Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.

Bilateral osteochondral defects (10 mm2 X 3 mm deep) were created on the distal articular surface of the radial carpal bone of ten, 2- to 3-year-old horses. One defect of each horse was repaired, using a sternal cartilage autograft (treated), and the other was left untreated (control). The horses were exercised on a high-speed treadmill at incrementally increased speed and duration over the course of 12 months. Horses were evaluated arthroscopically at 6 to 7 weeks, and clinical examinations were conducted weekly at exercise. Twelve months after surgery, carpuses of each horse were radiographed and clinically examined prior to euthanasia. A gross pathologic evaluation of each joint was conducted, and samples were collected for histologic, histochemical, histomorphometric, and biochemical evaluation. Radiographically, the grafted joints had more extensive evidence of arthropathy, and clinically, 8 of the 10 horses were more lame in the grafted limb. On the basis of histomorphometry, the repair tissue of the grafted defects contained a greater median percentage of hyaline cartilage (45%) than that of control defects 4.5%), and the control defects contained a greater percentage of fibrocartilage (82%) than did grafted defects (28.5%). A greater median percentage of repair tissue stained with safranin-O in the grafted defects (24.5%) than in the control defects (3.5%). On gross pathologic and histologic evaluation, repair tissue of the control defects had better continuity and was more firmly attached to the subchondral bone than was repair tissue of the grafted defects. Repair tissue of the grafted defects had extensive fissure and flap formation. Histologically, subchondral bone reactivity and fibroplasia was extensive in grafted joints. Repair tissue of grafted defects had a greater percentage of type II collagen (mean sem, 83.5 +/- 2.95%) than did controls (mean, 79.4 3.87%) that was not statistically significant. Hexosamine content was significantly higher (P < 0.05) in repair tissue of the grafted defect (mean, 28.9 +/- 3.00 mg/g of dry weight) vs control (mean, 20.6 +/- 1.85 mg/g of dry weight). On the basis of this experimental model, sternal cartilage autografts cannot be recommended at this time for repair of osteochondral defects in athletic horses.

The neutrophil plasma membrane has a major role in migration, phagocytosis, and destruction of microorganisms. Neutrophils isolated from blood and mammary secretions were homogenized, and the plasma membrane fraction was isolated on discontinuous sucrose gradient (20, 32, and 50%). Purity of plasma membrane preparation was determined by use of marker enzyme analysis. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of the membrane proteins was performed under reducing conditions for polypeptide characterization. The membrane proteins were also labeled with 125I externally, using 1,3,4,6-tetrachloro-3 alpha-6 alpha-diphenylglycouril, and proteins were separated by SDS-PAGE and autoradiographed. Compared with whole cell homogenate, the plasma membrane fraction obtained at the 20/32% interface was enriched for the marker enzymes, 5'-nucleotidase (16-fold), alkaline phosphatase (5.5-fold), and total phosphatase (26-fold). The membrane fraction had minimal specific activity for beta-glucuronidase (0.4-fold), compared with whole cell homogenate. Plasma membrane protein yield was about 500 micrograms/ 10(9) bovine blood neutrophils. The SDS-PAGE of plasma membrane proteins revealed 25 protein bands, of which 13 were major bands. There were 3 distinct bands (18, 36, and 65 kd) in the plasma membrane-enriched fraction (20/32 interface) that were not seen in other fractions (30/50% and pellet). Further, 125I-labeling identified 5 distinct protein bands (205, 140, 65, 35, and 30 kd). Blood and mammary neutrophils had similar polypeptide patterns, except that 36- and 65-kd bands were more prominent for blood neutrophils than for mammary neutrophils.

Efficacy of fenbendazole at 2 dosages for treating naturally acquired giardiasis in dogs was assessed. Giardia cysts were not detected in the feces of 6 of 6 group-1 dogs (as determined by use of the zinc sulfate concentration technique) after fenbendazole treatment (50 mg/kg of body weight, PO, q 24 h, for 3 doses). Cysts were not detected in the feces of 6 of 6 group-2 dogs after fenbendazole treatment (50 mg/ kg of body weight, PO, q 8 h, for 3 days). However, cysts were not detected in the feces of only 1 of 6 group-3 (nontreated control) dogs. Signs of toxicosis were not observed in any dog. These results indicate that the current label dosage (for the treatment of Toxocara canis, Toxascaris leonina, Ancylostoma caninum, Uncinaria stenocephala, Trichuris vulpis, and Taenia pisiformis, but not Giardia spp) of fenbendazole (50 mg/kg, PO, q 24 h, for 3 doses) is also effective for treating giardiasis in dogs.

The role of porcine parvovirus (PPV) in inducing reproductive failure in swine has been extensively documented. However, information is not available as to the risk of ppv transmission by embryo transfer. Using the polymerase chain reaction (PCR) technique, PPV-specific DNA was detected in association with 4-day-old porcine embryos incubated in vitro in the presence of NADL-8 strain of PPV, despite attempts to rid the embryos of virus by either washing or treatment with pronase or trypsin. The presence of PPV in embryos collected from acutely infected swine was not detected by PCR, although PPV DNA was detected in the proximal portion of the reproductive tract during the early stages of infection. Viral-specific nucleic acid was not detected in embryos transferred from infected donors to seronegative recipients and retrieved and assayed on the 15th and 32nd days of gestation. Results of the use of PCR to detect PPV associated with swine female reproductive tract and embryos ascribe minimal risk to the transmission of PPV to seronegative recipients through embryo transfer.

High serum alkaline phosphatase (ALP) activity is considered a sensitive marker of cholestasis in most mammalian species, including dogs. Induction of high serum ALP activity in association with cholestasis is dependent on high hepatic bile acids concentrations. Treatment of dogs with glucocorticoids also results in high serum ALP activity. The possible causal relation between serum ALP activity and bile acids concentration was investigated in dogs treated with glucocorticoids. The relation of glucocorticoid treatment to changes in the activity of individual ALP isoenzymes, alanine transaminase (ALT) and gamma-glutamyltransferase (GGT) also was investigated. Eight conditioned dogs were given 4 mg of prednisone/kg of body weight, IM, daily for 10 days. Blood samples were taken prior to treatment and on treatment days 3, 5, 7, and 10. Liver tissue was then taken from each dog. Serum total ALP activity was significantly (P < 0.05) high at day 3 in prednisone-treated dogs. Isoenzyme analysis indicated that this increase was attributable to an increase in the liver ALP isoenzyme (LALP). Significant increases in serum corticosteroid-induced ALP (CALP) and bone ALP were first observed on days 7 and 10, respectively. Serum ALT and GGT activities were significantly increased by day 5. Increased serum or hepatic tissue bile acids concentrations were not observed in prednisone-treated dogs, compared with values in 8 clinically normal (control) dogs, but were high in 3 dogs with complete bile duct ligation. Hepatic activities of LALP, CALP, and GGT were higher in prednisone-treated dogs than values in controls, indicating probable increased hepatic synthesis of these enzymes. Hepatic ALT activity was not increased. The ratio of serum to tissue LALP activity was increased in prednisone-treated dogs, compared with values in controls, indicating that LALP may have been preferentially released into serum. There was no difference in the ratio of serum to liver GGT activity between prednisone-treated dogs and controls. The LALP and GGT ratios were increased in bile duct-obstruction dogs. It was concluded that, although LALP is the principal ALP isoenzyme in serum during the first 10 days of prednisone treatment, hepatic bile acid concentrations are not increased and, therefore, are not likely to be responsible for induction and release of ALP into serum. Prednisone may, therefore, be directly responsible for induction of ALP activity in dogs treated thusly.

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10(-12) to 10(-4)M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10(-8) to 10(-6)M dexamethasone. Haptoglobin release was similarly induced by cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10(-8)M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

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.

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.

Analogues of a melanocyte-stimulating hormone (alpha-MSH) have been documented to be effective in inducing integumental melanogenesis in several species. These melanotropin analogues are more potent than the natural hormone and have prolonged biological activity, without apparent teratogenic or other toxic effects, at least in rodents. In a pilot study, a cyclic alpha-MSH analogue, Ac-[Nle4, Asp5 D-Phe7, Lys10] alpha-MSH4-10-NH2, was administered SC to a dog at a dose of 1 mg of analogue in 1 ml of 0.9% NaCl for 3 weeks, without noticeable adverse effects. There was gradual and extensive darkening of the coat, which originally was predominantly tan, with tips of black. Initially, the darkening involved face and extremities, then gradually expanded to include the trunk and tail hair. Visual pigmentation peaked approximately 2 months after injections were completed. As new hair growth continued subsequent to the injections, the original tan color appeared at the proximal end of the hair shaft, leaving a dark terminal band on all affected hairs. These observations clearly indicated that follicular melanogenesis can be induced in dogs by treatment with a melanotropic peptide.