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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.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1983.
|Date Available in IDEALS:||2014-12-16|
This item appears in the following Collection(s)
Dissertations and Theses - Veterinary Clinical Medicine
Graduate Dissertations and Theses at Illinois
Graduate Theses and Dissertations at Illinois