The purpose of this study was to investigate the mechanism by which 5-hydroxytryptamine (5-HT) modifies respiratory function, specifically, hyperventilation, diffuse bronchoconstriction, and pulmonary arterial hypertension in cattle. We determined whether the IV response to 5-HT in calves was attributable to stimulation of 5-HT2 receptors. Six healthy unsedated young bull calves of the Friesian (n = 4) and of the Belgian White and Blue (n = 2) breeds were used. A specific 5-HT2 antagonist (metrenperone, 0.05 mg/kg of body weight) was administered IM 30 minutes before the cattle were given a 5-minute IV 5-HT infusion. Pulmonary function values were registered before, during, and after the 5-HT challenge infusion. Minute volume increased significantly, because of an increase in respiratory rate. Conversely, lung dynamic compliance, total pulmonary resistance, and pulmonary arterial pressure were not changed. We concluded that in cattle, 5-HT-induced ventilatory response is not mediated through activation of 5-HT2 receptors. However, the 5-HT2 receptors are involved in 5-HT-induced broncho- and pulmonary vasoconstriction.

Changes in lateral cecal arterial blood flow, mean internal carotid arterial pressure, and heart rate caused by nasogastric administration of fenoldopam (3, 6, and 9 mg/kg of body weight), a selective agonist of dopaminergic receptors, were recorded in 7 healthy horses. Cecal arterial blood flow was significantly increased within 30 minutes after administration of fenoldopam at all 3 dosages, with the peak increases from baseline (67.8 +/- 17.5 ml/min) being 125 +/- 28, 120 +/- 22, and 153 +/- 32 ml/min for 3, 6, and 9 mg/kg, respectively. Although carotid arterial pressure did not change significantly after administration of fenoldopam at the dosage of 3 mg/kg, administration of fenoldopam at the dosages of 6 and 9 mg/kg significantly reduced carotid arterial pressure from 113 +/- 10 to 88 +/- 3 and 81 +/- 5 mm of Hg, respectively. Intravenous infusion of metoclopramide, a dopaminergic receptor antagonist, at the rate of 0.125 mg/kg/h, blocked the effect of fenoldopam on cecal arterial blood flow and carotid arterial pressure. It was concluded that dopaminergic receptors mediate alterations in local blood flow and systemic pressure in horses.

The sodium-dependent transporter system responsible for L-glutamine uptake by brush border membrane vesicles prepared from equine jejunum was characterized. Vesicle purity was ascertained by a 14- to 17-fold increase in activity of the brush border enzyme markers. Glutamine uptake was found to occur into an osmotically active space with negligible membrane binding. The sodium-dependent velocity represented approximately 80% of total uptake and demonstrated overshoots. Kinetic studies of sodium-dependent glutamine transport at concentrations between 5 micromolar and 5 mM revealed a single saturable high-affinity carrier with a Michaelis constant of 519 +/- 90 micromolar and a maximal transport velocity of 3.08 +/- 0.97 nmol/mg of protein/10 s. Glutamine uptake was not affected by changes in environmental pH. Lithium could not substitute for sodium as a contransporter ion. 2-Methylaminoisobutyric acid inhibited the sodium-dependent carrier only minimally, but marked inhibition (> 90%) was observed in the presence of histidine, alanine, cysteine, and nonradioactive glutamine. Kinetic analysis of the sodium-independent transporter revealed it to have a Michaelis constant = 260 +/- 47 micromolar and a maximal transport velocity of 0.32 t 0.06 nmol/mg of protein/10 s. We conclude that glutamine transport in equine jejunal brush border membrane vesicles occurs primarily via the system B transporter and, to a lesser extent, by a sodium-independent carrier.

Indirect immunofluorescent antibody (IFA), latex agglutination (IA), and enzyme immunoassay (EIA) methods were compared for evaluation of the serum antibody responses of dogs experimentally and naturally exposed to spotted fever-group rickettsiae. Selected sera (obtained on days 1, 42, 53, 124, 145, 236, 255, 264, and 292) were examined from three 8-month-old female Beagles inoculated with Rickettsia rickettsii on days 34 and 250 of the study. A second group of dogs comprised three 8-month-old female Beagles inoculated with R montana on days 34 and 102. Subsequently, these dogs were inoculated with R rickettsii on day 250. Serum samples were obtained from the second group of dogs on days 1, 96, 103, 132, 180, 215, 292, and 494. A third group consisted of 21 naturally exposed dogs, from which sequentially obtained serum samples were available, and which had clinical signs compatible with Rocky Mountain spotted fever. Clinical signs of disease in dogs of the third group resolved after treatment with tetracycline (22 mg/kg of body weight, Po, q 8 h) was instituted. At least 2 sequentially obtained serum samples from each dog were tested. In general, the first sample was obtained just prior to treatment and the convalescent serum samples were obtained at weekly or greater intervals thereafter. For correlation and reactivity data, an IFA test for IgG/IgM (using heavy and light chains-specific conjugate) was used as the reference standard for comparison of results with those of the other tests,

Power spectral analysis and digital filtering of brain stem auditory evoked potentials (BAEP) were performed in dogs. The BAEP were recorded in 7 dogs, using alternating clicks at frequency of 20 Hz. The clicks were delivered monaurally at intensity of 90-dB normal hearing level. Power spectral analysis indicated that the frequency compositions of the averaged responses were divisible into 4 frequency bands: A (30 to 390 Hz), B (390 to 680 Hz), C (680 to 910 Hz) and D (910 to 1960 Hz). The frequency limits of digital high-pass (HP) and low-pass (LP) filters, at which neither peak-to-peak nor absolute amplitudes were reduced, were 1,170 and 1,270 Hz for P1, 290 and 1,170 Hz for P2, 290 and 980 Hz for P3, 290 and 980 Hz for P4, and 200 and 880 Hz for P5, respectively. The dual structure of BAEP was confirmed in dogs. Below 200 Hz for the HP filter, peak-to-peak and absolute amplitudes of afl waves were not significantly reduced. Therefore, this frequency may be a boundary frequency between low- and high-frequency components of BAEP in dogs. The main source for the high- frequency components that constituted each positive peak and the following trough was derived from frequency bands C and D. The frequency limits of 200 Hz for a digital HP filter and of 1,270 Hz for a digital Lp filter, at which amplitudes of aU waves were not reduced, support the analog filter settings recommended for dogs (ie, less than and qual to 53 and 3,000 Hz for analog HP and LP filters, respectively).

Two types of sensory receptors were located in the equine foot, using anatomic techniques. Histologic examination of stained hoof sections revealed lamellated corpuscles in the hoof dermis, which had many of the morphologic characteristics of Pacinian corpuscles. These sensory receptors were restricted to the palmar (caudal) aspects of the solar dermis of the heel. A second type of receptor was detected by use of immunocytochemistry, indicating apparently naked nerve endings containing the neuropeptide calcitonin gene-related peptide-like immunoreactivity in skin, solar dermal tubules, and the digital cushion. This peptide is an example of a sensory neurotransmitter contained in dorsal root ganglion cells and is believed to exist only in unmyelinated sensory nerve fibers. These 2 morphologic structures may be used for detection of sensory stimuli, such as pressure (or vibratory senses) and pain, respectively, in horses during various locomotory gaits.

Ultrasound-guided brain biopsy of the cingulate gyrus and the head of the caudate nucleus was performed in clinically normal dogs. Dogs survived the surgery, and neurologic deficits were not detected in the 14-day postoperative period. Magnetic resonance imaging detected changes in the brain associated with biopsy in 9 dogs (90%) immediately after surgery and in 6 dogs (60%) 14 days after surgery. Fourteen days after surgery, sonography of the brain, performed through the skin overlying the burr hole, detected changes associated with biopsy in 9 dogs (90%). Histopathologic changes evident in the brain 14 days after surgery consisted of focal malacia and hemorrhage with associated subacute encephalomeningitis. Postmortem examination indicated that the biopsy specimen was accurately obtained from the desired site in 9 dogs (90%). Tissue specimens suitable for histologic examination were obtained from 10 dogs (100%). Accuracy and low morbidity of ultrasound-guided biopsy indicate that this may be a useful technique for diagnosis of focal brain disease in dogs.

Plasma catecholamine concentrations in response to onychectomy were examined in 27 cats receiving different anesthetic regimens. Each cat was anesthetized with a dissociative-tranquilizer combination, and onychectomy was performed on 1 forefoot. One week later, each cat was anesthetized with the same dissociative-tranquilizer combination plus either butorphanol or oxymorphone, and onychectomy was performed on the other forefoot. Four treatment groups were studied: tiletamine-zolazepam and tiletamine-zolazepam-butorphanol combinations were administered to group-1 cats, ketamine-acepromazine and ketamine-acepromazine-butorphanol combinations were administered to group-2 cats, tiletamine-zolazepam and tiletamine-zolazepam-oxymorphone combinations were administered to group-3 cats, and ketamine-acepromazine and ketamine-acepromazine-oxymorphone combinations were administered to group-4 cats. All drug combinations were administered IM. Central venous blood samples were drawn for catecholamine analysis after injection of drug(s), after onychectomy, and 1, 2, and 4 hours after injection. Tiletamine-zolazepam alone or tiletamine-zolazepam-butorphanol prevented epinephrine release for 2 hours after injection of drug(s). Norepinephrine concentration increased significantly (P < 0.05) from baseline after onychectomy for tiletimine-zolazepam-butorphanol and at 4 hours for tiletamine-zolazepam and tiletamine-zolazepambutorphanol. After onychectomy, there was no difference in epinephrine values between tfletamine-zolazepam and tiletamine-zolazepam-oxymorphone. Ketamine-acepromazine prevented increases in norepinephrine and epinephrine concentrations for up to 2 hours after surgery. Addition of butorphanol to ketamine-acepromazine decreased norepinephrine values immediately after onychectomy. Addition of oxymorphone to ketamine-acepromazine resulted in lower epinephrine values 4 hours after surgery.

Concentration of sulfamethazine was measured in plasma and tissues (fat, liver, kidney, spleen, lungs, and skeletal muscle) of pigs given the drug IV and PC. The plasma concentration vs time curve was best described by a 2-compartment model, with a distribution half-life of 0.46 hour and an elimination half-life of 16.9 hours. Bioavailability after oral administration was 85.8 +/- 5.3%. The tissue and plasma sulfamethazine concentration vs time data ,ere used to develop a multicompartment pharmacokinetic model of sulfamethazine disposition in pigs. Plasma and tissue concentrations of sulfamethazine in pigs were measured at various intervals after multiple oral doses of sulfamethazine, and were compared to concentrations predicted by the model. Model predictions for tissue concentrations of sulfamethazine after addition of the drug to feed (110 micrograms/g of feed for 98 days; 550 micrograms/g for 30 days) were compared to results from other studies. The model accurately predicted the number of days for sulfamethazine concentration to fall below 0.1 Kg of tissue/g (0.1 ppm. the tolerated concentration) in various tissues.

The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Pa(CO2)] = 35 to 45 mm of Hg), at hypercapnia (Pa(CO2) = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (Pa(O2)) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.