Akabane virus (AKV) strain OBE-1 was inoculated IV into 17 pregnant sheep. Ten fetuses infected at 29 to 45 days of gestation and examined 29 to 30 days later had AKV antigen in the following groups of cells: neuroglial cells in the brain and spinal cord, ganglion cells in the cranial and abdominal ganglia, layer of ganglion cells in the retina, ganglion cells (Auerbach's plexus) in small intestine, hepatocytes, cells in the arterial wall of mesenteric membrane, and trophoblast cells in the placenta. Prior to detection of circulating virus-neutralizing antibody, immunoglobulin-containing cells were found initially at 59 days of gestation in the peripheral portion of white pulp tissue in the spleen. After that, numbers of immunoglobulin-containing cells gradually increased. These results indicated that AKV may have strong affinity for neuronal and ganglional cells in infected fetuses and immunoglobulin-containing cells might be considered the earliest immunologic response to AKV replication in the fetus.

Microscopic examination of the nasal mucosa of clinically normal specific-pathogen-free pigs and of toxicogenic type-D Pasteurella multocida toxin challenge-exposed specific-pathogen-free pigs indicated that the surface epithelium in pigs of both groups was microscopically normal; erosions or appreciable inflammatory changes were not evident. In pigs of both groups and in aU 3 regions of the nasal cavity, the endothelial lining of all blood vessels appeared normal without detectable changes to the walls at postinoculation day 10. Vascular injury in the cartilage or the bone was not discernible in control or challenge-exposed pigs. There were marked differences in the osseous structures of the conchae when the 2 groups were compared. In control pigs, active bone formation and remodeling were observed, and the septal cartilage was normal. In toxin challenge-exposed pigs, there likewise was normal bone formation and remodeling in the vestibular region, and the septal cartilage was normal. In marked contrast, conspicuous changes were observed in the osseous core of the conchae of the respiratory and, sometimes, the olfactory regions. These changes consisted of bone necrosis and resorption by large numbers of osteoclasts with variable replacement by dense mesenchymal stroma, which resulted in conchal atrophy. In the absence of any discernible damage or injury (angiopathy) to the nasal vessels, it appears that the action of the dermonecrotoxin of P multocida serotype D is on the most active osteoblasts and the associated organic matrix of the bone, with subsequent disruption of normal bone formation and remodeling of the nasal conchae.

Somatosensory evoked potentials in response to tibial nerve stimulation were recorded from the scalp of 31 clinically normal mixed-breed dogs. The latency and amplitude of a main positive potential (P18), recorded with a frontal electrode referenced to the nose, were measured in subjects with body length ranging from 316 to 962 mm. A linear relation to body size explained the variations in latency among dogs (r2 = 0.81); the amplitude variations were explained in part by body size (r2 = 0.44). Bilateral tibial nerve stimulation significantly (P < 0.05) increased the amplitude of P18, but its latency was unaffected, compared with unilateral stimulation. Results of unilateral right and left tibial nerve stimulation were compared and were not different. Replacing acepromazine with xylazine as premedication before thiopental anesthesia did not influence the recordings.

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.

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the alpha 2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, alpha-adrenoceptor antagonists, were administered to isolate alpha 1- or alpha 2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/kg of body weight, IV) and esmolol (50 to 75 microgram/kg/min, IV) to induce parasympathetic and beta 1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10(-9)M) to 25.7 mg (10(-4)M) and medetomidine (n = 3), 0.000237 mg (10(-9)M) to 2.37 mg (10(-5) < M) after parasympathetic and beta 1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, IV) or medetomidine (n = 6, 0.05 mg/kg, IV) after parasympathetic and beta 1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, IV) followed by atipamezole (0.3 mg/kg, IV). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine. Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause significant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the alpha-adrenoceptor antagonists, prazosin (alpha(1)) and atipamezole (alpha(2)), did not cause significant changes in supraventricular or ventricular rate. alpha 2-Adrenoceptor agonists do not induce direct alpha 1- or alpha 2-adrenoceptor-mediated depression of supraventricular or ventricular rate in dogs with complete atrioventricular block.

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,

Random fragments of DNA were obtained from a cosmid library of Salmonella agona genomic DNA. from this library, 2 fragments were chosen and pooled to probe isolates of S typhimurium obtained during an episode of salmonellosis in a veterinary medical teaching hospital. Chromosomal DNA from the Salmonella isolates was digested with restriction endonucleases, and was probed with the random fragments of chromosomal DNA. This procedure resulted in a fingerprint pattern for each isolate. We found that the method permitted discrimination between isolates involved in the disease episode and S typhimurium obtained prior to the episode. We conclude that random fragments of chromosomal DNA are useful for fingerprinting isolates of S typhimurium. Analysis of plasmid DNA obtained from the isolates was not as useful. Some isolates found to be identical by restriction site analysis, had plasmids of different molecular weight. These results indicate that plasmid analysis may not be as useful a fingerprinting tool as previously reported.

Haptoglobin (HP), an acute-phase protein, is detected in serum of cows with hepatic lipidosis (fatty liver). To assess the relevance of Hp in fatty liver, induction of Hp was examined, using conditions similar to those involving development of fatty liver in cows. Induction of Hp was achieved by a combination of dexamethasone administration (0.1 mg/kg of body weight) and 2 days' starvation. Haptoglobin appearance in serum was not associated with the increase of alpha 1-acid glycoprotein (a marker for inflammation). This treatment increased serum nonesterified fatty acids concentration and decreased serum triglycerides concentration. Protein kinase C activity was decreased in the cytosolic fractions of liver and mononuclear cells. Reduction of protein kinase C-catalyzed endogenous protein phosphorylation also was observed, particularly in the cytosolic fractions of the tissue and cells. Detection of Hp in serum of cows with fatty liver appears to be explained by the fact that Hp is induced by dexamethasone administration and starvation, which are similar to the condition responsible for fatty liver development. The change of protein kinase C-catalyzed phosphorylation was suggested to be involved in the induction of Hp in cows.