The aim of this experiment was to determine CH4 production and energy partition for a range of diets fed to Bos indicus cattle. Six Brahman cattle were fed on three different diets in a replicated Latin square experiment over three periods. The diets were (1) long-chopped Angleton grass (Dicanthium aristatum) hay ad libitum (DM digestibility (DMD) 41 (se 2)%; 4 g N/kg), (2) long-chopped Rhodes grass (Chloris gayana) hay ad libitum (DMD 60 (se 1)%; 14 g N/kg) or (3) 2 kg long-chopped lucerne (Medicago sativa) hay/d plus a high-grain diet (ad libitum) (DMD 70 (se 1)%; 31 g N/kg). CH4 production was measured using confinement-type respiration chambers. Metabolizable energy intake (MJ/d) of cattle fed on Angleton grass (18·4 (se 2·0)) was lower (P< 0·01) than that for Rhodes grass (54·9 (se 2·1)), which was lower (P< 0·01) than that for the high-grain diet (76·7 (se 5·8)). CH4 production (g/d) for cattle fed on Rhodes grass (257 (se 14)) was higher (P< 0·01) than that for cattle fed on both the high-grain diet (160 (se 24)) and Angleton grass (113 (se 16)). CH4 conversion rate (MJ CH4 produced per 100 MJ gross energy intake) was not significantly different between cattle fed on Angleton (10·4 (se 1·1)) and Rhodes (11·4 (se 0·3)) grass, but was higher (P< 0·01) than for cattle fed on the high-grain diet (6·7 (se 0·7)). CH4 production (g/kg live-weight gain) was associated (P< 0·001) with both live-weight gain and feed: gain ratio. We conclude that the relationships between CH4 production, energy utilization and live-weight change of cattle fed on tropical forages differ from those of cattle fed on diets based on temperate forages.
Three experiments were conducted to determine the effects of dietary supplementation with a novel antimethanogenic compound (AM) on methane production and growth in Brahman (Bos indicus) steers. The compound was a chemical complex of bromochloromethane (BCM) and α-cyclodextrin, which is chemically stable when added to feed, thus overcoming the highly volatile nature of BCM. In these experiments the AM compound was administered to steers as a mixture with different feed supplements. In Expt 1 the effect on in vivo methane production of feeding steers the AM compound was determined using a confinement-type respiration chamber. Methane production of AM-treated steers (0 ± 2·4 mL/min) was lower (P < 0·001) than that of control steers (205 ± 5·2 mL/min) over 28 days. In Expt 2 we determined the effect of AM treatment over 12 weeks on growth of steers fed on a low quality roughage diet. The most marked effect of AM treatment was reduced (P < 0·01) voluntary roughage dry matter intake (DMI), and reduced (P < 0·01) acetate : propionate molar ratio (A : P) in rumen fluid. Average daily liveweight gain (ADG) (0·22 ± 0·01 kg/day) and feed : gain ratio (F : G) (20·7 ± 1·46 kg DMI/kg liveweight) were not significantly affected by AM treatment. In Expt 3 we determined the effect of AM treatment over 10 weeks on growth of steers fed on a medium quality roughage diet, in steers that were either treated or not treated with a hormonal growth promotant (HGP; oestadiol 17β). AM treatment reduced (P < 0·05) DMI below that of steers not treated with AM, whereas DMI was not significantly affected by HGP treatment. Both AM (P < 0· 1) and HGP (P < 0·05) treatments separately reduced A : P ratio in rumen fluid. AM treatment had no significant effect on ADG, whereas ADG of HGP-treated steers was higher (P < 0·05) than that of steers not treated with HGP (0·76 ± 0·27 v. 0·60 ± 0·027 kg/day). F : G was reduced (P < 0·01) by HGP treatment. F : G of both HGP-treated steers and those steers not treated with HGP was reduced (P < 0·05) by AM treatment. We conclude that feeding steers with this novel AM compound enables the potent antimethanogenic properties of BCM to be realised under commercial conditions, and that prolonged use over 10–12 weeks is associated with an improved feed conversion efficiency in steers fed on better quality roughage diets.
SUMMARYThe effect of maternal undernutrition between the 30th and 96th day of pregnancy on placental growth in single-bearing ewes was determined separately in two experiments in consecutive years (1986 and 1987) at Mount Derrimut Field Station, Deer Park, Australia. In the first experiment, placental growth measured on the 96th day of pregnancy was reduced (473 v. 596 g) by maternal undernutrition, while in the second, placental growth was increased (600 v. 496 g). Foetal weight and its linear dimensions on the 96th day of pregnancy were not significantly affected by maternal u dernutrition in either experiment. The only significant difference in the animals and experimental conditions between the two studies was the liveweight of the ewes at mating, which was c. 10 kg higher in the second experiment compared with the first (P < 0·01). Body condition score and the change in condition score during the respective nutritional treatments were not significantly different between the two experiments. The results suggest that maternal liveweight, possibly body reserves not quantifiable by condition score, protects and even enhances placental growth during a period of maternal undernutrition.
We tested the hypotheses that an episode of hypoxemia near mid-gestation in fetal sheep has long-term effects on brain development and that the extent and type of damage is related to the stage of development within a particular brain structure at the time of the hypoxemia. Fetal sheep (n = 8) were made hypoxemic at 90 +/- 2 days (term approximately 147 days) by restricting the maternal blood supply to the placenta for 12 hours (h) using a vascular clamp so as to reduce fetal arterial O2 saturation by 50%-60%. Fetuses were killed 35 days later and the brains analysed histologically and immunohistochemically. Age-matched fetuses (n = 8) were used as controls. Gross brain damage was observed in only 1 fetus, the most acidemic during the period of hypoxemia. There was a reduction of 12% (p < 0.05) in the cross-sectional area of the cerebral cortex in hypoxemic fetuses compared with controls. In lobule 6 of the cerebella of hypoxemic fetuses, significant reductions were seen in (a) the volume density of Purkinje cells (33%), (b) the width of the molecular layer (13%), (c) the area of the inner granule cell layer (13%), (d) the area of the white matter (18%), and (e) the total cross-sectional area (15%). There were also significant reductions in the area of arborization of Purkinje cell dendritic trees (50%), in the branching density (25%), and in the number of dendritic spines (31%). In the ventral hippocampi of hypoxemic fetuses, there was a 36% reduction (p < 0.05) in the volume density of CA1 pyramidal cells and a 50% increase (p < 0.05%) in the number of astrocytes. We conclude that an episode of hypoxemia near mid-gestation reduces neuronal numbers in the hippocampus and cerebellum and probably also in the cerebral cortex. The growth of neural processes in a particular region will be significantly retarded if the hypoxemia occurs at an early stage of the growth of neural processes (e.g. cerebellum) but not if development is well advanced at the time of the insult (e.g. hippocampus). Damage is sustained in the white matter of the cerebral hemispheres if the insult is particularly severe. Together, these deficits could affect neural connectivity and impair postnatal brain function.
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