Dear All,

Re: EFFECTS OF PGF2a ANALOGUES ON SUBSEQUENT LUTEAL FUNCTION

I begin by clarifying that my knowledge of luteal function in ruminants can
be written on the back of a postage stamp, and that I am more familiar with
the human CL. That having been said, I do vaguely recall that, in the
ruminant, there are waves of follicular development that are initiated in
the luteal phase of the preceding cycle. (Please correct me if I'm wrong).

Based on this limited undertsanding, I would go along with Milo's suggestion
that, in view of the short half-life of PGF2a and its structural analogues,
any effect of cloprostenol on the subsequent CL must reflect actions on the
follicle that gives rise to that CL. Specifically, shortening the luteal
phase of cycle 1 will cut short the time available for follicular
development in that luteal phase and drive follicles to develop prematurely
for cycle 2 with inevitable consequences for luteal function in that seecond
cycle.

If I understood correctly, Milo seemed to be suggesting that premature
follicular development limits the size of the follicle at ovulation, and
hence the number of cells available to synthesize progesterone in the
consequent CL. However, remembering the adage that "size isn't everything",
does anyone have (or know of) any data that the FUNCTION of luteal cells is
adversely affected by their endocrine or paracrine exposure in the follicle
prior to ovulation?

As a closing aside, I am glad to see that this topic has really captured the
international interest of this discussion group!

Best wishes,

Tony


Dr.Tony Michael
Lecturer in Biochemistry & Molecular Biology,
Dept.Biochemistry & Molecular Biology,    Tel :0171-794-0500 x.4999 (Office)
Royal Free Hospital School of Medicine,     Tel : 0171-794-0500 x.4988 (Lab)
Rowland Hill Street,                                   Fax : 0171-794-9645
London NW3 2PF