Cyclic proestrous LH release was investigated by endogenous and exogenous assay in rats exposed to light from 5:00 A.M. to 7:00 P.M. daily. Pituitaries were removed from proestrous rats at 10:00-11:00 A.M. and 4:00-5:00 P.M., injected into immature, primed recipient rats and tested for ovarian ascorbic acid depleting ability (exogenous assay). "Morning" pituitaries were significantly more potent than "afternoon" pituitaries, confirming the finding of drug and hypophysectomy studies that LH is released from the pituitary between 2:00 and 3:00 P.M. Ovaries removed from the proestrous donor rats showed no consistent ascorbic acid depletion on the afternoon of proestrus (endogenous assay). There was, however, a cyclic variation in ovarian ascorbic acid, the highest values occurring in metestrus, the lowest in proestrus. I N RECENT years Everett and his co-workers (1,2) have accumulated indirect evidence suggesting that when cyclic female rats are exposed to light daily between 5:00 A.M. and 7:00 P.M., LH is released from the pituitary starting at 2:00 P.M. and completed in 90% of animals by 3:30 P.M. on the day of proestrus. Ovulation then occurs around midnight. This timing of LH release was demonstrated by injecting a variety of centrally-acting blocking drugs (1) or hypophysectomizing (2) at the critical time in the afternoon and looking for presence or absence of ovulation the following morning.The use of endogenous ovulation as a criterion of LH release necessitates the presence of prepared follicles, limiting the variety of experiments which might be utilized to elucidate the factors triggering LH release. In order to avoid the need for a prepared ovary, changes in LH content must be measured directly, either in the anterior pituitary or in the body fluids. Acute decreases in pituitary gonadotrophin content have been demonstrated following coitus-induced ovulation in the rabbit (3, 4), following the onset of heat in the ewe (5) and sow (6), and following post-partum ovulation in the mouse (7). This encouraged us to look for acute decreases
A correlation between the use of halogenated anesthetic agents and liver necrosis is not yet established in man. In an attempt to resolve this dilemma, guinea pigs were immunized with a complex of guinea-pig albumin and trifluoroacetate (TFA), a common metabolite of halothane and fluorexene, and then exposed to halothane on multiple occasions. Histology and liver-function tests showed no difference in the incidence of liver damage between groups of animals immune to TFA with cellular immunity and untreated control animals. However, a difference in the liver enzyme levels was seen between controls and animals showing humoral immunity.
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