Interleukin-1 (IL-1) is a protein secreted by stimulated cells of the monocyte-macrophage line, which has a number of important biologic activities. Interleukin-1 has been implicated in the induction and augmentation of the pathologic processes involved in arthritis and articular cartilage destruction. Horses develop osteoarthritis with a frequency and degree of severity similar to human beings. To further document the similarity of the osteoarthritic process in people and horses, the synovial fluid from 5 horses with clinical osteoarthritis was tested for IL-1 bioactivity. Interleukin-1 activity was found in all tested synovial fluids. Upon column chromatography, the synovial fluid-derived factor had a molecular weight consistent with that of IL-1 in other mammalian species. Ion exchange chromatography of osteoarthritic synovial fluid revealed the principal peaks of bioactivity to be in the fractions with isoelectric points of 7.2, 5.4, and 4.7, which are characteristic of IL-I. A considerable degree of homology between human and equine IL-1 was demonstrated by the cross hybridization of a human IL-1 beta cDNA probe with RNA derived from IL-1-producing equine adherent monocytes. These results indicate that equine IL-1 is in all of the osteoarthritic equine joints tested and that equine IL-1 has many of the characteristics of IL-1 isolated from other species.

Sera and tracheal washings (TW) were used to identify antigens of Bordetella avium recognized during experimentally induced bordetellosis in young turkeys. Pooled sera and TW were examined for antibody by a microtitration agglutination test and by western immunoblotting. In addition, comparable samples collected from 1-day-old turkeys and uninoculated control turkeys also were examined. At least 8 outer membrane proteins of B avium were recognized in immunoblots of sera and TW from infected turkeys. Reactivity of TW in immunoblots was qualitatively similar but less intense, compared with reactivity of corresponding sera collected on postinoculation (PI) weeks 2, 3, and 4. Molecular weights of the major outer membrane proteins of B avium recognized by sera and TW at PI week 4 were 100,000, 97,000, 36,000, 31,000, 21,000, 18,000, 14,000, and < 14,000. A protein with a molecular weight of 55,000 reacted nonspecifically in all samples tested. Antibody, detectable by microtitration agglutination, was in sera of 1-day-old turkeys and in sera and TW of B avium-infected turkeys during PI weeks 2 to 4.

Fifty-six samples of feces and intestinal contents from nonvaccinated diarrheal pigs with rotavirus infections were tested, using a subgroup (SGP)-specific ELISA, to determine rotavirus SGP classification. Forty-one percent (23/56) were SGP 1, 25% (14/56) were SGP 2, and 34% (19/56) were not classifiable. For classifiable samples, the geographic distribution for SGP 1 and SGP 2, respectively was: 60%/40% from Ohio (n = 15), 63%/37% from other midwestern states (Iowa, Minnesota, Nebraska, South Dakota: n = 16), and 67%/33% from Canada (n = 6). Thirty-seven SGP-classifiable samples were categorized according to age of pigs. Of pigs less than or equal to 1 week old, 22% of samples were SGP 1 (n = 8), and 14% (n = 5) were SGP 2. Of samples from 1- to 2-week-old pigs, 8% were SGP 1 (n = 3), and 5% were SGP 2 (n = 2). Of samples from 2- to 3-week-old pigs, 5% were SGP 1 (n = 2), and 8% were SGP 2 (n = 3). Of samples from 3- to 4-week-old pigs, 5% were SGP 1 (n = 2), and 3% were SGP 2 (n = 1). Of samples from pigs > 4 weeks old, 22% were SGP 1 (n = 8) and 8% were SGP 2 (n = 3). Double-stranded RNA extracted from positive controls and from 10 selected field samples (5 from SGP 1 and 5 from SGP 2) was electrophoresed in polyacrylamide gels to detect correlation between subgroup classification by ELISA and long or short double-stranded RNA electrophoretic-migration patterns. All SGP-1 and -2 rotavirus samples tested had typical long double-stranded RNA electrophoretic-migration patterns.

Equine neutrophil antibody was raised in rabbits inoculated with equine neutrophils isolated to purity > 99.0%, using Percoll density-gradient sedimentation. Neutrophil antibody was detected by use of agar gel diffusion, leukoagglutination, indirect immunofluorescence, staphylococcal protein A and streptococcal protein G binding, and phagocytic inhibition techniques. Precipitin lines and leukoagglutination were seen in antiserum dilutions of 1:4 and 1:64, respectively. The specific nature of leukoagglutination was characterized by the formation of rosette-like clumps of neutrophils. Specific bright membranous fluorescence was seen in neutrophils treated with the antiserum and exposed to fluorescein-conjugated goat anti-rabbit immunoglobulin, and staphylococcal protein A and streptococcal protein G. Whereas the indirect immunofluorescence and protein G-binding tests were equally sensitive and resulted in titer of 1:256, the protein A-binding test was less sensitive and resulted in titer of only 1:32. Nonspecific binding of protein A and protein G was noticed as uniform or patchy cellular fluorescence in a small number of neutrophils. Treatment of neutrophils with antiserum up to dilution of 1:8 resulted in a significant (P < 0.05) suppression of phagocytosis of opsonized zymosan particles. Thus, protein G-binding and indirect immunofluorescence tests are highly sensitive to detect neutrophil antibody and may be used to diagnose immune-mediated neutropenias in horses and, possibly, in other animal species.

In 6 female goats, the mean threshold for glucosuria was 159.5 +/- 4.3 mg/dl. During increasing filtered loads of glucose, renal reabsorption of glucose reached maximal capacity, which was not exceeded when plasma glucose concentration was increased further. Measured in 10 female goats, the transport maximum for glucose was 119.1 +/- 9.1 mg of glucose reabsorbed/min. During infusion of glucose, there was a significant (P < 0.05) time-dependent reduction in inulin clearance indicating that IV glucose administration may be inappropriate in goats with compromised renal function.

The ventricular arrhythmogenic dose of epinephrine (ADE) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (TZ). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ADE. The ADE (mean +/- SD) was no different during anesthesia with use of halothane alone (8.9 +/- 4.3) than it was when injections of TZ preceded administration of halothane (6.7 +/- 2.8). Tiletamine/zolazepam was also administered IV immediately after determination of the ADE during halothane-induced anesthesia. The TZ administered in this manner did not alter the ADE. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of TZ did not alter blood pressure response. The ADE was also determined in 6 cats anesthetized with halothane preceded by administration of TZ. The ADE (mean +/- SD) was 0.7 +/- 0.23 microgram/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Myoelectric activity of the ileum, cecum, and right ventral colon (RVC) was studied in 4 mature ponies. Eight Ag-AgCl bipolar recording electrodes were sutured to the seromuscular layer of the ileum (2 electrodes), cecum (4 electrodes), and RVC (2 electrodes). Myoelectric activity was studied beginning 10 days after surgery. Eight, 60-minute recording sessions were performed in each pony during the interdigestive period, which was the period 3 to 7 hours after the morning feeding. On separate days, food was withheld for 24 hours, and 90-minute recordings were obtained during the nonfeeding period. Ponies were then fed a normal ration, and recordings were continued to obtain data for the digestive (feeding) period. All phases of the migrating myoelectric complex were seen at both ileal electrodes during the interdigestive period, including the periods of no spiking activity (phase 1), irregular spiking activity (phase 2), and regular spiking activity (phase 3). Phase 2 occupied 77% of the total recording time, and the mean duration of phases 1, 2, and 3 was 3.4 +/- 0.2, 12.8 +/- 1.2, and 6.7 +/- 0.7 min, respectively. Frequency of ileal slow waves was 11.8 +/- 0.1/min, and spike burst conduction velocity was 4.7 +/- 0.3 cm/s. A complete migrating myoelectric complex was seen in 11 of 32 tracings (34%) and had a mean duration of 24.2 +/- 2.6 min. The ileal migrating action potential complex, most often seen in phase 2, had a frequency of 4.8 +/- 0.5 spike bursts/h and a conduction velocity of 13.6 +/- 0.4 cm/s. The migrating action potential complex was detected directly before retrograde cecal myoelectric activity 73% of the time, indicating possible myoelectric coupling of the ileum and cecum. Motility patterns recognized in the cecum included: pattern I, spike bursts beginning at the apex and conducted to the cranial base; pattern II, spike bursts beginning at the caudal base and conducted to the apex; pattern III, spike bursts beginning at the cranial base and conducted to the apex; and pattern IV, termed the progressive pattern, beginning at the cecal apex, conducted through the cecal base and cecocolic orifice and into the RVC. The progressive pattern was detected at a frequency of 34.2 +/- 1.8 spike bursts/h and was often preceded by (71%), followed by (64%), or preceded and followed by (51%) pattern I or II. This recurring sequence of cecal myoelectric events was termed the cecal myoelectric complex. In the RVC, 2 patterns of myoelectric activity were seen: aborally directed propulsive spike bursts (3.6 +/- 0.6 spike bursts/h) and orally directed retropulsive spike bursts (7.2 +/- 1.2 spike bursts/h), confirming that propulsion and retropulsion exist in the RVC. Nonfeeding caused a significant decrease in the frequency of ileal migrating action potential complex (P = 0.008), cecal pattern III (P = 0.003), and the progressive motility pattern (P = 0.003). Nonfeeding caused a significant decrease (P less than or equal to 0.009) in the appearance of the cecal myoelectric complex. Feeding caused a significant increase (P = 0.003) in the mean frequency of the progressive pattern compared with the nonfeeding period, but this was significantly less than during the interdigestive period (P = 0.003).

The feasibility of renal arterial infusion of nonbiodegradable microspheres as a model of chronic renal disease in dogs was evaluated. Resin-coated, styrene-divinyl benzene copolymer microspheres were infused into the kidneys of healthy adult Beagles by direct injections of both renal arteries in a single surgical procedure. Injections of 25-micrometer diameter microspheres had minimal effect on either the clinical status or serum values of the dogs. Histologic examination revealed the majority of the microspheres lodged within the capillary beds of the glomeruli, and little change to the kidneys. However, injections of 50-micrometer diameter microspheres caused significant increases in serum concentrations of urea nitrogen and creatinine. Histologically, the larger microspheres obstructed afferent arterioles and small arteries, which caused diffuse glomerular necrosis and nephron damage. With doses ranging from 1 to 3 million microspheres/dog, a correlation between the quantity of microspheres injected and severity of renal damage was observed. The optimal dose for producing a model of moderate renal disease was determined to be 1.8 million microspheres/dog (0.9 million microspheres/kidney). During long-term studies, microsphere-injected dogs fed a moderately restricted protein ration remained relatively azotemic, compared with control dogs on the identical ration. During the 5-month postsurgical period, the serum urea nitrogen concentration averaged 18.41 +/- 1.59 mg/dl (mean +/- SE) for the microsphere-injected dogs vs 9.31 +/- 0.38 for the control dogs (P < 0.001). Similarly, the mean serum creatinine value was significantly higher (P = 0.020) for the microsphere-injected dogs, compared with the controls (1.23 +/- 0.12 mg/dl vs 0.94 +/- 0.03). In addition, the difference in mean endogenous creatinine clearance rates was statistically significant (microsphere-injected 1.02 0.05 ml/min/kg, vs control 1.53 +/- 0.06, P < 0.001).

In 6 adult horses anesthetized with pentobarbital, the hemodynamic responses of the equine digit to infusion of dopamine were evaluated by use of an isolated extra corporeal pump perfused digital preparation. Digital blood flow was maintained at a constant rate that was independent of systemic hemodynamic changes. Three sequential experiments were performed on each horse. In the first experiment (n = 6), dopamine was infused IV at rates of 1.0, 2.5, and 5.0 microgram/kg/min. For the second experiment (n = 5), dopamine (400 microgram/ml) was infused into the digital artery at the rates of 0.07, 0.7, and 1.2 ml/min. The third experiment (n = 5) consisted of a 5-minute intra-arterial infusion of phentoalamine followed by the intra-arterial infusion of dopamine while continuing the infusion of phentolamine. Digital venous, arterial, and capillary pressures, total digital vascular resistance, and precapillary to postcapillary resistance ratios were determined in each experiment. Systemic infusion of dopamine did not induce changes in the hemodynamics of the digital vasculature. Digital arterial infusion of dopamine alone resulted in a dose-dependent increase in arterial pressure, total digital vascular resistance, and an increase in the precapillary to postcapillary resistance ratio. Phentolamine attenuated the vasoconstrictive response elicited by intra-arterial infusion of dopamine.

Canine circulating neutrophils, isolated by a blood lysing technique, were incubated with 7-S nerve growth factor (NGF), at final concentrations between 12.5 and 800 ng/ml, for 30 minutes at 37 C. Neutrophil cytosolic H2O2 production, measured by flow cytometry, after 7-S NGF incubation was not significantly different from that produced at 37 C (baseline temperature controls) alone. Phorbol myristate acetate (PMA; 100 ng/ml) stimulation of neutrophils produced cytosolic H2O2 concentrations almost 13 times that of baseline temperature control neutrophils. Preincubation of neutrophils with 7-S NGF (100 to 800 ng/ml, 30 minutes, 37 C) and subsequent stimulation by PMA resulted in augmented H2O2 production in excess of twice that of neutrophils treated with PMA alone, and almost 30 times that of baseline temperature controls.