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It has been shown that the adrenal cortex gives a diminished secretory response to exogenous corticotrophin (ACTH) 2–3 h after exposure to moderate doses of ionizing radiation (Ungar, Rosenfeld, Dorfman & Pincus, 1955; Shima & Matsuba, 1963). The present paper describes observations made on adult dogs for up to 14 days after X-irradiation of one adrenal gland.

Adult mongrel dogs weighing 10·3–18·5 kg were used. Under sodium pentobarbitone anaesthesia, the left adrenal gland was exposed by the left lumbar route and irradiated with 2000 R of X-rays. The X-ray characteristics were: 180 kV peak, 20 mA, focus—surface distance 37 cm, filtration of 0·5 mm Cu and 0·5 mm Al, and half-value-layer 1·0 mm Cu. Dose-rate to the adrenal gland was approximately 130 R/min. Observations were carried out at 2, 7 and 14 days after irradiation.

On the day of observation, each animal was injected s.c. with 0·1 mg dexamethasone-21-phosphate/kg. One

The rate of secretion of 17-oxosteroids by the testes of anaesthetized dogs in vivo was used as an index of LH secretion. Intracarotid injection of luteinizing hormone releasing hormone (LH-RH, 1, 5 or 10 μg/kg body wt) resulted in an increase in the testicular 17-oxosteroid secretion which was roughly proportional to the dose administered and which reached a maximum 60 min after the injection. Testicular output of 17-oxosteroids was unaffected by administration of melatonin (10 or 100 μg/kg body wt) into the carotid artery. When LH-RH (5 μg/kg) was injected into the carotid artery 3 h after intracarotid injection of melatonin (10 or 100 μg/kg), the testicular response to LH-RH was considerably diminished. Pretreatment with melatonin (100 μg/kg) did not alter the testicular response to human chorionic gonadotrophin (20 i.u./kg body wt) given i.v.

It is concluded that melatonin may act directly on the anterior pituitary gland in dogs to inhibit the LH-RH-induced release of LH.

SUMMARY

The effect of prostaglandin E₂ (PGE₂) on the secretion of adrenaline and noradrenaline by the adrenal gland and the interaction between PGE₂ and acetylcholine in the adrenal medulla were examined in anaesthetized dogs. In splanchnicotomized dogs, i.v. injection of PGE₂ failed to induce any secretion of catecholamines from the adrenal gland, whereas administration of PGE₂ into the lumboadrenal artery resulted in a slight, approximately dose-dependent increase in catecholamine secretion within 2 min of the injection. This effect of PGE₂ was unaffected by i.v. administration of atropine. Intravenous administration of acetylcholine 1 min after the administration of PGE₂ into the lumboadrenal artery of splanchnicotomized atropine-treated dogs had a markedly greater effect on adrenal catecholamine secretion; the resultant output was about twice that evoked by acetylcholine in the absence of PGE₂. The effect was more than additive, since the response to acetylcholine was at least one order of magnitude greater than that to PGE₂. This indicates that PGE₂ and acetylcholine may act synergistically in the adrenal medulla.

Department of Pathophysiology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki 852, Japan

(Received 25 May 1976)

In a previous study (Yamashita, Shimizu & Waki, 1972), there was a decreased response of the adrenal medulla to acetylcholine after exposure of the adrenal area to moderate doses of X-rays. In this paper, we present the results observed on the secretory response of the adrenal medulla to exogenous insulin in dogs whose heads had been irradiated with lower doses of X-rays.

Adult mongrel dogs weighing 8·9–13·9 kg were used. The animals received 200 rad X-irradiation to their heads under pentobarbitone anaesthesia. Radiation was delivered at a rate of 60·6 rad/min, using a therapy unit (200 kV, 30 mA) with a filter comprising 1·5 mm copper– 0·5 mm aluminium. Target-to-skin distance was 37 cm. Approximately 18 h after irradiation, the animals were re-anaesthetized with pentobarbitone (25 mg/kg, injected i.v.) and the left

Exposure of the whole body to moderate doses of X-rays in the rat, rabbit and cat has been shown to reduce the adrenaline and noradrenaline content of the adrenal gland (Goodall & Long, 1959). The present experiments were performed to determine whether X-irradiation exerts a selective effect on the secretory function of the adrenal medulla.

Adult mongrel dogs weighing 9·8–16·3 kg were used. The left adrenal gland was exposed by the lumbar route under pentobarbitone anaesthesia by the method of Satake, Sugawara & Watanabe (1927). Simultaneously the left adrenal vein was cannulated and the left splanchnic nerves were sectioned. The exposed adrenal gland was then irradiated with 200–5000 R of X-rays. The X-ray characteristics were: 180 kV peak, 20 mA, focus—surface distance 37 cm, and half-value-layer 1·0 mm Cu. Dose-rate to the adrenal gland was approximately 130 R/min. Samples of adrenal venous blood were collected 30 and 10 min before,

In previous experiments in our laboratory, the dog testis exposed to low doses of X-rays has shown great secretory activity in response to pregnant mare serum within a few days of irradiation, and this effect continues for 30 days or so (Shimizu, Yamashita, Sugihara & Tsuchiyama, 1972). However, it has not been ascertained whether the effect occurs within a few hours of exposure. We now report the response of the testis to human chorionic gonadotrophin (HCG) 1·5 h or 24 h after exposure to 200 R of X-rays. The secretory response was determined by measuring total 17-oxosteroids in spermatic venous blood.

Eighteen adult mongrel dogs (9·0–16·3 kg) were studied. Under pentobarbitone anaesthesia (injected i.v.), X-irradiation of the scrotal area alone was administered to 12 dogs in single doses of 200 R. Radiation was delivered using a 200 kV peak therapy unit (200 kV, 20 mA) through a 0·5 mm copper—0·5

First Department of Internal Medicine, Kagoshima University, Medical School, Kagoshima 890, Japan

(Received 13 December 1977)

The role of brain noradrenaline in the regulation of pituitary-adrenocortical function is controversial. Ganong (1972) suggested that the central noradrenergic system inhibits the secretion of adrenocorticotrophin, but it has also been shown (Kumeda, Uchimura, Kawabata, Maeda, Okamota, Kawa & Kanehisa, 1974) that a drastic reduction in the hypothalamic noradrenaline content, resulting from intraventricular administration of 6-hydroxydopamine, has no effect on the basal levels of corticosterone in rat plasma and adrenal tissue. The stress response is also not affected, nor is the suppressive effect of dexamethasone on the plasma and adrenal concentrations of corticosterone. Almost identical results have been reported by Cuello, Shoemaker & Ganong (1974) and Kaplanski, van Delft, Nyakas, Stoof & Smelik (1974), and Cuello et al. (1974) suggested the possibility of denervation hypersensitivity developing as a result of intraventricular administration of 6-hydroxydopamine.