The Role of Escherichia Coli Endotoxins in The Pathogenesis of Lactation Failure in The Sow
Smith, Bradford Bixby
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/71313
Description
Title
The Role of Escherichia Coli Endotoxins in The Pathogenesis of Lactation Failure in The Sow
Author(s)
Smith, Bradford Bixby
Issue Date
1983
Department of Study
Veterinary Medical Science
Discipline
Veterinary Medical Science
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(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.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.