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Title:The Role of Escherichia Coli Endotoxins in The Pathogenesis of Lactation Failure in The Sow
Author(s):Smith, Bradford Bixby
Department / Program:Veterinary Medical Science
Discipline:Veterinary Medical Science
Degree Granting Institution:University of Illinois at Urbana-Champaign
Subject(s):Agriculture, Animal Pathology
Abstract:Previous studies have implicated E. coli endotoxins in the pathogenesis of insufficient milk production in the periparturient sow. Experiment I demonstrated that E. coli endotoxins (4, 8, or 16 mg 055:B5 strain) given subcutaneously to 150-170 kg sows on day 2 postpartum (PP + 2) decreased plasma prolactin (PRL) concentrations to 25-35% of pre-endotoxin concentrations within 4 hours. Piglet weight, an indirect indicator of milk production, declined significantly concomitant with the decline in PRL. Experiment II demonstrated that 8mg endotoxin suppressed PRL and piglet growth when administered on PP + 2 but not when given on PP + 6 for the first or second time. Endotoxin administration suppressed thyrotropin releasing hormone (TRH) (100 (mu)g IV) stimulated PRL release on PP + 2 but not on PP + 6. The results suggested that the suppressive effects of E. coli endotoxins on PRL are partially mediated directly at the adenohypophysis. Experiment III demonstrated that the dopamine vesicle depleting agent, reserpine (0.025 mg/kg), and the DA receptor blocking agents, haloperidol (10 mg/sow) and chlorpromazine (0.5 mg/kg), were ineffective in elevating PRL concentrations when given on PP + 5 or PP + 6. TRH (500 (mu)g IM) elevated PRL for 20-30 minutes. These results suggested that PRL is not under chronic inhibitory control by the hypothalamus as observed in other species. Experiment IV demonstrated that PRL concentrations did not increase following electric shock stimulation or restraint and venipuncture but did decline following removal of the suckling stimulus.
Results obtained in this thesis suggest that low concentrations of E. coli endotoxins exert a suppressive effect on milk production by suppressing PRL release and may be a significant factor in the pathogenesis of lactation failure in the periparturient sow.
Issue Date:1983
Description:229 p.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1983.
Other Identifier(s):(UMI)AAI8410048
Date Available in IDEALS:2014-12-16
Date Deposited:1983

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