Objective-To assess effects of body position on direct measurements of intra-abdominal pressure (IAP) and abdominal perfusion pressure (APP) in horses anesthetized with total intravenous anesthesia (TIVA). Animals-9 healthy adult horses. Procedures-Instrumentation in unsedated standing horses involved insertion of an arterial catheter for blood pressure measurements and 3 intraperitoneal cannulas (left flank, right flank, and ventral abdomen) for IAP measurements. Baseline values were measured for heart rate, respiratory rate, systolic arterial blood pressure, mean arterial blood pressure (MAP), diastolic arterial blood pressure, and IAP. Horses were medicated with xylazine, and pressures were measured again. Anesthesia was induced with ketamine-diazepam and maintained with a ketamine-guaifenesin infusion. Horses were positioned twice into left lateral recumbency, right lateral recumbency, or dorsal recumbency. Hemodynamic pressures and accessible abdominal pressures were measured for each recumbency position. The APP was calculated as MAP - IAP. Differences in IAP, MAP, APP and sedation (standing horses) or body position (anesthetized horses) were compared by means of repeated-measures ANOVA or paired t tests. Results-Baseline hemodynamic and IAPs were not different after xylazine administration. Ventral abdomen IAP and MAP were lower for horses in dorsal recumbency than in right or left lateral recumbency. Ventral abdomen APP remained unchanged. For lateral recumbencies, flank IAP was lower and APP was higher than pressure measurements at the same sites during dorsal recumbency. Conclusions and Clinical Relevance-Body position affected IAP and APP in healthy anesthetized horses. These effects should be considered when developing IAP acquisition methods for use in horses with abdominal disease.

Objective—To determine the pharmacokinetic parameters of xylazine, ketamine, and butorphanol (XKB) administered IM and sodium salicylate (SAL) administered PO to calves and to compare drug effects on biomarkers of pain and distress following sham and actual castration and dehorning. Animals—40 Holstein bull calves from 3 farms. Procedures—Calves weighing 108 to 235 kg (n = 10 calves/group) received one of the following treatments prior to sham (period 1) and actual (period 2) castration and dehorning: saline (0.9% NaCl) solution IM (placebo); SAL administered PO through drinking water at concentrations from 2.5 to 5 mg/mL from 24 hours prior to period 1 to 48 hours after period 2; butorphanol (0.025 mg/kg), xylazine (0.05 mg/kg), and ketamine (0.1 mg/kg) coadministered IM immediately prior to both periods; and a combination of SAL and XKB (SAL+XKB). Plasma drug concentrations, average daily gain (ADG), chute exit velocity, serum cortisol concentrations, and electrodermal activity were evaluated. Results—ADG (days 0 to 13) was significantly greater in the SAL and SAL+XKB groups than in the other 2 groups. Calves receiving XKB had reduced chute exit velocity in both periods. Serum cortisol concentrations increased in all groups from period 1 to period 2. However, XKB attenuated the cortisol response for the first hour after castration and dehorning and oral SAL administration reduced the response from 1 to 6 hours. Administration of XKB decreased electrodermal activity scores in both periods. Conclusions and Clinical Relevance—SAL administered PO through drinking water decreased cortisol concentrations and reduced the decrease in ADG associated with castration and dehorning in calves.

Objective—To compare cardiovascular effects of sevoflurane alone and sevoflurane plus an IV infusion of lidocaine in horses. Animals—8 adult horses. Procedures—Each horse was anesthetized twice via IV administration of xylazine, diazepam, and ketamine. During 1 anesthetic episode, anesthesia was maintained by administration of sevoflurane in oxygen at 1.0 and 1.5 times the minimum alveolar concentration (MAC). During the other episode, anesthesia was maintained at the same MAC multiples via a reduced concentration of sevoflurane plus an IV infusion of lidocaine. Heart rate, arterial blood pressures, blood gas analyses, and cardiac output were measured during mechanical (controlled) ventilation at both 1.0 and 1.5 MAC for each anesthetic protocol and during spontaneous ventilation at 1 of the 2 MAC multiples. Results—Cardiorespiratory variables did not differ significantly between anesthetic protocols. Blood pressures were highest at 1.0 MAC during spontaneous ventilation and lowest at 1.5 MAC during controlled ventilation for either anesthetic protocol. Cardiac output was significantly higher during 1.0 MAC than during 1.5 MAC for sevoflurane plus lidocaine but was not affected by anesthetic protocol or mode of ventilation. Clinically important hypotension was detected at 1.5 MAC for both anesthetic protocols. Conclusions and Clinical Relevance—Lidocaine infusion did not alter cardiorespiratory variables during anesthesia in horses, provided anesthetic depth was maintained constant. The IV administration of lidocaine to anesthetized nonstimulated horses should be used for reasons other than to improve cardiovascular performance. Severe hypotension can be expected in nonstimulated horses at 1.5 MAC sevoflurane, regardless of whether lidocaine is administered.

Objective-To evaluate effects of sedation on stability of resistance of the respiratory system (RRS) and measures of resting energy expenditure (REE) by use of open-flow indirect calorimetry (IC) and treatment with aerosolized albuterol on REE in horses with recurrent airway obstruction (RAO). Animals-9 clinically normal horses and 8 horses with RAO. Procedure-In phase 1, RRS was measured by using forced oscillometry (FOT) in 5 clinically normal horses before and after sedation with xylazine. In phase 2, REE was measured in 4 clinically normal horses between 20 and 25 minutes and again 35 to 40 minutes after sedation with xylazine. In phase 3, IC was performed between 20 and 25 minutes and FOT was performed between 30 and 35 minutes after xylazine administration in 8 horses with RAO; after administration of 450 µg of albuterol, IC and FOT were repeated. Results-In phase 1, RRS values were significantly lower 5 and 10 minutes after sedation. In phase 2, diminishing sedation did not significantly affect REE. In phase 3, there was a significant decrease in mean RRS (1.15 +/- 0.25 vs 0.84 +/- 0.14 cm H20/L/s) and REE (30.68 +/- 17.89 vs 27.46 +/- 16.54 kcal/kg/d) after albuterol administration. Conclusions and Clinical Relevance-FOT and IC are useful in obtaining repeatable measurements of RRS and REE, respectively, in sedated horses. Concurrent bronchodilation and decreased REE after albuterol administration suggest that increased work of breathing as a result of airway obstruction may contribute to increased energy demands in horses with RAO.

The effect of xylazine, cisapride, and naloxone on myoelectric activity of the ileum, cecum, and proximal loop of the ascending colon (PLAC) was determined in 4 healthy Jersey cows implanted with 8 pairs of bipolar electrodes. A 4 X 4 Latin square design was used. The treatments included xylazine (0.04 mg/kg of body weight), cisapride (0.08 mg/kg), naloxone (0.05 mg/kg), and 0.9% sodium chloride solution (20 ml). All treatments were administered IV during early phase I of the migrating myoelectric complex in the ileum. Myoelectric activity was recorded for 4 hours after treatment, and data were analyzed for each hour separately. Xylazine significantly (P < 0.05) increased the duration of phase I of the first migrating myoelectric complex in the ileum to 220.72 +/- 26.89 minutes, compared with 30.91 +/- 10.11 minutes after administration of 0.9% sodium chloride solution. The number of cecocolic spikes per minute per electrode and the duration of cecocolic spike activity (percentage of recording time) were significantly (P < 0.05) decreased for the first 3 hours, and the number of propagated spike sequences in the cecum and PLAC was significantly (P < 0.05) decreased for the first 2 hours after administration of xylazine. Significant difference was not found between control and either,cisapride or naloxone treatment of healthy cows. However, during hour 1 after treatment with cisapride, number of spikes per minute, duration of spike activity, and number of propagated spike sequences were highest, compared with the other treatments. It was concluded that naloxone at the dosage used in this study was not suitable for medical treatment of cecal dilatation in cattle, when hypomotility of the cecum and PLAC must be reversed. Xylazine should not be used for relief of signs of pain in cases of cecal dilatation, because it significantly reduced myoelectric activity of the cecum and PLAC for at least 2 hours after treatment. Furthermore, results of this study indicated a trend (P > 0.05) toward increase of cecocolic myoelectric activity after administration of cisapride. It is the authors' opinion that the potential benefit of cisapride for medical treatment of cecal dilatation in cattle needs further evaluation.

Intraocular pressure (IOP) was measured, using applanation tonometry, in both eyes of 20 horses after topical application of 0.5% proparacaine to the cornea. Ultrasonic pachymetry was used to measure central, mid-peripheral, and peripheral corneal thickness (CT) in all 4 quadrants of both eyes of 25 horses. All measurements were repeated after auriculopalpebral nerve block, sedation by IV administration of xylazine, or combination of nerve block and sedation. Mean IOP after topical anesthesia of the cornea was 20.6 +/- 4.7 mm of Hg for the left eye and 20.35 +/- 3.7 mm of Hg for the right eye. Mean central CT was 793.2 +/- 42.3 micrometers. The peripheral part of the cornea was significantly (P < 0.05) thicker, on average, than the central part of the cornea. Auriculopalpebral nerve block had no significant effect on IOP or CT. Intravenous administration of xylazine resulted in a significant (P < 0.05) decrease in IOP, but had no effect on CT.

Cardiopulmonary consequences of IV administered glycopyrrolate (0.01 mg/kg of body weight), followed in 11 +/- 2 minutes by butorphanol (0.2 mg/ kg) and xylazine (0.5 mg/kg), were evaluated in 6 dogs, with and without nasal administration of oxygen (100 ml/kg/min). Glycopyrrolate caused significant (P < 0.05) increases in heart rate and cardiac index and significant (P < 0.05) decreases in stroke index. Subsequent administration of butorphanol and xylazine was associated with significant (P < 0.05) increases in systemic vascular resistance, mean arterial blood pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, PaCO2, venous admixture, oxygen extraction ratio, and hemoglobin concentration. It caused significant (P < 0.05) decreases in cardiac index, stroke index, breathing rate, minute volume index, oxygen delivery, and oxygen consumption. Mean arterial blood pressure, pulmonary vascular resistance, tidal volume index, and minute volume index were significantly (P < 0.05) higher when dogs were breathing room air. The arterial and venous PO2, and PCO2, and venous oxygen content were significantly (P < 0.05) higher, and the arterial and venous pH, and oxygen consumption were significantly (P < 0.05) lower when oxygen was administered. Pulsus alternans and S-T segment depression were observed in dogs of both groups. Ventricular premature contractions were observed in 1 dog breathing room air. All dogs were intubated briefly 15 minutes after administration of butorphanol and xylazine. Time to first spontaneous movement was 45 minutes. All dogs remained in lateral recumbency without physical restraint for 60 minutes.

In horses with noninduced, reversible airway obstruction (heaves), pulmonary function is improved after sedation with the alpha-adrenergic agonist xylazine. The mechanism of this effect is undetermined. Because the predominant excitatory innervation of equine airways is cholinergic, the influence of alpha 2-adrenergic receptor stimulation on the response of isolated distal airways to cholinergic stimulation was determined. Distal bronchial segments from 22 healthy horses were suspended in isolated organ baths where their mechanical responses to various stimuli could be studied. Each tissue was incubated with one of several concentrations of clonidine, clonidine vehicle, or clonidine plus tolazoline. Then, the contractile response of the tissues to either cumulative acetylcholine (ACh) addition or cumulative electrical field stimulation (EFS) was recorded. All contractile responses evoked by EFS were mediated through stimulation of cholinergic airway nerves. Clonidine had no effect on the contractile response of distal airway segments to exogenous ACh. However, clonidine (at concentrations > 10(-5) M) significantly (P < 0.05) diminished the contractile response of the distal airway segments to EFS. This inhibitory effect of clonidine was not observed in the presence of tolazoline. Similar results were observed when the less-selective alpha 2-adrenergic agonist xylazine was exposed to the isolated segments instead of clonidine. Because EFS-but not exogenous ACh-induced contractions were inhibited, alpha 2-adrenergic receptor stimulation apparently causes presynaptic inhibition of the cholinergic nerves innervating distal portions of the bronchi of horses.

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the alpha 2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, alpha-adrenoceptor antagonists, were administered to isolate alpha 1- or alpha 2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/kg of body weight, IV) and esmolol (50 to 75 microgram/kg/min, IV) to induce parasympathetic and beta 1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10(-9)M) to 25.7 mg (10(-4)M) and medetomidine (n = 3), 0.000237 mg (10(-9)M) to 2.37 mg (10(-5) < M) after parasympathetic and beta 1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, IV) or medetomidine (n = 6, 0.05 mg/kg, IV) after parasympathetic and beta 1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, IV) followed by atipamezole (0.3 mg/kg, IV). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine. Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause significant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the alpha-adrenoceptor antagonists, prazosin (alpha(1)) and atipamezole (alpha(2)), did not cause significant changes in supraventricular or ventricular rate. alpha 2-Adrenoceptor agonists do not induce direct alpha 1- or alpha 2-adrenoceptor-mediated depression of supraventricular or ventricular rate in dogs with complete atrioventricular block.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs, were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively. Differences for groups IGS, IGX, and IGM could not be calculated because arrhythmias satisfying the ADE criteria were not observed at the maximum infusion rate of 5.0 micrograms/kg/min. Differences among groups IS, IX, and IM were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, IM) or medetomidine (15 micrograms/kg, IM) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either alpha 2-adrenergic receptor agonist.