Age-related Variation of Plasma Concentrations of Skatole, Androstenone, Testosterone, Oestradiol-17β, Oestrone Sulphate, Dehydroepiandrosterone Sulphate, Triiodothyronine and IGF-1 in Six Entire Male Pigs

This study describes the age-related variation in boar taint compounds, skatole and androstenone, and testosterone, oestradiol-17 beta (E17 beta), oestrone sulphate (ES), dehydroepiandrosterone sulphate (DHEAS), triiodothyronine (T(3)) and insulin-like growth factor-1 (IGF-1) in six boars. Three pairs of littermates of crossbred entire male pigs (from three Yorkshire x Duroc dams and one Hampshire sire) were included. Blood samples were taken at the age of 9-15 weeks and thereafter at weekly intervals from the age of 20-32 weeks. Plasma concentrations of skatole, androstenone, testosterone, E17 beta, ES, DHEAS, T(3) and IGF-1 were measured. We found that skatole levels in boars increased at the age around puberty after an increase in the levels of testicular steroids. Levels of skatole were not associated with the levels of sex steroids, T(3) and IGF-1. However, the increased level of testicular steroids is probably the underlying factor needed for high skatole levels to occur although the specific mechanism leading to increased skatole levels remains unknown.     

Effects of transportation on early embryonic death in mares

Incidence of early embryonic death (EED) and associated changes in serum cortisol, progesterone and plasma ascorbic acid (AA) in transported mares were investigated. Mares were transported for 472 km (9 h) during either d 16 to 22 (T-3 wk, n = 15) or d 32 to 38 (T-5 wk, n = 15) of gestation. Blood samples were drawn from control, nontransported mares (NT-3 wk, NT-5 wk, n = 24) and transported mares pre-trip, midtrip, and at 0, 12, 24, 48 and 72 h post-transport and daily for the next 2 wk. Incidence of EED between transported and nontransported mares was not different (P greater than .05). Serum cortisol in all transported mares increased (P less than .05) relative to pre-trip values at midtrip and 0 h post-transport. Relative to NT mares, serum cortisol was higher (P less than .05) at midtrip in T-3 wk mares and 0 h post-transport in T-5 wk mares. Serum progesterone in all T mares increased (P less than .05) at midtrip relative to pre-trip values and was higher (P less than .05) in T-3 wk mares than in NT-3 wk mares at midtrip and 0 h post-transport. Post-transport decreases (P less than .05) in concentrations of progesterone were observed in mares that aborted. Plasma AA in transported mares increased (P less than .05) at midtrip in T-5 wk mares and decreased (P less than .05) relative to pre-trip values at 24 and 48 h post-transport (T-3 wk and T-5 wk mares, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Exogenous eFSH, follicle coasting, and hCG as a novel superovulation regimen in mares

The objective of this study was to evaluate various equine follicle-stimulating hormone (eFSH) treatment protocols and the effect of “follicle coasting” on ovulation and embryo recovery rates in mares. Cycling mares (n = 40) were randomly assigned to one of four groups 7 days after ovulation: (1) 12.5 mg eFSH twice daily until follicles were 35 mm or larger; (2) 12.5 mg eFSH twice daily until follicles were 32 mm or larger; (3) 12.5 mg eFSH twice daily for 3.5 days followed by 12.5 mg eFSH enriched with luteinizing hormone (LH) twice daily until follicles were 35 mm or larger; and (4) 25 mg eFSH once daily until follicles were 32 mm or larger. Mares in groups 1 and 3 were injected with human chorionic gonadotropin (hCG) (2500 IU intravenously) at the end of eFSH treatment, whereas mares in groups 2 and 4 were given hCG approximately 42 and 54 hours, respectively, after the last eFSH treatment (“follicle coasting”). Nonsurgical embryo collection was performed 6.5 to 7.5 days after ovulation. Each mare experienced a nontreated estrous cycle before being reassigned to a second treatment. Ovulation rates for mares in treatment groups 1 to 4 were 3.3 ± 0.4, 4.1 ± 0.4, 3.5 ± 0.4, and 2.8 ± 0.4 (mean ± SEM; P < .05), respectively. One or more embryos were recovered from more than 80% of mares in each treatment group, and embryo recovery rate per flush was similar among treatment groups (1.9 ± 0.3, 2.6 ± 0.3, 1.9 ± 0.3 and 1.9 ± 0.3, respectively; P > .05). The overall embryo recovery rate was 2.1 ± 1.5 embryos per flush. In summary, ovulation rate was higher for mares treated with eFSH (3.4 ± 0.4) compared with non-treated controls (1.1 ± 0.2). Ovulation rate in mares in which hCG was delayed (follicle coasting) was higher (P < .05) when treatments were given twice per day versus once per day. Administration of equine luteinizing hormone (eLH) in conjunction with eFSH did not have an advantage over mares treated only with eFSH.     

The effects of dietary flax oil and antioxidants on ascites and pulmonary hypertension in broilers using a low temperature model

1. Three experiments were conducted using a low temperature model to induce pulmonary hypertension (PH) and ascites in broiler chickens. Diets containing 25 g or 50 g flax oil/kg food and control diets with an equivalent amount of animal/vegetable (A/V) blend oil, with and without supplemental antioxidants (vitamin C and vitamin E) were used. The amount of PH was assessed by the ratio of right ventricle weight to total ventricle weight (RV/TV ratio). Birds were considered to suffer from pulmonary hypertension syndrome (PHS) if the RV/TV ratio was greater than 0.299. 2. In experiment 1, the test diets contained 50 g oil/kg food and were given during the grower period only. Birds fed on the flax oil diet tended to have a lower incidence of PHS, ascites and lower RV/TV ratios than birds fed on the control diet. However, when the flax oil diet was supplemented with antioxidants, the incidence of ascites, PHS, haematocrit and whole blood and plasma viscosity increased compared with birds fed on the flax oil diet without antioxidants. These effects were not seen in experiment 2, when the test diets containing 30 g oil/kg food (25 g flax oil plus 5 g A/V blend oil/kg food compared to 30 g A/V blend oil/kg food) were given during the grower period. However, in experiment 3, when the test diets containing 30 g oil/kg food were given from day 1 to week 8, birds fed on the control diet supplemented with antioxidants had a higher incidence of PHS than those fed on the control diet alone. 3. In all 3 experiments, there was no significant effect of dietary fat source or supplemental antioxidants on total food intake or food conversion. 4. We conclude that diets containing 50 g flax oil/kg food tend to reduce the incidence of PHS and ascites in broilers using a low temperature model but the results were not statistically significant. In some cases, supplementing diets with a combination of vitamin E and vitamin C increased the incidence of ascites and PHS.     

The effect of dietary chloride and bicarbonate on blood pH, haematological variables, pulmonary hypertension and ascites in broiler chickens.

1. The effect of supplementing grower diets with bicarbonate or chloride on haematological variables, pulmonary hypertension syndrome and ascites in broilers exposed to cold temperature was investigated. 2. High concentrations of dietary chloride had no effect on the pH of the venous blood but a low chloride/high bicarbonate diet significantly increased blood pH. There was no consistent effect of dietary chloride or bicarbonate concentrations on growth performance, although in 1 experiment birds given a low chloride/high bicarbonate diet consumed less food and gained less weight than controls. 3. Birds fed on high-chloride diets tended to have a higher incidence of ascites and pulmonary hypertension than controls. Birds fed on low-chloride and high-bicarbonate diets had significantly lower pulmonary hypertension and lower heart weights, which may have indicated a decrease in pulmonary and systemic blood pressure. 4. We conclude that increasing dietary bicarbonate and reducing dietary chloride has potential as a low cost and effective method to reduce the pulmonary hypertension which leads to ascites in broiler chickens.