Administration of progesterone to cows with ovarian follicular cysts results in a reduction in mean LH and LH pulse frequency and initiates ovulatory follicular growth.

Abstract

Cows with ovarian follicular cysts were treated with progesterone to determine whether a reduction in LH concentrations and initiation of ovulatory follicular waves would occur. Cysts were diagnosed using transrectal ultrasonography when single follicular structures > 20 mm or multiple structures > 15 mm in diameter were present for 7 d in the presence of low progesterone concentrations. Three groups were studied: 1) cows with normal estrous cycles (CYC, n = 8); 2) cows with untreated cysts (CYST, n = 7); and 3) cows with cysts treated with two progesterone-releasing intravaginal devices (PRID, n = 8) for 9 d. Ovaries were examined with transrectal ultrasonography, and blood samples were collected daily for analysis of progesterone and FSH. Serial blood samples for determination of mean LH and LH pulse frequency were collected on d 0 (CYST and PRID cows only), 1, 5, 9, and 10. Progesterone concentrations were higher in PRID cows than in CYST cows throughout the PRID treatment period (P < .002). On d 0, LH pulse frequency was similar (P = .10) in PRID (6.6+/-.6 pulses/8 h) and CYST cows (5.1+/-.6 pulses/8 h), but mean LH tended to be higher (P = .054) on d 0 in PRID cows (2.5+/-.2 ng/mL) than in CYST cows (1.9+/-.2 ng/mL). Mean LH and LH pulse frequency decreased (P < .002) by d 1 in PRID cows (1.1+/-.2 ng/mL, 1.8+/-.6 pulses/8 h) compared with CYST cows (2.1+/-.2 ng/mL, 5.6+/-.6 pulses/8 h) and remained lower throughout most of the experimental period. The FSH concentrations were higher (P < .01) in PRID cows than in CYC and CYST cows on d 3 and 4. The increase in FSH concentrations preceded emergence of the PRID-induced follicular wave. All PRID cows and four of seven CYST cows initiated new follicular waves during the period of PRID treatment. Follicular waves were initiated later (P < .05) in CYST cows (d 5.2+/-1.7) and PRID cows (d 5.5+/-.6) than in CYC cows (d 1.8+/-.3). Cysts were smaller (P < .01) at the end of the treatment period in PRID cows compared with CYST cows. No CYST cows ovulated, but all PRID cows ovulated newly developed follicles 3 or 4 d after PRID removal. Treatment with exogenous progesterone reduced LH in cows with cysts, and this was followed by development of normal ovulatory follicles.

Follicular cysts occur after a normal estradiol-induced GnRH/LH surge if the corpus hemorrhagicum is removed

“…Numerous previous studies have hormonally induced cows to have follicular cysts, using large doses of exogenous E 2 . About 50% of cows became anovular following these treatments (Cook et al 1990, Hamilton et al 1995, Calder et al 1999. Cows with induced follicular cysts appear to be in a physiological state in which high circulating E 2 either produces a delayed However, this is the first study, to our knowledge, that has shown that this lack of hypothalamic responsiveness to E 2 and follicular cysts can be induced by the normal increase in E 2 simply by preventing the post-ovulatory rise in circulating P 4 .…”

“…The mechanisms by which P 4 can reinitiate normal cyclicity in cows with follicular cysts has been investigated in a number of studies (Johnson & Ulberg 1967, Nanda et al 1991, Calder et al 1999, 2005. First, P 4 can decrease GnRH and LH pulses leading to a lack of trophic support for follicular cysts (Calder et al 1999).…”

“…Follicular cysts can also be induced with a single E 2 injection if E 2 is given at a time when the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) surge will occur in the absence of a potentially ovulatory follicle . Conversely, cows with either induced or naturally occurring follicular cysts return to cyclicity after treatment with P 4 (Calder et al 1999, 2005. Thus, the pathophysiology underlying follicular cysts appears to involve an unresponsiveness of the hypothalamus to increasing E 2 due to elevated E 2 inducing a GnRH/LH surge that is not followed by an increase in P 4 .…”

“…Development of an appropriate model is essential for studies on the underlying physiology of follicular cysts. Several different methods have been used to induce animals into an anovular condition resembling follicular cysts including estradiol (E 2 ) treatment during diestrus (Wiltbank et al 1961, Nadaraja & Hansel 1976, multiple treatments with high doses of progesterone (P 4 ) and E 2 (Erb et al 1973, Cook et al 1990, Hamilton et al 1995, Calder et al 1999 and prolonged E 2 exposure (Dobson et al 1996(Dobson et al , Ö zturk et al 1998. Follicular cysts can also be induced with a single E 2 injection if E 2 is given at a time when the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) surge will occur in the absence of a potentially ovulatory follicle .…”

“…The subsequent increase in P 4 from the CL could reinitiate responsiveness to E 2 at the hypothalamus by inducing ERa (Blache et al 1991, Caraty & Skinner 1999. Removal of the CL after ovulation in the anovular cows prevents the rise in circulating P 4 , a new follicle wave grows and E 2 concentrations increase, so maintaining downregulation of hypothalamic ERa.The mechanisms by which P 4 can reinitiate normal cyclicity in cows with follicular cysts has been investigated in a number of studies (Johnson & Ulberg 1967, Nanda et al 1991, Calder et al 1999, 2005. First, P 4 can decrease GnRH and LH pulses leading to a lack of trophic support for follicular cysts (Calder et al 1999).…”