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The effect of Escherichia coli endotoxin on luteal function in Holstein heifers
Authors:Gilbert R O  Bosu W T  Peter A T
Affiliation:Department of Medical Sciences, School of Veterinary Medicine University of Wisconsin-Madison, Madison, WI 53706 USA.
Abstract:
This study was undertaken to elucidate the possible role of endotcxin in mediating premature luteolysis in the well- documented phenomenon of short estrous cycles in postpartum dairy cows. Four groups of Holstein heifers (n = 4 to 6 each) received either intrauterine infusion of sterile culture medium (Group I); intrauterine infusion of Escherichia coli (E. coli ) endotoxin (5 mug/kg) in sterile culture medium (Group II); intrauterine administration of 10 ml of a 24-h culture of a strain of E. coli isolated from the uterus of a cow with metritis (approximately 10(9) colony forming units/ml; Group III); or intravenous administration of E. coli endotoxin (5 mug/kg; Group IV) on Day 7-9 of the estrous cycle. Blood samples were collected every 48 h during the pretreatment estrous cycle and up to the administration of the experimental treatment, thereafter 4-h samples were collected for 5 d. Sample collection was then performed every 48 h for the remainder of the treatment cycle and the post treatment cycle. Serum concentrations of progesterone and plasma concentrations of 15-keto-13, 14-dihydroprostaglandin F(2alpha) (PGFM) were determined by radionmmunoassay. Intrauterine infusion of endotoxin had no effect on the cycle length or on hormone concentrations, while infusion of viable E. coli organisms tended to shorten the estrous cycle. Intravenous administration of endotoxin produced a sharp increase in both progesterone and PGFM concentrations, followed by a transient decrease in progesterone concentrations. Cycle length remained unchanged. It was concluded that the intact endometrium prevents the uptake of endotoxin although pathogenic E. coli organisms may disrupt the endometrial integrity sufficiently to shorten the estrous cycle by premature luteolysis. It is postulated that intravenous administration of endotoxin influences luteal function by the activation of the arachidonic acid cascade, by a direct effect on the corpus luteum, or via other mediators.
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