We compared the plasma cortisol and immunoreactive corticotropin (IR-ACTH) responses to incremental doses (1.25, 12.5 and 125 micrograms) of synthetic ACTH (cosyntropin) administered IV to 6 clinically normal cats. Mean plasma cortisol concentration increased significantly (P < 0.0001) after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-microgram doses, plasma cortisol concentration peaked at 30 minutes, then decreased to values not significantly different from baseline concentration by 90 and 120 minutes, respectively. In contrast, after administration of the 125-microgram dose, mean cortisol concentration peaked at 60 minutes and remained significantly (P < 0.05) higher than baseline values at 120 minutes. Compared with the 1.25- and 12.5-microgram doses, administration of the 125-microgram dose of cosyntropin induced significantly (P < 0.05) higher cortisol responses at 60, 90, and 120 minutes. Although individual cat's peak plasma cortisol concentration after administration of the 125-microgram dose was higher than the peak value determined after administration of the 2 lower doses of cosyntropin, these differences were not statistically significant. Mean plasma IR-ACTH concentration increased significantly (P < 0.0001) and reached a maximal value at 30 minutes after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-microgram doses, plasma IR-ACTH concentration decreased to values not significantly different from baseline concentration by 60 and 120 minutes, respectively, whereas mean IR-ACTH concentration remained significantly (P < 0.05) higher than baseline values 120 minutes after administration of the 125-microgram dose. Mean peak plasma IR-ACTH concentration attained after administration of the 125-microgram dose of cosyntropin was significantly higher than that attained after administration of the 2 lower doses. Peak plasma IR-ACTH concentration attained after administration of the 12.5-microgram dose of cosyntropin was significantly higher than that attained after administration of 1.25 micrograms of cosyntropin. Results of the study indicate that IV administration of cosyntropin at doses ranging from 1.25 to 125 micrograms induces similar peak plasma cortisol responses in clinically normal cats, indicating that all of the doses may maximally stimulate the adrenal cortex. Administration of the higher cosyntropin doses did, however, result in more prolonged adrenocortical response.

Four 1-year-old steers were each inoculated orally with 10,000 Toxoplasma gondii oocysts of the GT-1 strain and euthanatized on postinoculation days (PID) 350, 539, 1191, and 1201. Samples (500 g) of tongue, heart, semimembranosus and semitendinosus muscles (roast), intercostal muscles (ribs), longismus muscles (tenderloin), brain, kidneys, liver, and small intestine were bioassayed for T. gondii by feeding to cats and examination of cat feces for shedding of oocysts. Toxoplasma gondii was recovered by bioassays in cats from the 3 steers necropsied PID 350, 539, and 1191, but not from the steer euthanatized on PID 1201. Cats shed oocysts after ingesting tongue from 2 steers, heart from 3 steers, liver from 2 steers, and roast, ribs, brain, and intestines from 1 steer each. Taxoplasma gondii was not isolated from any of the other bovine tissues. In addition to tissues bioassayed in cats, homogenates of mesenteric lymph nodes, lungs, spinal cord, spleen, and eyes were bioassayed in mice for T. gondii infection. Toxoplasma gondii was not recovered from the 135 mice inoculated with tissue from each of the 4 steers. All 4 inoculated steers developed high T. gondii antibody titers (greater than or equal to 1:8,000) in the agglutination test, using formalin-fixed whole tachyzoites. In the steer euthanatized on PID 1201, agglutinating T. gondii antibody titers decreased from 1:4,000 to 1:320 between 2 and 5 months after inoculation and to 1:20 by 19 months after inoculation.

Combined blood pool and delayed images produced by use of 99mTc-methylene diphosphonate (99mTcMDP) were evaluated as an objective measurement of the response of equine joints with osteochondral defects to postoperative exercise and intra-articularly administered polysulfated glycosaminoglycan (PSGAG). Osteochondral defects (approx 2.4 X 0.9 cm) were induced arthroscopically in the dorsodistal radial carpal bones of 18 ponies. These ponies were randomized (while balancing for age [range 2 to 15; median, 5.0; mean, 5.1 years]) to 2 treatment groups. Nine ponies were assigned to be exercised, and 9 were stall-rested. Six ponies in each group were administered PSGAG (250 mg) in 1 joint (medicated) and lactated Ringer's solution (LRS) in the contralateral joint. The 3 remaining ponies in each group were administered LRS in both joints (nonmedicated). Medication was given at surgery, then weekly for 4 weeks. The exercise protocol (begun at postoperative day 6 and conducted twice daily) started with 30 minutes walking (approx 0.7 m/s), and, by postoperative month 3, the ponies were being walked for 15 minutes and trotted (approx 1.6 m/s) for 25 minutes. Simultaneous dorsal images of both carpi were made 2 to 3 minutes after IV administration of 99mTcMDP (blood pool image) and 90 to 120 minutes later (delayed image). Scintimetry, in counts per minute per pixel per millicurie, was done before, and at 1, 2, 4, 8, 10, 13, and 17 weeks after surgery, prior to euthanasia. Radionuclide uptake on blood pool images decreased faster than that on delayed images, in which uptake remained high for 17 weeks. This indicated that bone was metabolically active for at least 17 weeks after surgery. Exercise significantly (P < 0.05) decreased uptake on the blood pool images of medicated joints up to 1 month after surgery. Thus, exercise (in the presence of PSGAG) probably had a transient, beneficial effect on soft tissues of the joint. Exercise, without PSGAG, promoted increased bone remodeling, because the highest uptake on delayed images was observed in exercised, nonmedicated ponies up to 3 months after surgery. This was consistent with development of osteoarthritis in these ponies. Medication alone stimulated bone remodeling, and data indicated that an identical effect may take place in contralateral LRS-injected joints, because of systemic circulation of the drug. However, the combination of exercise and medication appeared to moderate the independent effects of each. The combination of exercise and medication in individual joints resulted in notably (P < 0.05) decreased bone remodeling. Medication caused a decrease in bone remodeling in exercised ponies, indicating a protective effect against development of osteoarthritis.

Two distinct monoclonal antibodies (MAB) were prepared for testing with kidney, spleen, and retrobular tissue imprints made from chinook salmon (Oncorhynchus tshawytscha) affected with plasmacytoid leukemia (PL). Hybridomas were prepared from mice immunized with whole and lysed cells purified from renal or retrobular PL-positive tissues, which had been obtained from naturally and experimentally infected fish from British Columbia, Canada. The MAB reacted with at least 4 morphologically different cell types; fluorescence was associated with the plasma membrane and cytoplasm. The MAB also reacted with kidney imprints made from chinook salmon affected with a PL-like lymphoproliferative disease in California, indicating that these 2 diseases might be caused by a similar agent. The MAB did not react with any of the kidney or spleen imprints made from wild chinook salmon collected from a river in Ontario, Canada.

The density of the cricoid cartilage from 29 equine larynges collected from an abattoir was determined by dual photon absorptiometry (DPA). Densities of the right and left cricoid cartilages were highly correlated. No correlation was found between age of the horse and the density of the cricoid cartilage.

Two experiments were performed to study the relationship between leukotriene B4 (LTB4) synthesis and placental separation and uterine involution in the cow. In experiment I, the concentration and synthesis of LTB4 by caruncular tissue was lower in cows with retained fetal membranes (RFM cows, n = 11) than in cows that expelled the fetal membranes normally (NFM cows, n = 19). The presence of bacterial cell wall, especially of alpha-hemolytic streptococci and coagulase positive staphylococci enhanced LTB4 synthesis by allantochorion only in NFM cows. In the RFM group, Escherichia coli lipopolysaccharide decreased allantochorionic LTB4 synthesis. With caruncle, only epidermal growth factor increased LTB4 production in NFM cows. In experiment II, the caruncular and endometrial secretion of LTB4 was lower in cows with subuterine involution (SUI cows, n = 5) or cows with SUI and RFM (SUI+RFM cows, n = 4) than in cows with normal uterine involution (NUI cows, n = 8). This decrease was especially noticeable in the previously gravid horn. In the three uterine involution groups, there were no differences in LTB4 synthesis by caruncular tissue taken from the previously gravid horn. However, progesterone and a bacterial suspension of E. coli reduced the synthesis of LTB4. Estradiol had no effect on LTB4 synthesis at the end of the postpartum period. These results suggest that LTB4 may play an important role in both placental separation and uterine involution in cattle and LTB4 synthesis may be modulated by endocrine and bacterial factors.

We determined whether administration of cisplatin in hypertonic saline solution would prevent significant decrease in renal function, as measured by exogenous creatinine clearance, in healthy dogs. A single dose of cisplatin (70 mg/m2 of body surface) was mixed in 3% saline solution and was infused IV (6.5 ml/kg of body weight) over a 20-minute period to 6 healthy dogs. Exogenous creatinine clearance was determined prior to treatment of dogs with cisplatin and again on days 3 and 21 after administration of cisplatin. All 6 dogs vomited at least once within 12 hours of treatment with cisplatin; however, clinically important changes in appetite, body weight, or hydration status were not apparent during the 21-day study. Although mean values for exogenous creatinine clearance decreased from baseline on days 3 and 21, changes were not significantly different. Renal histologic lesions included mild, chronic, lymphoplasmacytic interstitial nephritis in 5 dogs, and presumably, were unrelated to treatment with cisplatin. Mild renal tubular atrophy (n = 2) and tubular necrosis (n = 1) may have developed secondary to treatment with cisplatin. Results of this study indicated that administration of a single dose of cisplatin in 3% saline solution to healthy dogs was not associated with significant decrease in glomerular filtration rate. This is a convenient protocol for administering cisplatin; however, additional study is required before it can be recommended for clinical patients, especially those with preexisting renal disease or those receiving multiple doses of cisplatin.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs, were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively. Differences for groups IGS, IGX, and IGM could not be calculated because arrhythmias satisfying the ADE criteria were not observed at the maximum infusion rate of 5.0 micrograms/kg/min. Differences among groups IS, IX, and IM were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, IM) or medetomidine (15 micrograms/kg, IM) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either alpha 2-adrenergic receptor agonist.

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.

Motion of 6 clinically sound horses trotting at a speed of 4 m/s on a treadmill was captured by video cameras before and 9, 16, and 23 days after amphotericin-induced lameness to determine the quantitative variables of three-dimensional computer-assisted image analysis that objectively describe carpal lameness. Amphotericin-B was used to induce lameness, and phenylbutazone (2.2 mg/kg of body weight, PO, once) and butorphanol tartrate (0.1 mg/kg IM, q 6 h, to effect) were used to control discomfort. Four 60-Hz cameras were symmetrically placed around the treadmill to capture 6 seconds of images from retroreflective spheres taped to the trotting horses. Images were transferred to a video-based digitizer and a computer work station, where 4 files of two-dimensional data were reduced to 1 file of three-dimensional data. The effect of lameness on motion analyzed was assessed by use of two-way ANOVA. Differences between means were assessed, using the Student-Newman-Keul's test (P less than or equal to 0.05). Head and withers excursions, (dorsal vertical displacement of head and withers targets, respectively) during the sound forelimb support phase were increased significantly during all lameness measurement periods. Head excursion, but not withers excursion, during the lame forelimb support phase, was decreased significantly during all lameness measurement periods. Computer determinations of stride length swing phase, stance phase, forelimb abduction, and carpal and fetlock ranges of motion did not consistently characterize the lameness. It was concluded that three-dimensional computer-assisted image analysis could be used for objective lameness evaluation in horses and that head and withers excursions were the most consistent variables for assessing equine carpal lameness.