Somatosensory-evoked potentials (SEP) and spinal cord-evoked potentials (SCEP) were recorded in clinically normal adult cats in response to electrical stimulation of pudendal and tibial nerves to provide normative data that can be used in a clinical evaluation of pudendal nerve function in cats after sacral or sacrococcygeal luxations or fractures. Responses to tibial nerve stimulation were included in the study as an internal control because it is usually not involved in these types of injuries and because its SEP and SCEP are easily recorded. Evoked potentials were characterized by the latencies (ms) of positive (P or p) and negative (N or n) peaks. The SEP resulting from percutaneous pudendal nerve stimulation consisted of a prominent P-N-P potential in the 30- to 80-ms range. The pudendal SCEP was not successfully recorded because of large muscle artifacts evoked from the sacral area. The tibial SEP was similar to the pudendal SEP, except that the prominent P-N-P series in the 35- to 81-ms range was preceded by a smaller p-n-p-n sequence in the 7- to 23-ms range. The tibial SCEP consisted of a P-N-P series in the 2- to 4-ms range.

In healthy adult goats, closure of the esophageal groove was induced by thirst, IV administered vasopressin, and intracarotid administration of hypertonic NaCl solutions. The efficiency of stimulation was tested directly by visual inspection of the course taken by orally administered solutions through a ruminal or abomasal fistula, palpation of the lips of the esophageal groove through a ruminal fistula, and indirectly by following the glucose dynamics in the blood after oral administration of glucose solution. Esophageal groove closure was observed during drinking after a 48-hour period of water deprivation. Intracarotid administration of 1.5 ml of a saturated solution or 10.5 ml of a 1.5% solution of NaCl also stimulated groove closure; however, groove closure stimulated by administration of vasopressin is the most satisfactory procedure for passing compounds of therapeutic importance directly from the cardiac orifice to the abomasum.

We examined the electromyographic activity of the costal portion of the diaphragm and the transverse abdominal and external oblique muscles in 6 chronically instrumented awake adult horses during eupneic breathing during 2 levels of hypercapnia (fractional concentration of inspired CO2; FICO2 = 0.4 and 0.6), and during 2 levels of hypocapnic hypoxia (FIO2 = 0.15 and 0.12). Using the inert gas technique, we also measured the end-expiratory lung volumes of the 6 horses during eupnea, 6% CO2 challenge, and 12% O2 breathing. During eupneic breathing, phasic electrical activity of these 3 muscles was always present and was preceded by the onset of mechanical flow. At progressive levels of hypercapnia, the magnitude of inspiratory and expiratory electrical activity increased, and for the expiratory muscles, this recruitment coincided with significant (P < 0.05) increases in peak expiratory gastric pressure. However, during hypocapnic hypoxia, differential recruitment patterns of the respiratory muscles were found. The electrical activity of the diaphragm increased in magnitude and occurred sooner relative to the onset of mechanical flow. The magnitude and onset of abdominal expiratory activity failed to increase significantly during these episodes of hyperpnea and this pattern of activity coincided with decrements in peak expiratory gastric pressure. Despite alterations in muscle recruitment patterns during these hyperpneic episodes, end-expiratory lung volume remained unchanged. Thus, we conclude that adult horses respond similarly to awake dogs during peripheral and central chemoreceptor stimulation.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 microgram/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta, and beta-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dt(max)). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dt(max) responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dt(max) from baseline values and markedly reduced the response to dopexamine infusion. beta-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dt(max) These data indicate that baroreflex activity, beta- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.

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.

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.

Somatosensory-evoked potentials (SEP) and spinal cord-evoked potentials (SCEP) were recorded in clinically normal adult cats in response to electrical stimulation of pudendal and tibial nerves to provide normative data that can be used in a clinical evaluation of pudendal nerve function in cats after sacral or sacrococcygeal luxations or fractures. Responses to tibial nerve stimulation were included in the study as an internal control because it is usually not involved in these types of injuries and because its SEP and SCEP are easily recorded. Evoked potentials were characterized by the latencies (ms) of positive (P or p) and negative (N or n) peaks. The SEP resulting from percutaneous pudendal nerve stimulation consisted of a prominent P-N-P potential in the 30- to 80-ms range. The pudendal SCEP was not successfully recorded because of large muscle artifacts evoked from the sacral area. The tibial SEP was similar to the pudendal SEP, except that the prominent P-N-P series in the 35- to 81-ms range was preceded by a smaller p-n-p-n sequence in the 7- to 23-ms range. The tibial SCEP consisted of a P-N-P series in the 2- to 4-ms range.

Effects of 2 drugs commonly used for chemical restraint of cattle were evaluated for their effect on laryngeal and pharyngeal anatomy, function, and response to stimuli. Eighteen adult Jersey cows, free of respiratory tract disease, were studied. Cows were assigned at random to 1 of 3 treatment groups. Endoscopic evaluations were performed before and at a predetermined time interval after administration of each drug. Responses to stimuli were evaluated by stimulating 7 preselected sites (epiglottis, left and right arytenoid cartilages, left and right vocal folds, and left and right dorsolateral pharyngeal walls) with a closed, transendoscopic biopsy probe. Xylazine HCl (0.05 mg/kg of body weight, IV) was administered to group-1 cows (n = 6), and endoscopy was repeated 5 minutes after administration of the drug. Xylazine (0.07 mg/kg, IV) was administered to group-2 cows (n = 6), and endoscopy was repeated 5 minutes after administration of the drug. Acepromazine maleate (0.035 mg/kg, iv) was administered to group-3 cows (n = 6), and endoscopy was repeated 10 minutes after administration of the drug. Responses to stimuli were scored as brisk (0), moderate (1), slow (2), and absent (3). Scores for responses to stimuli were compared, using the Wilcoxon signed-rank test for data within groups, and a general linear models procedure, using the Kruskal-Wallis test between groups. Interobserver agreement rates were generated for each group. A value of P<0.05 was considered significant. Xylazine profoundly changed laryngeal sensitivity and function at both dosages. The corniculate processes of the arytenoid cartilages were observed to be in a markedly adducted position after sedation. Response to stimuli was significantly (P = 0.03) slower than normal after sedation, using both dosages. Displacement of the soft palate dorsal to the epiglottis was persistent in 50% of the cows after stimulation tests subsequent to sedation with xylazine. Acepromazine had a mild effect on laryngeal sensitivity and function. The corniculate processes of the arytenoid cartilages were observed in paramedian position after sedation. Acepromazine did not significantly affect responses to stimuli. Effects of sedation on responses to stimuli were not significantly different for groups 1 and 2. However, effects for group 3 were significantly different from those for groups 1 and 2 (P = 0.006 and 0.004, respectively). Endoscopic evaluation of the proximal portion of the respiratory tract of cattle should be performed without sedation, when possible. If sedation is required to facilitate restraint for endoscopy, acepromazine maleate is recommended over xylazine on the basis of results of this study.

The effects of single IV administered doses of dexamethasone on response to the adrenocorticotropic hormone (ACTH) stimulation test (baseline plasma ACTH, pre-ACTH cortisol, and post-ACTH cortisol concentrations) performed 1, 2, and 3 days (experiment 1) or 3, 7, 10, and 14 days (experiment 2) after dexamethasone treatment were evaluated in healthy Beagels. In experiment 1, ACTH stimulation tests were carried out after administration of 0, 0.01, 0.1, 1, and 5 mg of dexamethasone/kg of body weight. Dosage greater than or equal to 0.1 mg of dexamethasone/kg decreased pre-ACTH plasma cortisol concentration on subsequent days whereas dosages greater than or equal to 1 mg/kg also decreased plasma ACTH concentration. Treatment with 1 or 5 mg of dexamethasone/kg suppressed (P less than 0.05) post-ACTH plasma cortisol concentration (on day 3 after 1 mg of dexamethasone/kg; on days 1, 2, and 3 after 5 mg of dexamethasone/kg). In experiment 2, IV administration of 1 mg of dexamethasone/kg was associated only with low (P less than 0.05) post-ACTH plasma cortisol concentration in dogs on day 3. In experiment 2, pre-ACTH plasma cortisol and ACTH concentrations in dogs on days 3, 7, 10, and 14 and post-ACTH plasma cortisol concentration on days 7, 10, and 14 were not affected by dexamethasone administration. The results suggest that, in dogs a single IV administration. The results suggest that, in dogs, a single IV administered dosage of greater than or equal to 0.1 mg of dexamethasone/kg can alter the results of the ACTH stimulation test for at least 3 days. The suppressive effect of dexamethasone is dose dependent and is not apparent 7 days after treatment with 1 mg of dexamethasone/kg. The magnitude of the decrease in post-ACTH plasma cortisol concentration did not exceed 35% (compared with control values), regardless of the dose of dexamethasone used.