ADRENOCORTICAL HYPERPLASIAS AND TUMORS IN ORGAN CULTURE

Abstract

Adrenocortical hyperplasias experimentally produced in rats were placed in organ cultcue and studied as well as human adrenals from 16 surgical materials (5 controls; 11 hyperfunctioning human adrenocortinal tissues including 3 adenomas and each 2 hyperplasias from Cushing's syndrome and primany aldosteronism and 1 adenoma from adrenogenital syndrome) and the following results were obtained.
1. Adrenocortical hyperplasia by aniline injections was demonstrated in female rats (weight of adrenals 26.0±10.9mg by 7 day treatment; 57.0±6.0mg in controls).
2. Hyperplastic rat adrenals were cultured with and without ACTH, and the histological findings were comparatively studied. Adrenal hyperplasias cultured 7 days preserved better morphology than untreated group. The best histological preservation was found in hyperplasia cultured with 0.2IU/ml of ACTH for 7 days.
3. Sixteen human materials were cultured for 48 hour to 7 days (14 days in part) and tolerated for electron microscopy as well as routine histology.
4. Normal human adrenocortical tissues maintained the basic structures of cytoplasmic organellae during the 7 day culture period. By ACTH 0.02IU/ml in the culture media, mitochondria, smooth endoplasmic retuculi (SER) and vesicles were increasing while lipid granule decreased.
5. Adenoma cells from Cushing's syndrome maintained their basic structure with and without ACTH during the 7 day culture period. By ACTH 0.02IU/ml in the media, a better preservation of the tissues was obtained in 14 day cultures, while they tended to be degenerated by ACTH 0.2IU/ml.
6. In hyperplasias from Cushing's syndrome, the cytoplasmic basic structures were well maintained by ACTH. The optimum concentration, 0.02IU/ml of ACTH, increased the size and number of mitochondria and SER.
7. Adenoma cells from primary aldosteronism included a characteristic myelin-like structure in cytoplasm as well as non-tumor part of the adrenal before and after culture. With ACTH in the media, mitochondria as well as vesicles were enlarged.
8. In hyperplasia from primary aldosteronism, ACTH in the media decreased the size of mitochondria, which looked thinner like threads and the cristae disappeared. Lipid granules were also decreased. The results indicate the factors affecting on hyperplasia of primary aldosteronism other than ACTH.
9. Adenoma cells from adrenogenital syndrome well maintained the original structures in 48 hour to 7 day cultures. By ACTH, at a concentration of 0.02IU/ml in the media, mitochondria and lipid granules increased as well as abundant endoplasmic reticuli.
10. Characteristic myelin-like structures were seen in adenoma cells from primary aldosteronism treated with spironolactone. Similar lamellar structures were also recognized in hyperplasia of Cushing's syndrome and adenoma of adrenogenital syndrome.
11. The myelin-like structures changed the characteristic laminated configuration into fluidlike extension after culture with or without ACTH. This was more prominent in adenoma cells from adrenogenital syndrome, in which the laminated structure showed a closer relationship to SER and RER and the role of functional connection.
The above mentioned results partly disclosed the pathological physiology of adrenocortical hyperfunction, and the present research method was proved to be useful for further clnical investigation.