Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Ceftiofur sodium, a broad-spectrum cephalosporin antibiotic, was evaluated for safe use in horses. Male or female horses were allotted to groups and were given either saline solution (control), or 2.2, 6.6, or 11 mg of an aqueous solution of ceftiofur sodium/kg of body weight/d, IM, for 30 or 31 days. These dosages are expressed in terms of the ceftiofur free acid, and represent 1 to 5 times the proposed therapeutic dosage (2.2 mg/kg/d) administered for 3 times the maximal recommended duration of 10 days. Some of the horses were euthanatized and necropsied on day 31 or 32. The other horses were evaluated for an additional 30 days, and some were euthanatized and necropsied on day 60. The following types of data were collected: clinical observation; physical examination; pelleted food consumption; body weight; hematologic, serum biochemical, and urinalysis findings; organ weight; gross necropsy observations; and histopathologic findings. Ceftiofur sodium was generally well tolerated at the exaggerated doses and treatment durations used in these safety studies. Slight to mild decrease in pelleted food consumption was detected in horses given 6.6 or 11 mg of ceftiofur sodium/kg/d. Decreased food consumption began on day 2 and lasted for approximately 9 to 12 days. Generally, mild skeletal muscle irritation was detected by gross and microscopic examination of the injection sites of horses given ceftiofur sodium. Prevalence and severity of the muscle irritation tended to increase with increasing concentration of the dosing solution. Increases in serum aspartate transaminase and creatine kinase activities were detected in some of the ceftiofur-treated horses, and were attributed to mild skeletal muscle irritation at the injection sites. Slight increases in numbers of circulating neutrophils and plasma concentration of fibrinogen were detected in the blood of some ceftiofur-treated horses, and were attributed to mild inflammation at the injection sites or possibly in the large intestine because of a change in bacterial flora.

We determined the position, dimensions, and structure of the kidneys, ureters, bladder, and urethra of 62 female sheep by use of ultrasonography. A 5.0-MHz convex transducer was placed over the right flank to examine the kidneys, and a 5.0 MHz-linear transducer was used to examine the bladder and urethra transrectally. All examinations were performed on sheep in standing position. The left kidney was 7.1 to 8.9 cm long, 3.4 to 5.5 cm wide, and 3.3 to 4.7 cm deep. Diameter of the parenchyma and renal sinus of the left kidney ranged between 1.1 and 1.9 cm and 1.1 and 2.0 cm, respectively. Circumference of the medullary pyramids varied between 2.1 and 3.3 cm. Similar ultrasonographic measurements were obtained for the right kidney. The diameter of the bladder varied between 0.3 and 6.9 cm in 96.8% of the sheep. The diameter of the bladder could not be determined in 32% of the sheep because it was > 10 cm, and, therefore, was beyond the penetration depth of the scanner. The only part of the urethra that could be ultrasonographically visualized was the internal urethral orifice. It had diameter between 0.1 and 0.2 cm. The ureters could not be ultrasonographically visualized in any of the sheep examined. The urinary tract of 8 sheep was examined 10 times within 2 weeks to examine whether measurements were reproducible. The interassay variation coefficient determined ranged from 3.1 to 31.8%, although for most variables, it ranged between 5 and 11%. Measurements for the length and width of the kidneys had the smallest interassay variation coefficient, whereas values obtained for diameter of the bladder and urethra, as well as thickness of the bladder, had the largest. It was concluded that the ultrasonographic findings described in this study can be used as references for diagnosis of morphologic changes in the kidneys, bladder, and urethra of sheep.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.

The nature of Mycoplasma arthritidis antigens responsible for eliciting protective immunity in rats was studied by inoculation of rats with mycoplasmal components that had been subjected to a variety of physical and chemical treatments. All inocula tested induced good protection against development of clinical illness, as assessed by changes in body weight and appearance of joint swelling and/or temporary hind limb paralysis. Although all preparations stimulated development in inoculated rats of high titer of antimycoplasmal antibodies measured by ELISA, the complement-fixation antibody response was poor and, in some cases, lacking altogether. This indicated that completion-fixation antibodies may not be involved in protecting rats against M arthritidis-induced illness. Protective antigens were stable to heat (100 C for 10 minutes), formalin, and denaturation by sodium dodecyl sulfate (SDS). Inoculation with membrane and soluble cytoplasmic fractions was protective, as was inoculation with 5 M arthritidis fractions separated according to molecular weight by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). For this latter experiment, rat antisera obtained after vaccination, but prior to challenge exposure, were tested by immunoblot analysis against electrophoretically separated M arthritidis membrane proteins. Interestingly, all antisera from these rats recognized antigens migrating far outside the molecular weight range of the cell fractions with which rats were inoculated. This indicated either that the protective antigens may be composed of numerous antigenically related subunits that separated by SDS-PAGE into a variety of molecular weight ranges or that a few major antigens may exist in several forms or phases within a given population of M arthritidis.

Blood constituents and vascular volume indices were determined in 5 standing horses by use of 2-period crossover experimental design. Horses were either administered hypertonic (2,400 mosm/kg of body weight, IV) or isotonic (300 mosm/kg, IV) saline solution. Each solution was administered at a dosage of 5 ml/kg (infusion rate, 80 ml/min). Samples for determination of PCV, plasma volume, blood volume, plasma osmolality, total amount of plasma protein and plasma concentrations of protein, Na, K, and Cl were collected at 0 hour (baseline, before fluid infusion) and 0.5 hour (at the end of fluid infusion), and subsequently, at 0.25- or 0.5-hour intervals for 4.5 hours. All horses were given the predetermined dose of fluids by 0.5 hour after beginning the saline infusion. Values of P less than or equal to 0.05 were considered significant. Administration of hypertonic saline solution was associated with decreased mean body weight by 4.5 hours, but weight change after isotonic saline administration was not significant. Other than body weight and plasma protein concentration, between-trial difference (treatment effect) was not observed for any measured variable or index. The F values indicated that increasing the number of horses would have not changed these results. A time effect was evident across both trials, so that mean (+/- SD) plasma volume increased (12.3 +/- 1.07%) and mean plasma protein concentration (-12.1 +/- 1.03%) and PCV (-11.9 + 0.67%) decreased proportionately and transiently in association with administration of either fluid at that volume. Other time effects included increased plasma osmolality and Na and Cl concentrations. Blood volume estimates and total amount of plasma protein remained unchanged. These data indicate that in conscious clinically normal horses, changes in plasma protein concentration reflect changes in plasma volume and that blood volume may be regulated by alterations in plasma volume and red cell mass. These data also indicate that changes in plasma volume and constituent concentrations may be similar in response to administration of either 0.9% (300 mosm/kg) or 7.2% (2,400 mosm/kg) NaCl solutions (5 ml/kg) and that clinically normal horses can rapidly regulate variable Na loads.

The purpose of this study was to determine the safety and efficacy of a live Salmonella choleraesuis immunizing strain, obtained by repeated ingestion and recovery through porcine neutrophils. The strain was tested in mice and in pigs. The vaccine was safe and effective in controlled experimental trials, using clinical, pathologic, and microbiologic criteria. Vaccinated pigs were able to maintain normal weight gains during the 4-week observation period following challenge inoculation with a high dose of a virulent strain.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.

The effects of 2 liquid formula diets differing in protein source were evaluated in orphan foals. The response of 7 foals fed a diet containing casein as the protein source, and 6 foals fed a diet containing a combination of whey and casein, was compared with the response in a reference group of 8 mare-raised foals. Orphaned foals were fed 150 kcal/kg of body weight/d, divided into 6 equal feedings of 25 kcal/kg. Formula intake was comparable among the experimental groups, and foals fed the liquid formula diet grew as well as mare-raised foals. There was no difference among groups in mean daily body weight gain, wither height, heart girth, body temperature, pulse, respiration rate, capillary refill time, or skin tenting. Insulin and blood glucose concentrations increased in both groups of foals fed formula diets, returning to prefeeding values within 4 hours. Differences among groups were found for serum alkaline phosphatase, alanine transaminase, cholesterol, creatinine, and glucose values; all other serum chemical values were comparable among groups. Plasma amino acid determinations revealed that arginine and ornithine were significantly lower in foals in both experimental groups than in reference foals, suggesting that arginine may have been the limiting amino acid in these diets. Diarrhea developed in foals in all treatment groups, but in most cases was self-limiting. These results suggest that the protein source of liquid formula diets may be less important in foals than in infants.

The effects of 3 experimental diets that varied only in the source of dietary protein (ie, poultry, cereal, red meat) were compared in Basenjis (n = 8) with immunoproliferative enteropathy and healthy Beagles (n = 8). Significant differences in fecal character, serum IgA concentration, and intestinal digestive and absorptive function were not induced by the different sources of dietary protein. The results of this study do not support a causal role for dietary protein source in the pathogenesis of immunoproliferative enteropathy of Basenjis.