Seven mature thoroughbred horses, weighing between 400 and 541 kg, were each injected intra-articularly into three joints with 6 mg/joint of triamcinolone acetonide (Vetalog). The fourth joint, the control, was injected with saline. Synovial fluid was taken from all four legs of the horses on days 1, 2, 3, 4, 5, 6, 7, 8, 11, and 15 following the injections. Triamcinolone acetonide was assayed by a radioimmunoassay. Blood was collected at 1, 2, 4, 6, 12 h and on days 1, 2, 3, 4, 5, 6, 7, 8, 11, and 15 following injection of either triamcinolone or saline. Both cortisol and triamcinolone were assayed. The results show that the synovial fluid level of triamcinolone was 7.5 micrograms/ml 1 day following treatment and decreased to 10 ng/ml by the 4th day. These low levels were maintained for approximately 14 days. By the 15th day, the triamcinolone was below a detectable level. Serum levels of triamcinolone increased to 3 ng/ml within 1 h and further increased to a peak of 4.3 ng/ml at 4th h. The level then decreased to 2 ng/ml at 24 h and to nearly an undetectable level in 48 h. The mean level of serum cortisol, on the other hand, gradually decreased as the serum level of triamcinolone increased. As the serum level of triamcinolone reached an undetectable level on the 2nd day, the serum cortisol level gradually increased and returned to the pre-administration level by the 5th day. These results showed that the intra-articular administration of triamcinolone maintained triamcinolone in the synovial fluid for 4-14 days and that the triamcinolone reached the blood within 1 h. The serum level of triamcinolone was maintained for 2 days and resulted in the inhibition of adrenal function for 4 days.

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The relationship between the medial basal hypothalamus (MBH) LH-RH activity and LH release was studied following progesterone (P) treatment of oestrogen-primed ovariectomized rats (day 0). Following P administration at 10.00 h (day 2) serum LH levels increased rapidly after 13.00 h to peak levels attained at 15.00 h and maintained until 18.00 h. Coincident with the onset of augmented release and peak serum LH concentrations at 15.00 h there was a significant enhancement in the MBH LH-RH activity. Thereafter, the MBH LH-RH stores promptly fell and remained at morning low levels through the rest of the LH surge period. P treatment also stimulated release of FSH and prolactin in the afternoon. Administration of norepinephrine (NE) synthesis inhibitors, diethyldithiocarbamate (DDC) and U-14,624 before P blocked the afternoon increments in serum gonadotrophins and the MBH LH-RH levels; prolactin release was also suppressed in DDC treated rats. In contrast, lergotrile mesylate (dopamine agonist) treatment prior to P administration suppressed only the afternoon increase in prolactin release. These studies show that (1) P can stimulate MBH LH-RH activity in oestrogen-primed rats and these Supported by grant NIH HD 08634. 0 Eli Lily Research Laboratories, Indianapolis, Indiana. effects are transmitted to the LH-RH peptidergic neurons via NE synapses in the preoptic area and (2) a common central NE system may mediate the stimulatory feedback effects of P on gonadotrophin and prolactin release.Administration of progesterone ( ) to oestrogen-primed ovariectomized rats elicits a pro-oestrus-type surge of serum gonadotrophins (Caligaris et al. 1971; Kalra et al. 1972) and prolactin {Caligaris et al. 1974). Several studies have demonstrated that the stimulatory feedback action of on gonadotrophins is mediated primarily by central norepinephrine (NE) systems {Kalra et al. 1972; Kalra l'alia), however, the neurotransmitter(s) involved in prolactin release has not been identified. Besides these information, little is known about the neuro¬ endocrine mechanisms by which progesterone stimulates the secretion of pituitary gonadotrophins and prolactin. In this report we describe (a) the time sequence of changes in hypothalamic LH-RH activity associated with the Pinduced surge of serum LH and (b) the effects of two NE synthesis inhibitors, diethyldithiocarbamate (DDC, Magos 8c Jarvis 1970; Carr et al. 1977) and U-14,624 (l-phenyl-3-(2-thiazolyl)-2 thiourea, Johnson et al. 1970; Khalsa et al.