The hot flush is the only symptom specifically attributable to the menopause. Hot flushes appear to represent an episodic derangement of thermoregulation as a result of estrogen deficiency but the underlying physiological mechanisms are unknown. We have developed an animal model for the study of hot flushes. Two female monkeys (Macaca arctoides) were trained to accept monitoring of scalp cutaneous temperatures. After baseline temperature recordings were obtained both monkeys were ovariectomized. A few days after operation the previously stable scalp temperature changed to an undulating pattern with cycles lasting approximately 40-50 min. Ethinyl estradiol (20 micrograms orally or im) and (7 alpha,17 alpha)-17-hydroxy-7-methyl-19-nor-pregn-5(10)-en-20-yn-3-one (2.5 mg orally), a steroid with weak estrogenic, progestogenic, and androgenic properties, suppressed the characteristic undulating temperature pattern; this returned after withdrawal of replacement therapy. Clonidine (0.15 mg twice a day) suppressed the cyclic changes for 2 to 3 h. Domperidone and naloxone had no significant effect. This animal model may be useful for the investigation of alternative therapy for the management of menopausal flushes.

The specific activities of lactate dehydrogenase (LDH) and its M-type (M-LDH), β-glucuronidase (β-GR), acid phosphatase (ACP) and alkaline phosphatase (AP) were determined. The specific activities of the enzymes (LDH, β-GR) in the myometrium were lower and their changes less pronounced than in the endometrium. We, therefore, determined the enzymes in the rat endometrium only in further experiments. All enzymes react sensitively to the changes induced in the endometrium by endogenous hormones in the course of a 4-day cycle: pro-oestrus (P) is characterized by rather low enzyme activities, oestrus (E) by a peak of LDH and M-LDH and a rise of AP. In metoestrus (M) there is a peak of β-GR, ACP and AP. Dioestrus (D) is characterized by a significant decrease in LDH and M-LDH and by elevated values of all the other enzymes. The values on the individual days of the 4–day cycle were compared with days 4–6 of pregnancy. The reason for this was that if the rats were not mated, they would, respectively, return to pro-oestrus instead of being 4 days pregnant, to oestrus instead of being 5 days pregnant, or to metoestrus instead of being 6 days pregnant. We found the following differences: on day 4 of pregnancy LDH and M-LDH were lower and ACP and AP higher than in P. On day 5 of pregnancy the LDH, M-LDH, β-GR and AP were lower than in E On day 6 of pregnancy the LDH, M-LDH, ACP and especially β-GR, were lower than in M.

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Forty eight hours after unilateral nephrectomy, both in non-castrated and in castrated male mice the relative dry weight of the remaining kidney increased significantly. This compensatory hypertrophy was significantly stimulated as early as 96 hours after operation by the treatment with 19-nortestosterone phenylpropionate (= NPP) at the time of operation. The percentual increase of the kidney weight was approximately the same in non-castrated as in castrated mice. The absolute initial values as well as the resulting values 96 hours after operation were higher in non-castrated male mice than in castrated animals. The number of cells and the DNA concentration per g tissue decreased during the period of non-stimulated compensatory hypertrophy in both groups of animals. NPP caused a still further decrease. The concentration of DNA per cell did not change. Following non-stimulated compensatory hypertrophy, there was no change in the RNA concentration per g tissue or per cell in castrated mice. In non-castrated mice the concentration increased. NPP caused approximately the same percentual increase of RNA concentration in non-castrated as in castrated animals during the period of compensatory hypertrophy. The difference between both groups of mice in the RNA concentration in the remaining kidney following stimulation of the compensatory hypertrophy by NPP was statistically significant.