Objective--To determine whether larkspur-derived N-(methylsuccinimido) anthranoyllycoctonine (MSAL)-type alkaloids alter heart rate and electrically evoked electromyographic (eEMG) response of the external anal sphincter (EAS) in cattle and whether these effects can be reversed by acetylcholinesterase inhibitors. Animals--12 beef heifers and 4 cows. Procedures--3 or 4 heifers were used in 1 or 2 of 7 dose-response experiments; heart rate and EAS eEMG response were assessed before and 24 hours after oral treatment with larkspur (doses equivalent to 0.5 to 15 mg of MSAL-type alkaloids/kg). In 3 subsequent experiments, 3 heifers (1 of which was replaced with another heifer in the control experiment) each received 10 mg of MSAL-type alkaloids/kg and were injected IV with physostigmine (0.04 mg/kg), neostigmine (0.04 mg/kg), or saline (0.9% NaCl) solution 24 hours later, prior to assessment. Additionally, EAS eEMG response was measured in 4 cows before and after epidural administration of 2% lidocaine hydrochloride. Results--Larkspur-treated heifers developed dose-related increases in heart rate and decreases in EAS eEMG response. Twenty-four hours after administration of MSAL-type alkaloids, neostigmine decreased heart rate but did not affect eEMG response, whereas physostigmine did not affect heart rate but caused a 2-fold increase in eEMG response. In cows, epidural anesthesia did not alter eEMG response, suggesting that transdermal stimulation of the EAS pudendal innervation did not occur. Conclusions and Clinical Relevance--In cattle, cardiac effects and muscle weakness or loss of EAS eEMG response induced by larkspur-derived MSAL-type alkaloids were reversed by neostigmine or physostigmine, respectively. Treatment with anticholinesterase inhibitors may alter the clinical effects of larkspur poisoning in cattle.

Objective-To assess gait abnormalities associated with selective anesthesia of the suprascapular nerve (SSN) achieved by use of perineural catheterization and thereby determine the function of that nerve as it relates to gait in horses. Animals-3 adult horses with no preexisting clinically apparent lameness at a walk. Procedure-Each horse was anesthetized; the right SSN was exposed surgically for placement of a perineural catheter to permit delivery of 1 mL of 2% mepivacaine hydrochloride. Six hours after recovery from anesthesia, each horse was videotaped while walking (50-step data acquisition period) before and after administration of mepivacaine. Videotapes were reviewed and the proportion of abnormal steps before and after selective SSN anesthesia was assessed. A step was considered abnormal if a marked amount of scapulohumeral joint instability (ie, lateral luxation of the proximal portion of the humerus) was observed during the weight-bearing phase of the stride. Results-Clinically apparent gait dysfunction was detected in all 3 horses following perineural administration of the local anesthetic agent. Anesthesia of the SSN resulted in scapulohumeral joint instability as evidenced by consistent lateral excursion of the shoulder region during the weight-bearing phase of gait at a walk. The proportion of abnormal steps before and after SSN anesthesia was significantly different in all 3 horses. Conclusions and Clinical Relevance-These data support the role of the SSN in shoulder joint stability in horses and define SSN dysfunction as 1 mechanism by which the syndrome and gait dysfunction clinically referred to as sweeny may develop.

Maximal conduction velocities of compound action potentials evoked by stimuli of 2 times threshold in the caudal cutaneous sural (CCSN) and medial cutaneous antebrachial (MCAN) nerves were determined by averaging potentials evoked and recorded through percutaneous needle electrodes. Mean maximal conduction velocities of compound action potentials were: CCSN = 61.3 +/- 2.0 meters/second (m/s) and MCAN = 56.4 +/- 2.8 m/s. To confirm accuracy of our percutaneous recordings, compound action potentials were recorded through bipolar chlorided silver electrodes from the exposed surfaces of fascicles of the CCSN and the MCAN. The maximal conduction velocities of these potentials were in agreement with the conduction velocities of compound action potentials that were evoked and recorded through percutaneous needle electrodes. The specificity of stimulating and recording sites was verified by recording before and after section of the nerves. Stimuli from 3 to 5 times threshold evoked a second, longer latency, compound action potential that consisted of a variable number of components in the CCSN and MCAN. The configurations and conduction velocities of the shorter latency potentials were the same as those of the single compound action potentials evoked by stimuli of 2 times threshold. Mean conduction velocities of the longer latency potentials were: CCSN = 24.4 +/- 2.6 m/s and MCAN = 24.5 +/- 2.2 m/s. Needle electrode and direct stimulation of either the CCSN or the MCAN at 3 to 5 times threshold failed to evoke contractions of limb muscles. Therefore, action potentials that contributed to the evoked compound potentials recorded in these horses arose, most likely, from afferent nerve fibers.

Although healthy and diseased bovine respiratory tracts have been intensively studied during the last years, to the authors' knowledge, there have been no attempts to objectively examine the inspiratory drive from the brain to the nerves and muscles and its transformation in pressure. Such technique would be useful in assessing the possibility of altered ventilatory drive or inspiratory muscle fatigue in the context of an animal with ventilatory failure. The relation among ventilation, airway opening occlusion pressure generated 100 milliseconds after onset of inspiration (Pawo100ms) and 6 indexes describing diaphragmatic electromyographic activity (EMGdi) recorded via implanted fishhooks was evaluated during free and impeded CO2, rebreathing in 6 young bulls. The best significant linear correlations (r > 0.8) with inspiratory center afferent stimulation, as judged by end-tidal CO2 concentration in expired air, were found for Pawo100ms, peak moving time average or variance EMGdi, and mean integrated EMGdi, whatever had been the respiratory impedance. However, with an inspiratory load, Pawo100ms responses systematically had greater increase for a given change in the driving EMGdi, implying dependence of the former not only on neural input, but also on configurational factors that determine inspiratory muscle excitation-pressure generation couplings. The reproducibility of EMGdi absolute values and changes was satisfactory up to 10 hours, but could not be repeated from one day to the other. It was concluded that, provided the constancy of the electrical coupling of the recording system to the tissue being studied is ensured, specific EMGdi and Pawo100ms values correlate reliably with amount of CO2 during free and loaded breathing. Simultaneous collection of both values during experimentally induced pulmonary disease in calves could, therefore, produce information to help answer questions about the role of CNS and inspiratory muscle dysfunction in case of ventilatory failure. Careful interpretation, however, requires additional measurements, such as end-expiratory lung volume, and some familiarity with the underlying physiologic processes that link phrenic nerve discharge to generation of negative pressure at the airway opening.

Spinal-evoked potentials were recorded from 2 litters of clinically normal mixed-breed dogs between 35 and 300 days of age. Summated responses to tibial nerve stimulation were recorded from percutaneous needle electrodes placed at L7-S1, L4-5, T13-L1, C7-T1, and the cisterna cerebellomedullaris. The ulnar nerve was stimulated with recordings at C7-T1 and the cisterna cerebellomedullaris. Amplitudes did not change significantly with age, but were significantly (P < 0.05) different between various recording sites. On day 35, segmental and overall (L7-cisterna cerebellomedullaris) conduction velocities were less than half of the adult values. Spinal cord conduction velocities increased with age, reaching adult values at approximately 9 months of age. It was determined that quadratic equations best predicted the conduction velocities during maturation.

The concentrations of dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindole-3-acetic acid (5-HIAA) in CSF obtained from the cisterna magna of 21 nonneurologically compromised dogs were determined by high-pressure liquid chromatography and electrochemical detection. A rapid method of sample preparation, which involved single filtration through a deproteinizing membrane, was used. Canine CSF obtained in this manner contained 5.78 +/- 0.78 ng of DOPAC/ml, 72.19 +/- 4.09 ng of HVA/ml, and 29.95 +/- 1.67 ng of 5-HIAA/ml. Linear regression analysis between HVA and 5-HIAA yielded a correlation coefficient of 0.4804. The neurotransmitter index, HVA/5-HIAA, was found to be more indicative of the dopaminergic metabolite HVA than the acid metabolite of serotonin, 5-HIAA (correlation coefficient with HVA = 0.5529 vs a correlation coefficient with 5-HIAA = -0.4462). A poor relationship (correlation coefficient = -0.1715) was found to exist between the 2 dopaminergic metabolites DOPAC and HVA in the CSF.

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.

The motor-evoked potential can be reliably recorded in anesthetized dogs by use of percutaneous placement of active recording electrodes near the dorsal lamina of the vertebral column. Two types of responses were observed in this study; short (< 5.5 ms at T9-10)- and long (> 5.8 ms at T9-10)-latency waves. Short-latency waves are larger in amplitude and appear with higher stimulus intensities than do long-latency waves. Short-latency waves are conducted at > 80 m/s and may not reflect pyramidal tract activation. The safety of using higher intensity stimuli to generate short-latency waves has not been determined.