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.

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.

Thirty mares with normal estrous cycles were allotted equally to 5 groups and infused with 250 ml of saline (NaCl) solution in utero on the seventh day after ovulation to test the effects of temperature, osmolarity, or pH of the saline solution on prostaglandin F2 alpha (PGF2 alpha) release and luteolysis. Intrauterine infusion of phosphate-buffered saline solution failed to alter the duration of the luteal phase, compared with the control group. Similarly, increasing the temperature of phosphate-buffered saline solution to 42 C or increasing (600 mosm) or decreasing osmolarity (less than 10 mosm) did not change the duration of the luteal phase. Decreasing the pH of saline solution to 3 caused significant (P less than 0.0001) re leases of PGF2 alpha from the uterus within the first hour after infusion, and the luteal phase was shortened to 8.8 +/- 1.0 days (mean +/- SEM; control, 15 +/- 1.2 days). The results of this study showed that pH is main factor in eliciting PGF2 alpha release by intrauterine infusion of a saline solution, whereas increased temperature and osmolarity have no effect on the release of PGF2 alpha. The intrauterine infusion of sterile water or physiologic saline (NaCl) solution has been used to induce estrus in mares for the past 50 years. Many investigators 1-10 have reported that intrauterine infusion of physiologic saline solution or water at body temperature (37 C or warmer up to 45 C) causes most "anestrous" mares to return to estrus in 1 to 8 days. The mare's ability to respond to intrauterine infusion was further defined when Arthur 11,12 demonstrated that estrus could be initiated only in mares in middiestrus or in pseudopregnancy, and Ginther and Meckley 13 reported intrauterine infusion was effective only during days 5 to 9 of diestrus. We subsequently demonstrated that the effect of intrauterine infusion of saline solution involved shortening the luteal phase.

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.

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.

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.

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.

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.