and ∑UG is the sum of accelerations of unsuccessful attempts to stand. CONCLUSIONS AND CLINICAL RELEVANCE Subjective scoring of recovery of horses from anesthesia resulted in poor agreement among diplomates. Subjective scoring may lead to differences in conclusions about recovery quality; thus, there is a need for an objective scoring method. The 3AA system removed subjective bias in evaluations of recovery of horses and warrants further study.

Field Sedation and Anesthesia of Ruminants.

Many surgical procedures on ruminants can be performed humanely and safely using local or regional anesthesia and physical restraint, but sedation and general anesthesia are necessary in order to perform some procedures. Although anesthesia-associated risks are greater in ruminants than monogastrics, ruminants can be anesthetized relatively safely in a field setting if the risks are understood, and adequate planning and precautions are in place. This article discusses the important features impacting sedation and anesthesia of cattle and small ruminants, and describes some commonly used drug protocols.