Heat stress (HS) causes seasonal infertility in sows and decreases reproductive efficiency. The objective was to examine thermoregulation, metabolic responses, and reproduction in sows exposed to HS or thermoneutral (TN) conditions during different phases of a production cycle (gestation, lactation, and breeding). Fifty-eight first-parity Landrace (n = 26) or Landrace × Large White F1 (n = 32) sows were rotated through environmental chambers for 57 d beginning in late gestation. The ambient temperature sequences included either TN (18°C to 20°C) or HS (24°C to 30°C) for each production phase with the following treatment groups: TN-TN-TN (n = 15), TN-HS-TN (n = 14), HS-TN-HS (n = 14), and HS-HS-HS (n = 15) for gestation-farrowing-breeding (20, 24, and 13 d, respectively). Regardless of the temperature treatment, rectal temperatures were greater (P < 0.001) during lactation (39.36°C ± 0.01°C) than during the gestation (38.27°C ± 0.01°C) or the breeding period (38.77°C ± 0.01°C). The increase in rectal temperature (P < 0.001) and respiration rate (P < 0.001) in response to the HS was greatest during lactation. There was an effect of day (P < 0.001) on serum IGF-1 and insulin concentrations because both insulin and IGF-1 increased after farrowing. Compared with HS sows, the TN sows had greater feed intake (P < 0.001) and greater serum concentrations of insulin (early lactation; P < 0.05) and IGF-1 (late lactation; P < 0.05) when they were lactating. The effects of HS on sow BW, back fat, and loin eye area were generally not significant. Average BW of individual piglets at weaning was approximately 0.5 kg lighter for the sows in the HS farrowing room (P < 0.05). Weaning-to-estrus interval, percentage sows inseminated after weaning, subsequent farrowing rate, and subsequent total born were not affected by treatment. In summary, regardless of ambient temperature, sows undergo pronounced and sustained changes in rectal temperature when they transition through gestation, lactation, weaning, and rebreeding. The effects of HS on rectal temperature, respiration rate, feed intake, and metabolic hormones were greatest during lactation. The controlled HS that we imposed affected piglet weaning weight, but rebreeding and subsequent farrowing performance were not affected.

A study was conducted to develop a model for fescue toxicosis using rats fed a diet containing endophyte-infected tall fescue seed (E+). Rats implanted with telemetric transmitters to continuously monitor core body temperature (Tc) and activity were housed at thermoneutrality (21 degrees C) and were fed a diet containing endophyte-free fescue seed (E-). After 2 wk, they were assigned to either E+ or E- diets and initially maintained at thermoneutrality (preheat) for 8 d. They were then exposed to heat stress (31 degrees C) for 22 d, followed by 1 wk of recovery at thermoneutrality (post-heat). Body weight and feed intake were measured daily. Rats receiving the E+ diet showed decreased feed intake (P = 0.001) and weight gains (P = 0.003) during the preheat period. The decrease in Tc from the pre-treatment level was greater in E+ than in E- rats during the preheat (P = 0.001) and postheat (P = 0.001) periods. With heat stress, both groups showed parallel decreases in feed intake. The increase in Tc from pre-heat to heat conditions was greater in E+ vs. E- rats (P = 0.001). Activity level was lower in E+ than in E-rats during heat stress (P = 0.009) and postheat (P = 0.037) periods. These results show that the rat model for fescue toxicosis is extremely useful because many of the observed responses to E+ diet are similar to those noted for cattle, and additional variables that are difficult to measure in cattle, such as activity, can be easily evaluated.

Fescue toxicosis is caused by consumption of toxins produced by an endophytic fungus, Neotyphodium coenophialum, in tall fescue [Lolium arundinaceum (Schreb.) Darbysh]. Microarray analysis was used to identify shifts in genetic expression associated with the affected physiological processes to identify potential targets for future pharmacological/toxicological intervention. Male rats (n = 24) were implanted with temperature transmitters, which measure core temperature every 5 min. After an 8-d recovery, the rats were fed an endophyte-free diet for 5 d. During the following 5-d treatment period, rats were fed either an endophyte-free or an endophyte-infected (91.5 microg of ergovaline.kg of BW(-1).d(-1)) diet. At the end of treatment, rats were euthanized and a sample of the liver was obtained. Feed conversion efficiency was calculated for both treatment groups. Serum prolactin concentrations were measured using ELISA. Liver tissue RNA was reverse transcribed and hybridized to an oligonucleotide microarray chip. Microarray data were analyzed using a 2-step ANOVA model and validated by quantitative real-time PCR. Significant reductions in mean core temperature, feed intake, feed conversion efficiency, BW, liver weight per unit of BW, and serum prolactin concentrations were observed in endophyte-infected rats. There was downregulation (P < 0.05) of various genes associated with energy metabolism, growth and development, and antioxidant protection, as well as an upregulation of genes associated with gluconeogenesis, detoxification, and biotransformation. This study demonstrated that even short-term exposure of rats to tall fescue endophytic toxins under thermoneutral conditions can result in physiological responses associated with altered gene expression within the liver.

Ergovaline, found in Acremonium coenophialum-infected tall fescue, is considered to be responsible for many symptoms associated with fescue toxicosis. Rats were tested to determine time-related thermoregulatory responses to acute treatment with ergovaline during specific thermal challenges. Isolated ergovaline was administered to rats (15 micrograms/kg body mass, i.p.) at controlled ambient temperatures (Ta) of 7 to 9 degrees C (cold) and 31 to 33 degrees C (hot). Treatment at cold Ta resulted in a decrease in rectal temperature (Tre) from 38.0 to 37.0 degrees C at 50 min after injection (P < .05) without complete return to preinjection value at 100 min. Tail temperature (Ttail) exhibited a concomitant 1C degree decrease (P < .05) after ergovaline injection at cold Ta. Also, metabolic heat production decreased from 15.7 to 11.7 W/kg at 20 min after injection of ergovaline (P < .05), with return to normal value at 40 min after injection. Injection of ergovaline at hot Ta increased Tre from 39.0 to 40.6 degrees C at 80 min after injection (P < .05), with no return to preinjection value at 100 min. This was attributed to a reduction in heat transfer across the tail as indicated by the decrease in Ttail from 37.1 to 36.4 degrees C at 40 min after injection (P < .05) and an initial increase in metabolic heat production from 8.4 to 9.4 W/kg at 3 min after injection (P < .05). Ambient temperature was found to be a major determinant of ergovaline response, which included alterations in both thermogenic and thermolytic mechanisms that control thermal balance.

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