(range 0.02-17.8s). Although fetal activity states were taken study, so far the influence has appeared to be small.
into account
in this
Prolactin during the transition from anoestrus to oestrus in sheep
H.A.I.M. van Leusden’, P.M. Meulendijk ’ and T. Kruip 2, ‘Department of Obstetrics and Gynaecology, St. Elisabeth’s Gasthuis, Arnhem, and 2Department of Veterinary Obstetrics and Gynecology ‘De Uithoj’, University of Utrecht, The Netherlands
The sheep has a restricted breeding season. Texel ewes - in the Northern hemisphere - only ovulate from September until February. Observations are presented of the changes that occur from the endocrinological point of view in sheep during the interval of transition from anoestrus to oestrus. In this study, emphasis is given to what happens with prolactin during that transition. Since hyperprolactinaemia is associated with amenorrhoea in women we decided to measure the changes in prolactin levels over this period. Fifty-eight complete cycles were meticulously studied in the transition period: thirty-six first cycles and twenty-two subsequent cycles. All observations were performed under field trial conditions. Oestrus behavior was assessed with the use of vasectomized raddled rams. Blood was sampled at regular intervals, and plasma prolactin, LH and progesterone were determined by means of a radioimmunoassay. In addition the LH response to lowering the prolactin levels by bromocriptine was measured in twenty-five animals in the anoestrus season and conversely metoclopramide was used to induce hyperprolactinaemia in the oestrus season to study its effect on LH surge and ovulation. The constant hyperprolactinaemia normally present in the anoestrus season of the ewe diminishes during the transition from anoestrus to oestrus. During the first luteal phase prolactin is lowered further. After luteolysis, paralell with LH, prolactin surges - not due to a coital reflex mechanism - come into existence. Therefore the fall in prolactin levels is phasic rather than gradual. Evidence is presented that in spite of the simultaneous occurrence, the regulatory reflex mechanisms for the LH and prolactin surge are different. From the relationship progesterone-prolactin, and from the failure of LH to rise in bromocriptine treatment it is concluded that there is no short-loop feed-back prolactin-LH surge. As introduction of rams during the hyperprolactinaemic transition period elicits LH surges and ovulations in the absence of ‘heat’, hyperprolactinaemia per se does not prevent ovulation. Likewise pharmacological induction of prolactinomas by metoclopramide - a dopamine receptor blocking agent - does not block the LH surge or ovulation. It is concluded that during the transition from anoestrus to oestrus season a number of complex changes take place leading to the disappearance of hyperprolactinaemia by a change in centrally located sensitivity of more than one regulatory mechanism. There are a number of analogies between naturally occurring prolactinomas in sheep and prolactinomas in man.