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ARS Home » Research » Publications at this Location » Publication #97730


item Matteri, Robert - Bob
item Carroll, Jeffery - Jeff Carroll
item Dyer, Cheryl

Submitted to: Journal of Animal Science Supplement
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Loss of body temperature is a well-recognized contributing factor to morbidity and mortality in piglets. Using LPS as a model for infectious challenge, we recently reported a significant hypothermic response in early neonatal pigs. The objective of this study was to evaluate the effect of pretreatment with indomethacin (IND), a prostaglandin synthesis inhibitor, on sickness and hypothermic responses to LPS in one-day-old piglets. Ten m IND/kg or vehicle (0.1 M Na2C03) was administered i.p. 1 hr prior to i.p. injection of 150 ug LPS (0111:B4, Sigma Chem. Co.) or sterile saline. Forty-one piglets were utilized (LPS, n = 11; IND, n = 9; IND + LPS, n = 11; Control, n = 10). Piglets were injected with IND or vehicle while still with their sows. One hr following IND the animals were quickly moved to a pen contained in an 18 deg C environmental chamber and injected with LPS or saline (time 0). Rectal temperatures were obtained from -1 to 3 hr at 15 min intervals and signs of sickness (diarrhea, vomiting, not huddling) wer monitored continuously. A significant incidence of vomiting was observed in the LPS group at .75 and 1 hr (P<.01). Diarrhea occurred in a significant number of the LPS piglets from .25 to 1.5 hr (P<.05). Huddling was reduced in the LPS piglets from .5 to 1.25 hr (P<.05). Injection of LPS induced a transient loss of body temperature between 1 and 2.75 hr (P<.0001). Body temperatures did not differ among Control, IND, and IND + LPS groups. There was no observable hypothermia or signs of sickness in LPS-injected animals pretreated with IND. Treatment with IND alone had no effect on any of the endpoints. Pretreatment with IND, likely through inhibition of prostaglandin synthesis, completely prevented the presently observed immunophysiological responses to LPS.