Responses of the skin over the dorsum to solar UV irradiation (2 hours/d for 6 consecutive days) were investigated in hairless descendants of Mexican hairless dogs. Assessment of skin color changes, using a spectrophotometer, indicated that luminance values began to decrease from the third, day of UV irradiation, reached the minimal value at 3 weeks, and almost recovered 12 weeks after completion of UV irradiation. The number of the dihydroxyphenylalanine-positive melanocytes increased significantly (P < 0.01) from the third day of UV irradiation, reached its maximal value at 2 weeks, and recovered to normal at 12 weeks after completion of UV irradiation. On the second day of UV irradiation, the epidermis became focally thick, with disarrangement of component cells that had degenerative changes. In addition, a few so-called sunburn cells with pyknotic nuclei were seen in the epidermis. On the third day of UV irradiation, apparent suntan reaction developed, and a large number of epithelial cell in the epidermis were heavily pigmented with melanin granules. At 12 weeks after completion of UV irradiation, the epidermis appeared almost normal. On the other hand, significant changes were not detected in the dermis throughout the study.

Effects of isoflurane on the CBC in ferrets were studied. There was rapid decrease in all hematologic variables after induction of anesthesia. Percentage reductions in indices of the erythron (hematocrit, RBC count, hemoglobin concentration) exceeded those of plasma protein concentration and WBC count at the first postinduction time point. There was little additional decrease in these variables for the duration of anesthesia. The values had partially recovered to preanesthetic baseline at 45 minutes after anesthesia. Although these alterations appear to be well tolerated in healthy ferrets, care should be exercised when subjecting anemic, geriatric, or debilitated ferrets to isoflurane-induced anesthesia.

Although healthy and diseased bovine respiratory tracts have been intensively studied during the last years, to the authors' knowledge, there have been no attempts to objectively examine the inspiratory drive from the brain to the nerves and muscles and its transformation in pressure. Such technique would be useful in assessing the possibility of altered ventilatory drive or inspiratory muscle fatigue in the context of an animal with ventilatory failure. The relation among ventilation, airway opening occlusion pressure generated 100 milliseconds after onset of inspiration (Pawo100ms) and 6 indexes describing diaphragmatic electromyographic activity (EMGdi) recorded via implanted fishhooks was evaluated during free and impeded CO2, rebreathing in 6 young bulls. The best significant linear correlations (r > 0.8) with inspiratory center afferent stimulation, as judged by end-tidal CO2 concentration in expired air, were found for Pawo100ms, peak moving time average or variance EMGdi, and mean integrated EMGdi, whatever had been the respiratory impedance. However, with an inspiratory load, Pawo100ms responses systematically had greater increase for a given change in the driving EMGdi, implying dependence of the former not only on neural input, but also on configurational factors that determine inspiratory muscle excitation-pressure generation couplings. The reproducibility of EMGdi absolute values and changes was satisfactory up to 10 hours, but could not be repeated from one day to the other. It was concluded that, provided the constancy of the electrical coupling of the recording system to the tissue being studied is ensured, specific EMGdi and Pawo100ms values correlate reliably with amount of CO2 during free and loaded breathing. Simultaneous collection of both values during experimentally induced pulmonary disease in calves could, therefore, produce information to help answer questions about the role of CNS and inspiratory muscle dysfunction in case of ventilatory failure. Careful interpretation, however, requires additional measurements, such as end-expiratory lung volume, and some familiarity with the underlying physiologic processes that link phrenic nerve discharge to generation of negative pressure at the airway opening.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum nine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.

We measured glomerular filtration rate (GFR) estimated by plasma disappearance of 99mTc-labeled diethylenetriaminepentaacetic acid, serum concentrations of thyroxine (T4), creatinine, and urea nitrogen, and urine specific gravity in 13 cats with naturally acquired hyperthyroidism before and 30 days after treatment by bilateral thyroidectomy, and in a group of 11 control cats. Mean (+/- SD) serum T4 concentration decreased from a pretreatment value of 120.46 (+/- 39.21) nmol/L to a posttreatment value of 12.15 (+/- 6.26) nmol/L (P < 0.0001; reference range, 10 to 48 nmol/L). Treatment of hyperthyroidism resulted in a decrease in mean (+/- SD) glomerular filtration rate, from 2.51 (+/- 0.69) ml/kg of body weight/min to a posttreatment value of 1.40 (+/- 0.41) ml/kg/min (P < 0.0001). Mean serum creatinine concentration increased from 1.26 (+/- 0.34) mg/dl to 2.05 (+/- 0.60) mg/dl (P < 0.01). Mean serum urea nitrogen concentration increased from 26.62 (+/- 6.83) mg/dl to a mean postthyroidectomy concentration of 34.92 (+/- 8.95) mg/dl (P < 0.01). All changes were significant. Two cats developed overt renal azotemia after treatment of hyperthyroidism. Our results provide further evidence that treatment of hyperthyroidism can result in impaired renal function. In addition, our results suggest that, in some instances, thyrotoxicosis might mask underlying chronic renal insufficiency.

Ursodeoxycholic acid (UDCA; 10 mg/kg of body weight) was administered orally to 5 healthy cats for 3 months. Signs of illness were not apparent in any cat during treatment with UDCA. Results of monthly CBC, serum biochemical analysis, and urinalysis were unchanged during drug administration. There was a decrease in serum cholesterol concentration in 4 cats. Total postprandial serum bile acids (PPSBA) concentration was significantly (P = 0.0003) increased over total preprandial serum bile acids (PRSBA) concentration at all sample collection periods. The PRSBA and PPSBA concentrations were significantly (P < 0.05) increased at all sample collection periods after administration of UDCA, compared with baseline values. Ursodeoxycholic and tauroursodeoxycholic acids were not detected in serum prior to initiating administration of UDCA. Both bile acids were detected in the serum of all cats 1 and 2 months after UDCA administration and were detected in the serum of 2 cats 3 months after initiating UCDA administration. Hepatic ultrasonographic findings were normal before and after completion of UDCA administration. A mild, focal lymphocytic infiltrate was observed in 3 cats 3 months after initiating UDCA administration. Results of the study indicate that UDCA is absorbed into the systemic circulation of cats after oral administration, undergoes hepatic conjugation, and appears to be safe.

Pharmacologically induced splenic contraction might be useful during certain medical or surgical procedures in horses. The effects of phenylephrine, an alpha 1-adrenergic receptor agonist, on hemodynamic function and splenic dimensions were examined in 6 healthy adult horses. Phenylephrine infusion (1, 3, or 6 microgram/kg of body weight/min for 15 minutes) resulted in a dose-related increase in mean pulmonary artery pressure; right atrial pressure; systolic, mean, and diastolic arterial pressures; and packed cell volume (P = 0.0001). Concurrent decreases in heart rate and specific cardiac output (P = 0.0001) were detected, but stroke volume did not vary significantly. The rate-pressure product was increased only at the highest phenylephrine dosage (P = 0.012). Bradycardia was observed at all dosages during drug infusion, and second-degree atrioventricular block was detected in 88% of horses during infusion. Phenylephrine administration caused dose-dependent splenic contraction, as detected by ultrasonographic measurements of splenic area and thickness (P = 0.0001). At the 3- and 6-microgram/kg/min infusion rates, splenic area was reduced to 28 and 17% of baseline measurement, respectively. Splenic dimensions had returned to baseline values by 35 minutes after the end of infusion. Infusion of phenylephrine at a dosage of 3 microgram/kg/min for 15 minutes can be used to induce splenic contraction in horses.

We performed dual-energy x-ray absorptiometry (craniocaudal and lateromedial views) on 10 pairs of humeruses, radiuses, femurs, and tibias from dogs, using an alignment jig, to determine the homotypic bone mineral density variations of long bones. The bones were divided into 3 regions: proximal, middle, and distal parts of the diaphysis. The bone mineral density of cortical bone, medullary bone, and total bone was determined. Of 160 homotypic comparisons, 21 indicated significant (P less than or equal to 0.05) differences between right and left bones at either a region or location. These differences were observed most frequently in the craniocaudal view and were probably secondary to positioning errors. Evaluation of elliptical bones, such as the radius, also indicated that, when the thicker dimension, such as the lateromedial view of the radius was measured, the bone mineral density of regions-of-interest in that view was greater than that in the opposite view (ie, craniocaudal view of the radius). This study validates the concept of using the contralateral limb as the control condition in orthopedic studies of dogs, particularly when evaluating the densitometric properties of long bones. This study also emphasizes the importance of accurate positioning to prevent inadvertent alteration of bone mineral density results when using dual-energy x-ray absorptiometry. Dual-energy x-ray absorptiometry is particularly susceptible to positioning errors, because it converts a 3-dimensional structure into a 2-dimensional image.

A former secondary lead smelter was in operation in Granite City, Ill, until the early 1980s. As a result, the surrounding area is heavily contaminated with lead. Soil concentrations as high as 5,000 ppm have been measured in prior studies. Because of growing concerns about health defects associated with low levels of lead exposure in human beings, a major study has been conducted on people living in the area. The study reported here was a corollary to the human exposure study. Lead concentration was determined in 84 dogs and 26 cats in the town and ranged between < 5 and 28 microgram/dl. None of the dogs had clinical signs of lead poisoning. The CBC and serum biochemical values did not indicate many significant differences between dogs with a high (larger than or equal to 10 microgram/dl) or low blood lead concentration (BLC). Hemoglobin concentrations were lower, and WBC counts were higher in dogs and cats with higher BLC, but they were still within reference ranges. Free erythrocyte protoporphyrin concentration was determined. Normal values appeared to be similar for dogs and cats. Only animals with BLC larger than or equal to 20 microgram/dl were found to have somewhat increased concentration of free erythrocyte protoporphyrin. Delta-aminolevulinic acid dehydratase activity was measured and found to be negatively correlated with BLC. The relation was strong, even at low BLC (5 to 10 microgram/dl) in both species. Age or sex difference was not observed. Therefore, biological changes associated with low BLC were limited to BLC in the 10- to 30-microgram/dl range.

The alpha 1-proteinase inhibitors of trypsin, Spi1, Spi3A, and Spi3B, in bronchoalveolar lavage fluid (BALF) and serum of horses were separated by electrophoresis, and their proportions were quantified in 12 control horses and 12 with chronic obstructive pulmonary disease (COPD). A significantly lower proportion of Spi3B (P < 0.05) and higher proportion of Spi1 (P < 0.02 to P < 0.01) were detected in BALF, compared with serum, in control and COPD-affected horses and appeared to be attributable to reduced Spi3 activity in BALF. There was no significant difference between the control and COPD groups in this respect, indicating that the decrease in Spi3 may be a physiologic phenomenon. The differences observed may be associated with proteolytic damage to or preferential complex formation by Spi3.