Search Results

You are looking at 1 - 2 of 2 items for

  • Author: R. A. Nowak x
  • Refine by access: All content x
Clear All Modify Search
R. A. Nowak
Search for other papers by R. A. Nowak in
Google Scholar
PubMed
Close
,
M.-W. Wang
Search for other papers by M.-W. Wang in
Google Scholar
PubMed
Close
, and
R. B. Heap
Search for other papers by R. B. Heap in
Google Scholar
PubMed
Close

ABSTRACT

The anti-fertility effect of passive immunization against progesterone is influenced by genotype in mice. In order to quantify this finding we determined the effective dose that blocks pregnancy in 50% of treated mice (ED50) for two different anti-progesterone monoclonal antibodies (DB3 and 11/32) in four different strains of mice (BALB/cJ, CBA/Ca, Tuck's no. 1 and F1C). Efficacy was greatest in the two inbred strains (BALB/cJ and CBA/Ca) with ED50 values of 0·46–1·4 nmol. The F1C hybrid mice were more resistant to antibody treatment (ED50 2·2–3·0 nmol), while the outbred Tuck's no. 1 strain required much higher doses (ED50 7·0–8·2 nmol). There were no intrastrain differences between the two monoclonal antibodies.

We have examined the possible role of the H-2 haplotype on antibody efficacy in different strains and crosses. The antibody was highly effective in blocking implantation in three congenic BALB strains of different H-2 haplotype, in another inbred strain CBA/Ca, and in reciprocal BALB/cJ×CBA/Ca crosses. The F1 hybrid crosses were somewhat resistant, but the C57BL/10Sn and B10.BR congenic strains were most resistant to treatment. The results show that the pregnancy-blocking effect of the anti-progesterone antibody was not influenced by the H-2 haplotype, but rather by background genes.

Journal of Endocrinology (1990) 125, 257–262

Restricted access
R. A. Nowak
Search for other papers by R. A. Nowak in
Google Scholar
PubMed
Close
,
J. S. Klein
Search for other papers by J. S. Klein in
Google Scholar
PubMed
Close
,
D. M. Pulido
Search for other papers by D. M. Pulido in
Google Scholar
PubMed
Close
, and
J. M. Bahr
Search for other papers by J. M. Bahr in
Google Scholar
PubMed
Close

ABSTRACT

The present study was undertaken to determine (1) whether the rabbit feto-placental unit maintains corpora lutea systematically and/or locally and (2) the interrelationships between conceptus number, luteal weight, luteal progesterone concentrations and serum progesterone levels. Thirty-three does were divided into the following treatment groups: (I) bilaterally pregnant, two ovaries; (II) unilaterally pregnant, two ovaries; (III) bilaterally pregnant, one ovary; (IV) unilaterally pregnant, one ovary, contralateral and (V) unilaterally pregnant, one ovary, ipsilateral. Blood samples were obtained from all rabbits on days 6, 9, 12, 15, 18 and 21 post coitum. Does were killed on day 21, and the percentage of viable fetuses, fetal weights, and luteal weights recorded. Blood samples and corpora lutea were analysed for progesterone.

Serum progesterone levels were similar for all groups until day 9 post coitum. Levels in groups III, IV and V declined significantly between days 9 and 12 following removal of one ovary at day 9. Fetal viability, fetal weights and luteal progesterone concentrations did not differ among any of the groups. Luteal weights did not differ among groups I, III, IV and V, but luteal weights of animals in group II were lower than those of group I (P<0·05). Ratios of viable fetuses to number of corpora lutea ranged from 1:11–10:5. No differences were observed in serum progesterone, luteal weights or luteal progesterone concentrations among animals with two conceptuses and those with seven or more, but serum progesterone levels in does with only one conceptus were lower than those in does with more (P<0·05). These results indicate that the feto-placental unit maintains corpora lutea systemically and that the high rate of pregnancy failure by day 21 in does with only one conceptus is due to the inability of a single conceptus to maintain normal serum progesterone levels even though the corpus luteum weight is not affected.

J. Endocr. (1986) 109, 107–110

Restricted access