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.

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.

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.

Release of enzymes from cytoplasmic granules has been postulated to have a major role in neutrophil-mediated tissue injury. Secretion or release of primary granules, specific granules, and cytosolic enzymes by bovine neutrophils was examined by quantifying the release of beta-glucuronidase, B12-binding protein, and lactate dehydrogenase, respectively, in response to predetermined amounts of phorbol myristate acetate, calcium ionophore, and opsonized zymosan. These responses were compared with the enzyme release induced by exposure to live or dead, unopsonized or opsonized Pasteurella haemolytica. The greatest release of beta-glucuronidase, B12-binding protein, and lactate dehydrogenase was observed in neutrophils exposed to live organisms partially because of neutrophil lysis. Bovine neutrophils respond markedly to particulate agonists, live or dead, pathogenic or nonpathogenic, by a selective release of specific granules, an effect enhanced by opsonization. Particulate agonists induce minimal primary granule release other than that induced by cell death. Because bovine neutrophils contain quantitatively high numbers of specific granules, the high rate of secretion/ release in response to P haemolytica organisms could have a major role in the tissue responses that characterize the lesions of pneumonic pasteurellosis.

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.