To evaluate the effect of ketoprofen on fecal output during secretory diarrhea, 16 calves were given approximately 200 micrograms of heat-stable Escherichia coli enterotoxin by suckling on 2 occasions. On one day, treatment was not administered. On the other day, either 3 mg of ketoprofen/kg of body weight (n = 8) or 6 mg of ketoprofen/kg (n = 8) was administered 1 hour before and 3 hours after administration of enterotoxin. Fecal output was no different after 8 or 24 hours from calves given 3 mg/kg, but fecal output was less at 8 hours and 24 hours for calves given 6 mg/kg (P = 0.0588), compared with the control day.

Effects of phenylbutazone (PBZ) and furosemide (FUR) on the respiratory tract of horses were evaluated, focusing on bronchial responsiveness. Four healthy Thoroughbreds were used and data were analyzed by use of a Latin square design. Histamine provocation tests (0.5, 1, 2, and 4 micrograms/kg/min, IV) were done: (1) without prior treatment with PBZ or FUR, (2) 30 minutes after administration of PBZ (8 mg/kg, IV), (3) 1 hour after administration of FUR (1 mg/kg, IV), and (4) after administration of PBZ plus FUR. Pulmonary function tests (dynamic compliance, resistance, respiratory frequency, and tidal volume) and heart rate were monitored throughout the experiments. Phenylbutazone did not influence basal pulmonary function test results, whereas FUR caused a significant (P < 0.05) increase in dynamic compliance and decrease in resistance. Histamine infusion resulted in a dose-dependent decrease in dynamic compliance and a dose-dependent increase in resistance, respiratory frequency, and heart rate. Phenylbutazone administration significantly (P < 0.05) attenuated most of the changes induced by histamine, whereas FUR had less protective action. Administration of PBZ plus FUR before administration of histamine was less effective than administration of PBZ alone.

The ability of viral glycoproteins (VP) VP4/VP7 reassortant swine rotaviruses (RV) to induce cross-neutralizing antibody against parental serotypes was investigated in guinea pigs. Using selective culture conditions, we produced 10 reassortant viruses that contained gene segment 4 of the OSU RV strain and gene segment 9 of the Gottfried RV strain. These reassortant RV grew to high titer in cell culture and were neutralized by monospecific antisera against both parental RV strains. The reassortant RV were chemically inactivated with binary ethylenimine, adjuvanted with aluminum hydroxide, and used to produce antisera in guinea pigs. The hyperimmune antisera had high neutralization titer against both parent RV strains. These results indicate that several of the reassortant RV may be capable of inducing neutralizing antibodies to VP4 and VP7 and may have future use as bivalent vaccine strains.

Histomorphometric and scanning electron microscopic analyses were performed on 74 embryos and fetuses and 20 sheep (early postnatal to adult age). Histologic differentiation of the omasum took place at 33 days of fetal life, with the appearance of first-order laminae. Second-, third-, and fourth-order laminae appeared at 39, 50, and 59 days, respectively. Neutral mucopolysaccharides first appeared in epithelial cells at 46 days of fetal life, decreasing quantitatively until birth, before subsequently stabilizing in postnatal life. Acid mucopolysaccharides, mucins, and mucoid compounds were not detected. Growth curves and formulas were constructed for each tissue layer. Initial tests involved multiplicative (y = axb), exponential (y = EXP [a + bx]), linear (y = a + bx), and polynomial models [y = a + bx + cx(2) + dx(3)].

Gastric pH was monitored in neonatal foals from birth to 3 months of age. Background pH decreased, especially during the first week of life. Milk had complex effects that depended on pH prior to sucking, confounded by the age of the foal: nearly neutral background pH tended to be acidified after milk intake; moderately acid background pH tended to be neutralized; low background pH was only slightly increased by milk. Absolute magnitude of the effects of milk decreased with age. Existence of a proulcerative intragastric environment in preweaning foals is postulated, but this must be considered in the context of what probably is a multifactorial pathogenesis.

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 X 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus. Age at puberty was similar between gilts exposed to low or moderate concentration of ammonia (208 vs 205 days; SEM, 1.3 days), even though weight at puberty was less (P < 0.03) for gilts exposed to low concentration of ammonia than for gilts exposed to moderate concentration of ammonia (109.7 vs 118.2 kg; SEM, 4.5 kg). At day 30 of gestation, number of live fetuses (10.6 vs 11.7), fetal length (2.53 vs 2.57 cm), and fetus-to-corpus luteum ratio (0.85 vs 0.78) were similar between gilts at low and moderate ammonia environments. These data indicate that exposure of gilts to mean aerial ammonia concentration of 35 ppm in environmentally regulated rooms depressed MDG for 2 weeks, but failed to alter onset of puberty or litter size at day 30 of gestation.

The effects of exogenous platelet-activating factor (PAF) were determined in anesthetized ponies. Administration of PAF induced a decrease in cardiac index that resulted in systemic hypotension. This was followed by tachycardia, hypertension, and a return of cardiac index to baseline. Pulmonary arterial pressure increased markedly because of pulmonary vasoconstriction. Exogenous PAF also caused leukopenia and thrombocytopenia. The specific PAF receptor antagonist (WEB 2086) blocked all PAF-induced changes. Flunixin meglumine, a cyclooxygenase inhibitor, abolished the pulmonary hypertension and tachycardia, and attenuated the systemic hypotension but did not change the PAF-induced peripheral cellular changes. The PAF antagonist also inhibited platelet aggregation induced by PAF in vitro. The PAF-induced changes are similar to those reported after endotoxin exposure in horses.

Rectal swab specimens were collected from 362 apparently healthy dogs of different origin, age, breed, and sex. Specimens were obtained in summer, autumn, and winter. Ninety-five thermophilic Campylobacter spp were isolated: C jejuni biotype I, n = 57, C jejuni biotype II, n = 1, C coli, n = 36, and C laridis, n = 1. Biotypes of C jejuni recovered were the same as those associated with Campylobacter-induced enteritis in human beings. Prevalence of C jejuni was significantly (P < 0.05) greater: in dogs < 6 months old than in adult dogs; in dogs living under high density and cohabitation housing conditions for long periods; and in autumn.

Free, autogenous, full-thickness skin grafting was performed on 10 dogs; 5 dogs were given an iron chelator, deferoxamine-10% hydroxyethyl pentafraction starch (DEF-HES; 50 mg/kg of body weight, IV), and 5 dogs were given 10% hydroxyethyl pentafraction starch (HES) in 0.9% saline solution (5 ml/kg, IV). The percentage of viable graft on day 10 was higher, but not significantly so, in DEF-HES-treated dogs (mean +/- SD, 72.6 +/- 24.8%; median 76.5%) than in HES-treated dogs (mean +/- SD, 46.7 +/- 34.3%; median, 48.8%). A trend for a positive correlation between the percentage of viable graft (on day 10) and the percentage of original graft area (on day 28) was observed in HES- and DEF-HES-treated dogs; this trend was significant in HES-treated dogs (P = 0.012). Both groups had significant positive correlation between percentage of viable graft on day 10 and percentage of haired skin on day 28 (HES, P = 0.000002; DEF-HES, P = 0.0148). A unique finding in DEF-HES treated dogs was the consistent observation of foamy macrophages in the dermis adjacent to the grafts, in deep subcutaneous tissue below the grafts, and in normal dermis.

The mechanism of estrogen-induced myelotoxicosis is unknown, although evidence indicates that estrogen does not directly damage the bone marrow granulocyte-macrophage progenitor cells and that the thymus is a probable mediator of the bone marrow suppression. Estrogen-induced production of a myelopoiesis-inhibitory factor by canine thymic stromal cells in vitro has been observed. Then, presence of a myelopoiesis-inhibitory factor in canine serum was investigated immediately after estrogen administration in vivo. Maximal reduction in colony-forming units-granulocyte/macrophage growth by sera from individual dogs varied. Individual dog sensitivity to estrogen-induced myelotoxicosis is seen clinically, and the cause is unknown. This serum factor could have a role in the eventual bone marrow hypoplasia seen in estrogen-treated dogs and is possibly the same factor produced by cultured thymic stromal cells exposed to estrogen.