title: Monoclonal antibodies specific for rat relaxin. IV. Passive immunization with monoclonal antibodies during the antepartum period reduces cervical growth and extensibility, disrupts birth, and reduces pup survival in intact rats.
abstract: The purpose of this investigation was to use an approach targeted specifically on endogenous relaxin to determine the influence of antepartum (days 20-22) relaxin on cervical modifications and birth in the rat. To that end, a monoclonal antibody specific for rat relaxin, designated MCA1, was used to neutralize endogenous relaxin in intact pregnant rats. MCA1 or PBS vehicle was administered iv to intact rats daily from days 20-22 of pregnancy. Cervices were removed at 1200 h on day 22. Cervices obtained from MCA1-treated rats were less extensible than cervices obtained from PBS-treated control rats. Furthermore, wet weight, dry weight, water content, and uronate content were lower in cervices obtained from MCA1-treated rats than in cervices from PBS-treated controls. Birth and maternal behavior of MCA1-treated and PBS-treated control rats were observed continuously from 2100 h on day 22 until day 2 postpartum (d2PP). MCA1-treated rats exhibited significantly prolonged durations of litter delivery as well as reduced incidences of live pups on d2PP compared with controls. There were lower incidences of normal maternal behavior observed at birth and on d1PP with MCA1-treated rats than with control rats. In addition, little or no milk was observed in the abdomen of most live pups of MCA1-treated rats on d2PP, whereas abundant milk was observed in the abdomen of all live pups of control rats. The mean live pup weight on d2PP was lower in the litters of MCA1-treated rats than in control litters. The present study indicates that in the rat endogenous relaxin is needed during the antepartum period for normal cervical growth and extensibility, normal litter delivery, and high postpartum pup survival. This work supports the hypothesis that the influence of endogenous relaxin on birth is attributable, at least in part, to its effects on the cervix.
authors.affiliation: Department of Physiology and Biophysics, University of Illinois, Urbana-Champaign 61801.
authors.forename: J J
authors.initials: JJ
authors.lastname: Hwang
authors.forename: R D
authors.initials: RD
authors.lastname: Shanks
authors.forename: O D
authors.initials: OD
authors.lastname: Sherwood
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D001723:Birth Rate; D002584:Cervix Uteri / Q000502:physiology*; D036861:Delivery, Obstetric; D005260:Female; D007116:Immunization, Passive; D009026:Mortality; D049590:Postpartum Period; D011247:Pregnancy; D051381:Rats / Q000502:physiology*; D012065:Relaxin / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D012065:Relaxin