Prostaglandins (PGs) are known to exert profound physiological and pharmacological effects on the female reproductive system in women and in many other species (Weeks, 1972; Labhsetwar, 1974). Indomethacin and aspirin, inhibitors of prostaglandin biosynthesis, block PMSG-induced ovulation in immature (Armstrong & Grinwich, 1972; Orczyk & Behrman, 1972) and adult female rats (Tsafriri, Lindner, Zor & Lamprecht, 1972). In the rabbit, ovulation induced by HCG, LH or coitus was blocked by indomethacin (O'Grady, Caldwell, Auletta & Speroff, 1972). In mice, ovulation was blocked with indomethacin and the effect was reversed by injecting prostaglandins E2 or F2α (Saksena, Lau & Shaikh, 1974). All these studies provide indirect evidence that PGs are involved in the process of ovulation. A more direct approach, namely the specific binding of endogenous PGs by anti-PG sera raised in rabbits, was used in the present study. Attempts were also made to reverse the antiovulatory effect of
I. F. LAU, S. K. SAKSENA and M. C. CHANG
I. F. LAU, S. K. SAKSENA and M. C. CHANG
Evidence has accumulated that insertion of a foreign body into the uterine lumen (Spilman & Duby, 1972; Wilson, Cenedella, Butcher & Inskeep, 1972; Chaudhuri, 1973; Saksena & Harper, 1974; Saksena, Lau & Castracane, 1974) or its distension (Poyser, Horton, Thompson & Los, 1971) induces a significantly greater production of prostaglandin (PG) than in control uteri in several species including man (Batta, Mukerjee & Santhakumari, 1972). Likewise, the elevated levels of PG in the presence of an IUD and its effect on luteal regression (Spilman & Duby, 1972) and the antifertility effect induced by an IUD has been successfully reversed in rabbits by administering indomethacin (Saksena & Harper, 1974), an inhibitor of prostaglandin biosynthesis (Vane, 1971). All this evidence suggests that prostaglandins are involved in the mechanism of action of an IUD. We reported a preimplantation rise of uterine prostaglandin F (PGF) content and concentration in rabbits, rats and hamsters bearing
S. K. SAKSENA, I. F. LAU and M. C. CHANG
Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545, and Department of Biology, Boston University, Boston, Massachusetts 02215, U.S.A.
(Received 29th April 1974)
Recent studies implicate prostaglandins (PGs) of the E and F series in the release of anterior pituitary hormones (see Carlson, Barcikowski, & McCracken, 1973). Increases in serum levels of LH (Sato, Taya, Tyujo, Hirono & Igarashi, 1974) FSH and prolactin (Sato, Jyujo, Iesaka, Ishikawa & Igarashi, 1974) were observed following a single injection of PG E1, E2 or F2α in rats which were spayed and primed with oestrogen plus progesterone. Intrauterine insertion of a Silastic-PVP implant containing PGF2α has been shown to stimulate the release of LH in rats and hamsters (Saksena, Lau & Chang, 1974). Experiments in which PGs did not affect LH release have also been reported (Chamley & Christie, 1973). Here we report the results of the time sequence of LH
S. K. SAKSENA, I. F. LAU, A. BARTKE and M. C. CHANG
Treatment of adult male rats with indomethacin, an inhibitor of prostaglandin (PG) synthesis, caused a significant decrease in LH and testosterone levels in the blood plasma and in the weight of the seminal vesicles, but the weight of the testes and ventral prostate, the levels of FSH in the plasma and fertility were not affected. The concentration of PGF in the blood plasma of the treated animals was reduced, even though measurable amounts of PGs were present in every group. The results of this study, together with the known effects of PG administration on LH release, suggest that the reduction of plasma LH levels in rats injected with indomethacin was due to decreased PG synthesis. It appears that PGs are normally involved in the regulation of LH release.
T. A. Parkening, T. J. Collins, I. F. Lau and S. K. Saksena
Summary. Plasma and pituitary hormones of young (3–5 months of age) dioestrous hamsters with normal cycles and aged (13–17 months of age) anoestrous hamsters were compared. The anoestrous hamsters exhibited lower plasma values of progesterone (P < 0·001), oestradiol-17β (P < 0·005) and prolactin (P < 0·001) and higher levels of plasma gonadotrophins (P < 0·001) than did the dioestrous animals. Pituitary concentrations of LH were higher (P < 0·005) in anoestrous hamsters, but pituitary FSH and prolactin values did not differ. In another series of experiments three groups of hamsters (3–5- and 13–17-month-old with normal cycles and 13–17-month-old in anoestrus) were ovariectomized. Blood samples were taken by cardiac puncture every 3–4 weeks after receiving s.c. injections of oestradiol-17β (1 or 10 μg/100g body wt) for 2 or 9 consecutive days. The markedly lower levels of gonadotrophins in aged anoestrous hamsters indicated that the hypothalamic–hypophysial complex was incapable of responding to the same degree as it did in young and aged cyclic animals. Prolactin values were similarly depressed in all 3 groups. Oestradiol-17β treatment caused reduced gonadotrophin and increasing prolactin concentrations in all 3 groups. These results indicate that the ovaries of the senescent anoestrous hamster produce less steroids and suggest that age-related changes in the hypothalamic–hypophysial complex are largely responsible for the cessation of regular oestrous cycles.
C. M. LUBICZ-NAWROCKI, NANCY I. F. LAU and M. C. CHANG
Mouse and hamster spermatozoa from the cauda epididymidis were deposited into the female tract at various periods following ligation of the corpus epididymidis. It was found that the number of spermatozoa in the cauda epididymidis decreased sooner in the hamster than in the mouse but the initial decrease in fertilizing ability occurred much earlier in the mouse than in the hamster. The fertilizing life of spermatozoa in the cauda epididymidis is approximately 25 days in both species.