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A. R. BELLVÉ

Summary.

Albino ICR mice, 384 females and 48 males, were allocated to control or stress treatments. For the latter, animals were exposed to 34·5° C and 65% relative humidity for a period of 24 hr. The treatment of males commenced 48 hr before a 6-day mating schedule and of females, at 16.00 hours on the day a copulatory plug was detected. The females were killed 54 hr or 10 days after a plug had been detected. The developmental stages of embryos recovered at 54 hr were recorded and four-cell and eight-cell ova were incubated in [3H]uridine and subjected to autoradiography. Females killed at Day 10 of gestation gave estimates of pre- and postimplantation embryonic mortality.

A significant increase in rectal temperatures (approximately 2° C) following treatment was taken as indicating stress had occurred. Extensive developmental retardation and/or arrest among embryos recovered from stressed females at 54 hr resulted in an increase in the proportion of two-, three- and four-cell embryos. This retardation was coincident with fewer blastomeres of four-cell (P<0·01) and eight-cell embryos (P<0·05) being able to incorporate [3H]uridine in comparison to those from control females. After male stress, developmental retardation was evident as an accumulation (P<0·05) of four-cell embryos but only the eight-cell embryos exhibited a reduction (P<0·05) in the number able to incorporate [3H]uridine.

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A. R. BELLVÉ

Summary.

Albino ICR mice were used in a factorial experiment to study abnormal embryonic development that was induced by a 24-hr exposure of parent mice to an ambient temperature of 34·5° C and 65% relative humidity. Two-cell embryos recovered from eighty females killed at 48 hr were cultured in vitro to the stage reached 120 hr after HCG. The pattern of embryonic development in vivo was determined by observing embryos recovered from 240 females killed at 64, 72, 88 or 96 hr after HCG.

Exposure of females caused an accumulation of two-, three- and four-cell embryos (P<0·01) following development in vivo or in vitro. Complete developmental arrest at the two-cell stage accounted for the major portion of embryonic mortality. In some partially affected two-cell embryos, one blastomere was able to undergo a limited number of divisions, asynchronous cleavage, to form three- or five-cell trophoblastic vesicles, or false blastocysts. Following exposure of males, developmental retardation and/or arrest at the morula stage accounted for a major portion of the embryonic death that had occurred by Day 10 of gestation. Significant male × female treatment interactions in the data on number of morulae, blastocysts and viable fetuses indicated that embryonic mortality due to male and female stress may be operating through similar mechanisms.

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A. R. Bellvé and W. Zheng

Departments of Anatomy and Cell Biology, Obstetrics and Gynecology, and Urology, and the Center for Reproductive Sciences, College of Physicians and Surgeons, Columbia University, 650 West 168th Street, New York, NY 10032, USA

Keywords: growth factors; testis

Introduction

Growth and differentiation of the male gonads involves a complex sequence of interactions between soma and germ cell elements. These interactions are mediated principally by the trophic hormones, FSH, LH, GH and prolactin, and the sensitive autocrine and paracrine actions of growth factors. During fetal and neonatal life, development of the gonads requires the differential expansion of epithelial and mesenchymal tissues to form the interstitial and epithelial compartments, respectively, of the testes (Bellvé & Feig, 1984). In pubertal and adult animals, the onset and maintenance of spermatogenesis require an exact temporal regulation of germ cell proliferation and differentiation. For both events there must be an array of local growth factors

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M. F. McDONALD and A. R. BELLVE

Summary.

The volumes of Fallopian tube secretion which pass into the peritoneal cavity (ampullar flow) and uterus (isthmic flow) were recorded at 12-hr intervals in ovariectomized ewes, and after injection of 30 μg, 90 μg or 500 μg oestradiol benzoate (ODB). Ovariectomized ewes were also treated sequentially with progesterone, oestrogen, and, in some animals, a further series of progesterone injections in an attempt to achieve the pattern of directional flow of tubal fluid found in the intact, cyclic ewe.

A decline in total daily secretion and fluid flow followed ovariectomy and was counteracted by the administration of ODB. Both ampullar and isthmic flows were markedly increased at all dose levels of ODB until the flows were comparable with, or exceeded, those which occurred during oestrus in the intact ewe. But the sequence of maximum ampullar flow and maximum isthmic flow was reversed by ODB, the difference being further accentuated by each increase in dose level. As isthmic flow was stimulated at all dose levels of ODB, an effective restriction of the tubo-uterine junction and/or isthmus was not apparent. Progesterone in combination with ODB did not effectively restrict the isthmic flow relative to the ampullar flow.

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A. R. BELLVE and M. F. McDONALD

The secretion of fluid in the Fallopian tube is greatest about oestrus and diminishes during the luteal phase of the cycle (e.g. Perkins, Goode, Wilder & Henson, 1965). Cannulation of both ends of the Fallopian tube in the ewe and volumetric collection of the secretion has shown that most of the fluid flowed through the ampullar orifice, but that there was marked increase in flow of fluid through the tubo-uterine junction about 4 days after the onset of oestrus (Bellve & McDonald, 1968). With the ovariectomized ewe injected with oestrogen, the peak flow through the tubo-uterine junction preceded that through the ampullar end (McDonald & Bellve, 1969). The mechanism which prevents a similar premature surge in isthmic flow in the intact ewe during the pre-ovulatory period, when oestrogen is in dominance (Moore, Barrett, Brown, Schindler,