Objective-To investigate effects of isoflurane at approximately the minimum alveolar concentration (MAC) on the nociceptive withdrawal reflex (NWR) of the forelimb of ponies as a method for quantifying anesthetic potency. Animals-7 healthy adult Shetland ponies. Procedure-Individual MAC (iMAC) for isoflurane was determined for each pony. Then, effects of isoflurane administered at 0.85, 0.95, and 1.05 iMAC on the NWR were assessed. At each concentration, the NWR threshold was defined electromyographically for the common digital extensor and deltoid muscles by stimulating the digital nerve; additional electrical stimulations (3, 5, 10, 20, 30, and 40 mA) were delivered, and the evoked activity was recorded and analyzed. After the end of anesthesia, the NWR threshold was assessed in standing ponies. Results-Mean +/- SD MAC of isoflurane was 1.0 +/- 0.2%. The NWR thresholds for both muscles increased significantly in a concentration-dependent manner during anesthesia, whereas they decreased in awake ponies. Significantly higher thresholds were found for the deltoid muscle, compared with thresholds for the common digital extensor muscle, in anesthetized ponies. At each iMAC tested, amplitudes of the reflex responses from both muscles increased as stimulus intensities increased from 3 to 40 mA. A concentration-dependent depression of evoked reflexes with reduction in slopes of the stimulus-response functions was detected. Conclusions and Clinical Relevance-Anesthetic-induced changes in sensory-motor processing in ponies anesthetized with isoflurane at concentrations of approximately 1.0 MAC can be detected by assessment of NWR. This method will permit comparison of effects of inhaled anesthetics or anesthetic combinations on spinal processing in equids.

During acute bouts of recurrent airway obstruction (heaves) in horses, neutrophils that are capable of increased production of reactive oxygen species accumulate in the airways. In the study reported here, the effect of hydrogen peroxide (H2O2; 1 micromolar to 0.1M), one of these reactive oxygen species products, on the responses of isolated trachealis muscle of horses was determined. Before and after incubation with H2O2, contractile responses to acetylcholine, electrical field stimulation (EFS), 127 mM KCl, and relaxation responses to isoproterenol and activation of the nonadrenergic noncholinergic inhibitory response (iNANC) were evaluated. Beginning at 1 mM, H2O2 contracted trachealis muscle in a concentration-dependent manner. This contraction was unaffected by atropine (1 micromolar), tetrodotoxin (1 micromolar), or 1 micromolar meclofenamate. Contraction of trachealis muscle in response to H2O2 is, therefore, not attributable to release of prostaglandins, acetylcholine, or other neurotransmitters. Above a concentration of 0.1 mM, H2O2 depressed the responses to EFS. acetylcholine, and KCl in a concentration-dependent manner. At 0.1M, H2O2 decreased the maximal responses to EFS, acetylcholine, and KCl by 62.7 +/- 7.2, 60.58 +/- 6.12, and 37.8 +/- 9.54%, respectively. In the presence of meclofenamate (1 micromolar), partial but significant protection against 1 to 100 mM H2O2 was observed. In tracheal strips contracted with 0.3 micromolar methacholine, H2O2 had no effect on the isoproterenol concentration-response curve. Up to a concentration of 100 mM, H2O2 had no effect on iNANC response. However, in the presence of 100 mM H2O2, this response was abolished in 2 of 4 horses. We conclude that high concentrations of H2O2 affected the responses of airway smooth muscle by actions on neurotransmission, muscarinic receptors, and downstream from receptors; some of the H2O2 effects were in part mediated by cyclooxygenase products; and H2O2 had no effect on beta-adrenergic- or iNANC-induced relaxation.

Anesthesia was induced in 8 healthy llamas by administration of guaifenesin and ketamine, and was maintained with halothane in oxygen. On 2 separate experimental days, atracurium was given to induce 95 to 99% reduction of evoked hind limb digital extensor tension (twitch). For the first part of the study, atracurium was given iv as repeat boluses, with muscle twitch strength being allowed to return without intervention to 75% of baseline after each bolus before the subsequent bolus was given. A total of 5 bolus doses of atracurium was given. For the first bolus, 0.15 mg/kg of body weight iv, and for subsequent boluses, 0.08 mg/kg, induced desired relaxation. Onset of relaxation was slightly more rapid for repeat, compared with initial, bolus. Duration of relaxation and recovery time were similar to initial and repeat doses. Maximal twitch reduction was observed in 4 +/- 0.2 minutes (mean +/- SEM). Duration from maximal twitch reduction to 10% recovery was 6.3 +/- 0.4 minutes. Twitch recovery from 10 to 50% of baseline took 11.6 +/- 0.6 minutes. Twitch recovery from 10 to 75% recovery took 19.5 +/- 1.1 minutes. Recovery from 10% twitch to 50% fade took 12.8 +/- 0.5 minutes. Fade at 50% recovery of twitch was 39 +/- 0.02%. Significant (P < 0.05) animal-to-animal variation was observed in twitch recovery times. For the second part of the study, atracurium was initially given IV as a 0.15-mg/kg bolus, followed by infusion for 1 to 2 hours. Infusion rate required some early adjustment to maintain desired relaxation, but the rate that prevailed was 1.07 +/- 0.07 ml/kg/h (0.4 mg of atracurium/ml of saline solution). Recovery of muscle twitch was similar to that previously mentioned for repeat bolus administration, At the end of the study, edrophonium (0.5 mg/kg) with atropine (0.01 mg/kg, IV) was effective in antagonizing residual neuromuscular blockade by atracurium. All llamas recovered without injury from anesthesia, although 1 llama had a rough recovery. It was concluded that atracurium can provide neuromuscular blockade by either repeat bolus administration or continuous infusion in llamas.

Distal airway segments (ID, 3 to 4 mm; length, 5 mm) from 2 groups of horses were isolated and suspended in tissue baths filled with Krebs solution, aerated with 5% CO2 in oxygen and maintained at 37 C. Responses to exogenous acetylcholine, isoproterenol, or electrical field stimulation were compared. Control horses (n = 30) had no history of recurrent airway obstruction, whereas principal horses (n = 15) had recurrent airway obstruction and were studied during an acute episode of airway obstruction. Although the distal airways contracted in response to the cumulative half-logarithmic addition of acetylcholine (10(-10)M to 10(-3)M) in both groups, bronchi obtained from principals were less sensitive to acetylcholine than were bronchi obtained from controls. Tetrodotoxin-sensitive electrical field stimulation-induced contractions were observed in both groups of airways, but the tension achieved in principal bronchi was less than in controls. All electrical field stimulation-induced contractions were abolished by atropine, indicating that the only excitatory innervation of equine distal airways is through the parasympathetic system. To examine the effect of isoproterenol and determine inhibitory innervation, bronchi were precontracted with histamine. Electrical field stimulation did not cause relaxation of precontracted bronchi in either group, thus indicating that distal airways lack inhibitory innervation. Isoproterenol caused similar, dose-dependent relaxation in both groups.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Strips of trachealis muscle were dissected from the mid-cervical portion of the trachea from horses that were free of respiratory tract disease. The epithelium and mucosa were removed from one group of tissues and were left intact in a second group of tissues. Each tissue was suspended in a bath filled with Krebs-bicarbonate solution that was aerated with 5% CO2 in oxygen and maintained at 37 C. Isometric tension was continuously recorded. The contractile response to square-wave electrical stimulations increased as frequency (3, 5, 10, 15, 20, 25, and 30 Hz), voltage (10, 15, 18, and 25 V), and pulse duration (0.2, 0.5, 1.0, 1.5, and 2.0 ms) increased in tissues with the epithelium and mucosa intact. A stimulus of 18 V, 20 Hz, and 0.5 ms induced maximal contraction. Atropine (10(-6) M) abolished the response to 18 V and 0.5 ms at all frequencies. The increase in active isometric tension was concentration dependent when acetylcholine (10(-9) to 10(-4) M) was added to the baths in 0.5-logarithmic increments. Tissues that were contracted in response to acetylcholine (10(-5) M) had a concentration-dependent decrease in active isometric tension when isoproterenol was added to the baths in 0.5-logarithmic increments (10(-9) to 10(-4) M). The contraction and relaxation curves were qualitatively similar, but quantitatively different in tissues with and without the epithelium and mucosa. Removing the epithelium and mucosa increased the contractile response to acetylcholine at bath concentrations of 3.1 X 10(-7) M and 10(-6) M. The presence of epithelium and mucosa enhanced the magnitude of isoproterenol-induced relaxations. We concluded that electrical stimulation released acetylcholine from isolated equine trachealis muscle, that isoproterenol induced relaxation of the trachealis muscle, and that the magnitude of the responses to exogenous agonists depended on the presence of epithelium and mucosa.

In 25 adult dogs of various breeds, recurrent laryngeal nerve fibers were electrically stimulated at 2 points along their extralaryngeal course. Evoked compound muscle action potentials were recorded in this ipsilateral intrinsic laryngeal muscles, using a percutaneous needle electrode. Latencies, amplitudes, and durations were measured. Latencies were correlated with neck length (r = 0.88 on left and 0.82 on right). Five of the dogs were euthanatized, and the nerve length between the 2 stimulating needle electrodes was measured; calculated conduction velocities (mean +/- SD) were 55 +/- 6 m/s (left) and 57 +/- 6 m/s (right). In 38 additional canine cadavers, the lengths of the exposed left and right recurrent laryngeal nerves were correlated with neck length (r = 0.44 on left and 0.56 on right). A linear regression model is proposed for predicting normal latencies, despite variations in neck length among different breeds of dogs.

Objective-To determine the relationship between the output of an electrical treatment device and the effective field strength in the superficial digital flexor tendon of horses. Sample Population-Cadaver horse forelimbs without visible defects (n = 8) and 1 live pony. Procedure-Microcurrents were generated by a microcurrent electrical therapy device and applied in proximodistal, dorsopalmar, and mediolateral directions in the entire forelimbs, dissected tendons, and the pony with various output settings. Corresponding field strengths in the tendons were measured. Results-A linear relationship was detected between current and field strength in all conditions and in all 3 directions. In dissected tendons, significant differences were detected among all 3 directions, with highest field strength in the proximodistal direction and lowest in the dorsopalmar direction. In the entire forelimbs, field strength in the proximodistal direction was significantly lower than in the mediolateral direction. Results in the pony were similar to those in the entire forelimbs. Conclusions and Clinical Relevance-Electrode placement significantly affected field strength in the target tissue. Many surrounding structures caused considerable reduction of field strength in the target tissue. These factors should be taken into account when establishing protocols for electrical current-based therapeutic devices if these devices are proven clinically effective.

Effects of alpha 2-adrenergic receptor stimulation on the cholinergic contractile response of bovine tracheal smooth muscle were studied. To determine the presence and function of alpha 2-adrenergic receptors on cholinergic nerves innervating bovine tracheal muscle, effects of 2 alpha 2-adrenoceptor agonists and an antagonist were determined. Muscular contractions were elicited by either electrical field stimulation (EFS) or exogenous acetylcholine (ACH). The contractile response to EFS and exogenous ACH was examined for each tissue. Electrical field stimulation of bovine tracheal smooth muscle caused contractions that were completely abolished by atropine, indicating the predominant excitatory innervation of bovine trachea is cholinergic. The alpha 2-adrenoceptor agonists clonidine and medetomidine (10(-6)M to 10(-4)M) concentration-dependently inhibited the contractile response to EFS but not the response to exogenous ACH. Contractions induced by EFS were significantly (P < 0.05) inhibited in clonidine (10(-4) M)-treated tissues at low frequencies (0.1 to 10 Hz), whereas medetomidine (10(-5)M, 10(-4)M) inhibited contractions at all frequencies (0.1 to 30 Hz). Inhibitory effects of the alpha 2-adrenoceptor agonists clonidine and medetomidine were attenuated by the alpha 2-adrenoceptor antagonist tolazoline. The alpha 2-agonists used in this study appear to cause prejunctional inhibition of cholinergic nerves, because the smooth muscle contractions elicited by EFS, but not exogenous ACH, were inhibited, compared with controls.

Muscle potentials evoked by stimulation of the sciatic nerve were evaluated in 4- and 15-week-old chickens. Each bird was anesthetized and slowly cooled externally from a normal body temperature of 40 C to 28 C, and motor nerve conduction velocities were measured at various intervals during cooling. Motor nerve conduction velocity decreased linearly with decreasing limb temperature in both groups. The rate of change in motor nerve conduction velocity per degree in 2 groups (2.13 m/s/C vs 1.84 m/s/C) fell just short of a statistically significant difference (P = 0.0508), indicating that an age-related effect on temperature-associated variation in motor nerve conduction velocity may be present.