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Ovarian Compensatory Hypertrophy Following Unilateral Ovariectomy in Hysterectomized and Early Pregnant Gilts¹

University of Wisconsin, Madison 53706³

Abstract

SIXTY-THREE crossbred nulliparous gilts were bred and used in a 2³ factorial experiment: (1) intact pregnant uterus vs. total hysterectomy, (2) unilateral ovariectomy (1-ov) vs. both ovaries intact (2-ov), and (3) slaughtered at day-15 vs. day-27 after breeding. Gilts were bred on the first day of estrus (day-0) and the appropriate surgery, or sham surgery was performed on day-3. There was a highly significant day x ovariectomy interaction (P<.01) on log luteal tissue weight adjusted for the log C.L. number. One-ovary gilts had a greater increase in luteal tissue weight at day-27 than at day-15. Log follicular fluid weight was, also increased (P<.001) in 1-ov gilts but was not affected significantly by uterine condition or day of slaughter. Analysis of follicle size frequencies showed fewer small follicles but more large follicles in 1-ov gilts than in 2-ov gilts. Also, pregnant gilts had more medium follicles and a greater number of total follicles than did the hysterectomized gilts.

Compensatory ovarian hypertrophy in hysterectomized and early pregnant pigs was due to an increase in both luteal tissue weight and follicular development. Luteal hypertrophy was dependent on stage of pregnancy, showing greater hypertrophy in the later stage than in the early stage of pregnancy, while follicular development was unaffected by stage. Follicular development was influenced by uterine condition as shown by changes in the follicle-diameter frequencies, while luteal hypertrophy was unaltered by uterine condition. Since luteal hypertrophy occurred in the hysterectomized gilts, we conclude that factors mediating the prolonged lifespan of the C.L., and not pregnancy itself, are responsible for this hypertrophy.

¹ Research supported by the College of Agricultural and Life Sciences, University of Wisconsin, Madison, and by Public Health Service Training Grant No. T01-HD-00104-07, from the National Institute of Child Health and Human Development, and by the Ford Foundation, Grant No. 630-0505A.

² Present address: Department of Genetics, University of Wisconsin, Madison 53706.

³ Paper No. 604 from the Department of Meat and Animal Science and 1528 from the Laboratory of Genetics.