Pituitary function and short-term clinical effects after transsphenoidal hypophysectomy were investigated in clinically normal dogs. In study, I, 8 dogs were given polyionic fluids IV during the first 12 hours after surgery. In study II, 4 dogs were given polyionic fluids IV and glucocorticoid supplementation for 7 days. Pituitary function was assessed by evaluating basal ACTH concentrations and results of a growth hormone stimulation test before and 1 and 12 weeks after hypophysectomy, an ACTH stimulation test, a thyrotropin-releasing hormone-stimulation test, and a modified water deprivation/vasopressin response test before and 1, 4, 8, and 12 weeks after hypophysectomy. Gross and histologic evaluations of the surgery site, thyroid and adrenal glands, and skin were done at 12 weeks after surgery. Four dogs from study I died within 27 hours after hypophysectomy. Postmortem examinations of these dogs revealed liver and lung congestion compatible with circulatory collapse. None of the dogs in study II died. For the surviving dogs in both studies, diabetes insipidus developed immediately after hypophysectomy and resolved within 2 weeks. Hypernatremia also developed immediately after hypophysectomy and resolved by 1 week. Production of ACTH was evident at 1 and 12 weeks after hypophysectomy in all dogs, and results of ACTH stimulation tests after surgery were not notably different from results obtained before surgery. Results of thyrotropin-releasing hormone stimulation and growth hormone-stimulation tests supported the diagnosis of hypothyroidism and hyposomatotropism attributable to hypophysectomy. Histologic examination revealed thyroid atrophy, epidermal and dermal atrophy, and normal adrenal glands in all dogs and remnants of the hypophysis in 2 dogs from study I. Continued ACTH production suggested that complete hypophysectomy was not accomplished in any dog.

The patency of mammary papillae was reestablished after surgically induced injury. Perforated prosthetic tubes with affixed Dacron tubing or Teflon strips were implanted in 18 abrabed papillae of lactating dairy cows and were secured with sutures. Wound healing was assessed by palpation and visual inspection. All wounds, with one exception, healed by first intention. Machine milking, reinstituted on day 5 after surgery, caused no apparent discomfort. Grossly and histopathologically, all implants stimulated a variable degree of mucosal metaplasia and hyperplasia. Only implants with Teflon strips became anchored by fibrotic invasion. Mastitis, tube migration, and milk fistulas were complications of the procedure.

Five mature Holstein cows and 6 first-lactation Holstein cows were administered 100 mg of glucose/kg of body weight, IV, over a 20-minute period on postpartum day 30. A series (preinfusion, glucose infusion, and postinfusion) of blood samples was collected at -15, -10, -5, 5, 10, 15, 20, 30, 45, 60, 75, 90, 105, and 120 minutes from the start of the infusion. Serum was obtained and was assayed for glucose, immunoreactive insulin (IRI) growth hormone (GH), and free fatty acid concentrations. Baseline glucose and free fatty acid concentrations were similar in cattle of both groups throughout the sample collection period. Both groups of cattle disposed of the infused glucose in a similar manner. The first-lactation cows secreted significantly (P < 0.0001) more IRI to utilize the glucose load than did the mature cows, 71 +/- 13 microU/ml vs 38 +/- 7 microU/ml, respectively (mean +/- SEM). Preinfusion and glucose infusion GH concentrations were similar in cattle of both groups. In the postinfusion period, GH values were significantly (P < 0.0002) higher in the first-lactation cows (8.7 +/- 1.8 ng/ml) than in the mature cows (5.8 +/- 1.6 ng/ml). Compared with that in the mature cows, the higher IRI concentration required by the first-lactation cows to utilize approximately the same glucose load suggested that first-lactation cows were insulin resistant. The increased insulin response to increased glucose concentration may be one reason first-lactation cows produce less milk than do mature cows. Other factors, such as variation in the ability of the mammary gland to synthesize milk cannot be excluded.

Using an avidin-biotin-peroxidase complex immunoperoxidase staining method, respiratory syncytial virus (RSV) antigen was demonstrated in glutaraldehyde-fixed, parraffin-processed lung sections from calves with induced RSV pneumonia. The virus also was detected in formalin-fixed, paraffin-processed lung sections from calves with naturally occurring RSV pneumonia. Specific immunoperoxidase staining was detected within the cytoplasm of epithelial cells and syncytia in small bronchi, bronchioli, and alveoli. Staining also was detected within exudates in airway lumina and in mononuclear and multinucleate cells within alveolar lumina. Optimal intensity of staining was achieved by proteolytic enzyme treatment of lung sections, using 0 .1% pronase and overnight incubation in diluted primary antiserum. The distribution of antigen had a close correlation with presence of lesions. Antigen-staining patterns were similar in lung tissue from calves with naturally occurring and induced RSV disease.

Neuromuscular and cardiovascular effects of atracurium, a nondepolarizing neuromuscular blocking agent, were evaluated in 10 halothane-anesthetized adult horses. Hind limb digital extensor tension (hoof twitch) was measured with a strain gauge to quantitate the muscle relaxant effects of atracurium. Response of facial muscles was compared with hoof twitch. Five injections of atracurium were given. Initial mean (+/- SEM) dosage of 0.07 +/- 0.01 mg of atracurium/kg of body weight caused 98.6 +/- 0.8% reduction of the preinjection hoof twitch. Subsequent dosages of 0.04 +/- 0.003 mg/kg induced a degree of relaxation similar to that induced by the initial dose. Duration of paralysis from maximal effect to 10% recovery of twitch was 12.2 +/- 1.5 minutes for the first injection. This was significantly (P less than 0.05) different from subsequent paralysis periods, which lasted approximately 7 miutes. The 10% to 75% recovery time after all injections was similar--approximately 16 minutes. The facial muscles were less affected objectively by atracurium than was the hind limb. Atracurium did not cause cardiovascular changes. When the hoof twitch had recovered to 95% of its tension before atracurium administation, 0.5 mg of edrophonium/kg, was given to antagonize neuromuscular blockage. Within 5 minutes of edrophonium administration, twitch tension exceeded that measured before atracurium administrations. Within 2 minutes of edrophonium administration blood pressure began to increase and continued to increase approximately 10 mm of Hg above the value measured before edrophonium administration. Heart rate was not affected by edrophonium. Other muscarinic side effects of edrophonium were not observed. Of the 10 horses, 9 had good, unremarkable recovery to standing position. One horse had a violent recovery period.

The efficacy of water vapor-saturated air as a treatment for horses with exercise-induced pulmonary hemorrhage (EIPH) was studied. Horses selected for study (n = 14) had grade 1 or greater hemorrhage in the trachea after a minimum of 4 breezes between 0.8 and 1 km, as determined by endoscopy. Nine horses were treated with water vapor-saturated air; 5 horses were not treated. When the mean and maximal EIPH scores from the pretreatment period were compared with the mean and maximal EIPH scores from the treatment period in both treated and nontreated groups, there was no significant difference between groups. There was a suggestion of a linear relationship between exercise speed and the mean EIPH score of the first 4 breezes in all 14 horses.

Studies were undertaken to assess the chicken embryo and newly hatched chicken as models for studying the effects of bone-active agents. Initially, 1,25-dihydroxycholecaliferol (1,25[OH]2D3), sodium fluoride (NaF), parathyroid extract, epidermal growth factor, and prostaglandin E2, were tested for lethality over a broad dose range. One or 3 injections of 1,25(OH)2D3 into the yolk sac of chicken embryos resulted in death of embryos given greater than 0.1 ng/injection, whereas 0.01 ng was tolerated by the embryos. Administering 1,25(OH)2D3 intraperitoneally to newly hatched chickens as a single injection or weekly for 3 weeks resulted in no deaths at doses up to 50 ng. One or 3 IV injections of less than 400 micrograms were tolerated by the embryo. Giving chickens feed and water containing 2.4 g of NaF/kg was lethal but no deaths occurred when chickens were given feed containing less than 1.2 g of NaF/kg. Mortality associated with the administration of epidermal growth factor to embryos was inconsistent, in that death occurred in embryos given a single injection of greater than 250 ng, but no deaths occurred in embryos given 3 injections at similar doses. Parathyroid extract and prostaglandin F2 were not lethal when administered to embryos and chickens in a single-injection or multiple-injection regimen. Overall, lethality in chicken embryos given a particular agent reflected the dose of bone-active agent injected, rather than the number of injections. Three of the bone-active agents were selected to characterize their microscopic bone effects in chicken embryos and chickens. Administration of 1,25(OH)2D3 to embryos on day 14 at doses of 100, 10, 1, and 0.1 ng led to subperiosteal hyperosteoidosis in all 5 of the tibiotarsi examined from the high-dose (100 ng) group necropsied on day 18 of incubation. Three of 5 of the tibiotarsi from the 10-ng treatment group were similarly affected. Bone effects were noticed in chickens hatched from the aforementioned treatment groups or in chickens given 1,25(OH)2D3 intraperitoneally and examined at 3 and 6 weeks of age. Administration of NaF to chicken embryos on the 10, 12th, and 14th days of incubation via the IV route at doses of 160, 80, 40 and 20 micrograms/embryo led to subperiosteal hyperosteoidosis in tibiotarsi from 3 of 10 embryos (examined at 18 days of incubation) from the 2 high-dose groups. Tibiotarsi of chickens from this treatment group were microscopically normal at 3 weeks after hatching. When newly hatched chickens were given a diet containing NaF at dosages of 1.2 g/kg, 0.6 g/kg, and 0.3 g/kg, a dose-dependent increase in osteoid was seen at 3 and 6 weeks. In addition, cortical thinning and expansion of the medullary canal were observed only at 3 weeks. In contrast to the effects observed with 1,25(OH)2D3 and NaF, parathyroid extract caused no microscopic bone alterations when given to embryos or chickens. Overall, the bone alterations in the embryo were attributed to increased subperiosteal osteoid formation and defective mineralization. These findings were consistent with known effects of NaF and 1,25(OH)2D3 on bone, and they establish the chicken embryo as a sensitive model for studying bone-active agents.

Strains of the suspensory ligament and deep digital flexor, superficial digital flexor, and long digital extensor tendons in the equine (pony) hind limb were recorded in vivo, using implanted strain gauges consisting of silicone rubber tubes filled with mercury. The relationship between strain gauge signals and tendon strains was obtained from tension-strain tests performed on isolated tendons after death of the ponies. During normal walking, maximal tendon strain (elongation over initial length, relative to the length of the structures at first ground contact) was 3.1% in the suspensory ligament and 3.4%, 2.3%, and 0.3% in the deep digital flexor, the superficial digital flexor, and the long digital extensor tendons, respectively. Changes (that occurred during walking) in the distance from origin to insertion of these musculotendinous structures were computed from limb geometric configuration and limb conformation. Maximal increase in origin to insertion length was 3.1% in the suspensory ligament and 2%, 1.6%, and 1.5% in the deep digital flexor, superficial digital flexor, and long digital extensor musculotendinous structures, respectively. The differences in strain, comparing the entire musculotendinous structure and its tendon, were explained by muscular contraction or relaxation.

Inoculation of lambs with an ovine isolate of respiratory syncytial virus (RSV) by a combined intranasal and intratracheal route resulted in mild respiratory tract illness, with respiratory tract lesions. Lung lesions were characterized by bronchitis and bronchiolitis, hyperplasia of bronchial and bronchiolar epithelium, peribronchiolar and perivascular accumulations of lymphocytes, alveolar and perivascular accumulations of lymphocytes, alveolar septal thickening, and collapse. Respiratory synctial virus was recovered from the respiratory tract of inoculated lambs, and RSV antigen was demonstrated by immunoperoxidase staining of bronchiolar and alveolar epithelial peroxidase staining of bronchiolar and alveolar epithelia cells in pneumonic lesions of lambs euthanatized on post-inoculation days 5 and 6. Other primary respiratory tract pathogens were not isolated. Clinical signs of respiratory tract illness or respiratory tract lesions did not develop in the in-contact control lamb. Inoculation of the ovine RSV isolate into calves and deer fawns resulted in infection in both species, and at necropsy, pneumonic lesions were present. A mild to moderate respiratory tract illness developed in the calves, but clinical disease was not seen in the fawns. Lung lesions in fawns were similar to those seen in lambs; lesions in calves were characterized by collapse, scattered areas of parenchymal necrosis, and bronchiolitis. Respiratory synctial virus was reisolated from the lower respiratory tract of inoculated calves and fawns, and immunoperoxidase positive epithelial cells were seen in pneumonic lesions Other primary respiratory pathogens were not detected. Respiratory syncytial virus infection was not demonstrable in control animals that were in contact with inoculated animals. We concluded that an ovine RSV isolate, when inoculated in a severe challenge regime, caused mild primary pneumonia in lambs and lesions similar to those described in epizootics of naturally occurring ovine respiratory tract disease. Also, the ovine RSV caused lower respiratory tract lesions in infected calves and deer.

Adult Beagles were used to evaluate clinical signs and serologic response after inoculation with, or exposure to, Borrelia burgdorferi. An indirect immunofluorescent assay (IFA) and 2 ELISA were used to monitor the serologic response to B burgdorferi. Feeding infected ticks on 4 dogs (group 1) failed to cause seroconversion, and SC inoculation with 500 organisms caused minimal seroconversion in 2 of 4 dogs (group 2). At 56 days, approximately 3.01 X 10(8) B burgdorferi organisms were injected IV into group-1 dogs, and intraperitoneally into group-2 dogs. A control group of 4 dogs (group 3) had noninfected ticks feed on them, and then were given IV injection of physiologic saline solution. Increases in immunoglobulin M (IgM) titers were detected in 2 of 4 group-2 dogs approximately 7 days after the initial exposure. These titers returned to negligible values 20 days later. Immunoglobulin G titers increased approximately 10 days after the initial exposure and were mildly increased 56 days later, when dogs were exposed a second time. Both the IV and intraperitoneal injections (second exposures) resulted in increased IgM titers, which in both groups eventually returned to preexposure values after approximately 2 months. Immunoglobulin G titers increased within a week after the second exposure, and in 3 dogs monitored for 8 months, returned to negligible values after the 8-month period. One control dog had a slightly increased IgG titer 24 days after the second inoculation. The possibility of urine transmission is suggested. Clinical status, hemograms, serum biochemical profiles, ECG and results of urinalyses remained normal throughout the study. Borrelia burgdorferi was not isolated from either the blood or urine of these dogs. Gross or microscopic pathologic changes were not detected on necropsy.