An in vitro bioassay system was used to study the effects of cyclopiazonic acid (CPA) mycotoxin on cardiac muscle. Acute exposure to 6 microgram of CPA/ml of modified Krebs-Henseleit solution significantly (P < 0.05) decreased 5 in vitro turkey cardiac muscle performance criteria: maximal weight a muscle could lift; maximal contraction velocity; relaxation velocity; time to peak contraction; and total time for muscle contraction and relaxation. The effect on these 5 criteria appeared to result from intracellular changes partially associated with calcium availability and were irreversible, suggesting that physiologic changes had developed after acute exposure to CPA.

Concentrations of total, free, and esterified carnitine were determined in plasma, liver, and skeletal muscle from cats with idiopathic hepatic lipidosis and compared with values from healthy cats. The mean concentrations of plasma, liver, and skeletal muscle total carnitine; plasma and skeletal muscle free carnitine; and plasma and liver esterified carnitine were greater (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. The mean for the ratio of free/total carnitine in plasma and liver was lower (P < 0.05) in cats with idiopathic hepatic lipidosis than in control cats. These data suggest that carnitine deficiency does not contribute to the pathogenesis of feline idiopathic hepatic lipidosis.

Protein profiles of whole homogenates of anconeus (slow twitch) and biceps femoris (fast twitch) muscles of clinically normal dogs and of Labrador Retrievers with hereditary myopathy (HM) were resolved on flat bed polyacrylamide isoelectric-focusing gels. Three methods of sample solubilization were performed. The solubilization buffer, with high concentrations of urea, precipitated the zwitterionic detergent, but use of the buffer containing 3% NP-40, 9.2M urea, and 0.1M arginine resulted in better resolution and stability of pH gradient. Gels of anconeus muscle from clinically normal dogs contained 2 protein bands specific to anconeus muscle, whereas gels of biceps femoris muscle from clinically normal dogs contained 3 protein bands amplified in biceps femoris muscle that were barely detectable in anconeus muscle. The staining intensity of protein bands in biceps femoris muscles from Labrador Retrievers with HM was decreased, relative to controls. The quantitative analysis of peak height ratios of biceps femoris muscle revealed significant (P less than 0.05) differences between profiles of clinically normal dogs and Labrador Retrievers with HM.

Tissue specimens from muscle, liver, kidney, and injection sites were collected, and serum was obtained from 3 calves euthanatized on each of posttreatment days 5 and 22. Calves were treated with 6.7, 13.4, or 20 mg of oxytetracycline (OTC)/kg of body weight, IM, once daily for 3 days; these dosages are 1, 2, and 3 times the label dose, respectively. One control calf was euthanatized on each of posttreatment days 5 and 22. In treated male calves killed 2 days after the last injection, OTC residues were detected in all tissues and serum, using high-performance liquid chromatography. Tissues from all injection sites also were considered positive for antimicrobial residues, using swab test on premises (STOP), microbial inhibition test (MIT), and thin-layer chromatography-biautography (TLCB) test. Kidney tissues from a calf given 13.4 mg of OTC/kg and kidney and liver tissues from a calf given 20 mg of OTC/kg also were considered positive, using the MIT and TLCB. Results of the STOP only were considered positive for the liver and kidney of a calf given 20 mg of OTC/kg, but substitution of Saskatoon antibiotic medium-3 for the original medium (antibiotic medium-5) allowed the STOP to detect residues in these tissues from all treated calves. In female calves killed 19 days after the last injection, the STOP, MIT, and TLCB procedures revealed positive results for tissues from some injection sites, but revealed negative results for other tissues. High-performance liquid chromatographic analyses detected OTC in tissues from injection sites from all treated calves, in muscle and liver from a calf given 20 mg of OTC/kg, and in kidneys from calves given 13.4 or 20 mg of OTC/kg. The STOP, MIT, and TLCB procedures lacked the sensitivity of high-performance liquid chromatography for detection of OTC residues.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: greater than or equal to 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C. Antibodies against Trichinella spp were found in 6 (1.8%) of 319 bear sera; Trichinella spp larvae were detected in muscle digests of 2 of 63 bears, and in histologic sections of muscles from 3 of 162 bears. Genetic typing indicated that the 2 Trichinella isolates from bears were a sylvatic genotype and were not the species found in domestic pigs.

Ouabain, a cardiac glycoside, binds to the Na+-K+i-adenosine triphosphatase (Na+ pump) and prevents active transport of Na+ and K+ across cell membranes. We used [3H]ouabain to quantify the number and affinity of Na+ pumps in skeletal muscle from Quarter Horses with the muscular disorder hyperkalemic periodic paralysis (HYPP). [3H]Ouabain-binding properties of gluteal muscle from clinically normal and affected horses were used to determine whether altered Na+ pump number or affinity could contribute to the pathologic features of muscle in affected horses. Foals and adult horses with HYPP were compared with age-matched clinically normal horses. The number of [3H]ouabain-binding sites in adult gluteal muscle was not different between the 2 types of horses (85.7 +/- 8.9 pmol of [3H]ouabain-binding sites/g [wet muscle weight] in horses with HYPP vs 100.2 +/- 8.8 pmol/g in clinically normal adult horses). Gluteal muscles in HYPP-affected and clinically normal foals also contained a similar number of [3H]ouabain-binding sites (222.3 +/- 21.0 pmol/g vs 225.3 +/- 24.2 pmol/g, respectively). The affinity of these binding sites for ouabain was not different, between adults or foals, in clinically normal or affected horses. Our results indicate that membrane events underlying the periodic episodes of paralysis in horses with HYPP are not attributable to quantitative changes in Na+ pump number or affinity. Our data cannot exclude the possibility that the specific activity of the Na+ pump is altered in muscle from HYPP-affected horses.

Vascular medial thickening is a prominent finding in people and animals with refractory neonatal pulmonary hypertension. Smooth muscle cells are capable of 2 distinct growth responses in vivo: hypertrophy or hyperplasia. Hypertrophic smooth muscle cells may undergo DNA synthesis without cell division, leading to a polyploid state. To better understand the nature of smooth muscle cell growth in healthy and pulmonary hypertensive neonatal calves, we measured incorporation of the thymidine analog bromodeoxyuridine (BrdUrd) and total DNA content in medial cells from control (pulmonary arterial pressure = 32 +/- 2 mm of Hg) and hypobaric hypoxia-exposed (pulmonary arterial pressure = 120 +/- 7 mm of Hg) calves. Labeling of medial cells with BrdUrd measured by flow cytometry was increased (P < 0.02) in pulmonary arteries of hypoxia-exposed calves (n = 5), compared with control calves (n = 5). Immunohistochemical localization of BrdUrd indicated that BrdUrd labeling of large elastic pulmonary arteries from hypoxia-exposed calves was increased almost exclusively in the outer half of the medial wall. Increased BrdUrd labeling of muscular pulmonary arteries from hypoxia exposed calves was observed in the arterial media and adventitia, and tended to exit in clusters. Analysis of DNA content by flow cytometry indicated a decrease (P < 0.05) in percentage of tetraploid medial cells in pulmonary arteries from hypoxia-exposed calves, compared with control calves. Bivariate analysis for BrdUrd labeling and DNA content of cells from the pulmonary arteries of hypoxia-exposed calves indicated a subpopulation of diploid cells with positive BrdUrd labeling, suggestive of DNA synthesis and subsequent cell division. Results are suggestive of smooth muscle cell hyperplasia in the vascular media of hypoxia-exposed calves.