Bahn, Robert C.

In 12 children with hyperadrenocorticism caused by tumor of the adrenal cortex the most common clinical picture was that of a mixture of adrenogenital and Cushing's syndromes. All tumors were surgically removed; adrenal steroids were used in the preparation of 11 patients for operation. One patient died with extensive metastasis 5 months after operation, while 11 were alive and well 18 months to 29 years after operation. Data from the 12 cases in this series and from those in the literature suggest that the likelihood of metastasis may be correlated with the relation of tumor weight to body weight.

Effects of hypophysectomy on aldosterone and sodium excretion were studied in a group of seven dogs with ascites secondary to thoracic inferior vena cava constriction. In another group of three dogs, the pituitary was removed first and after 6–8 weeks the thoracic inferior vena cava was constricted. Following hypophysectomy of the seven dogs with the initial ascites, aldosterone became undetectable in urine and sodium excretion increased concurrently; adrenocorticotrophic hormone (ACTH) failed to prevent these effects. However, additional constriction of the vena cava with a consequent further elevation in venous pressure was followed by a return of nearly complete sodium retention. In two of the dogs in which hypophysectomy was performed first and the thoracic inferior vena cava constricted later, there resulted increased aldosterone output, marked sodium retention and ascites. In these dogs the adrenal cortex was markedly atrophic but the atrophy was limited to the two inner layers. The data suggest that in pathological states accompanied by edema and ascites the increased excretion and presumably increased secretion of aldosterone are not solely dependent upon pituitary hormonal function.

The concentration and distribution of sodium and potassium in small consecutive portions of kidneys of potassium-depleted and vitamin D-intoxicated hydropenic rats were estimated by a procedure based on the principle of specific activity. By this method sodium and potassium could be measured in bits of tissue weighing less than 2 mg. The results were correlated with the corresponding urinary osmolality. In both experimental groups, a marked impairment of the elaboration of osmotically concentrated urine was observed. The relative distribution of sodium and potassium in the kidney was not altered significantly. Associated with the decreased osmolality of the urine, however, was an approximately proportionate or slightly greater reduction in the content of sodium in the papilla. The findings suggest that a failure to establish maximal medullary hypertonicity, as indicated by the diminished accumulation of sodium, may be an important factor in the impairment of concentrating mechanisms.

Effects of hypothalamic lesions were studied in 10 dogs with chronic ascites produced by constriction of the thoracic inferior vena cava. During the first three postoperative days, the high rate of urinary aldosterone excretion and the marked Na retention characteristic of dogs with chronic experimental ascites were unaltered in all 10 animals. Every area of the hypothalamus was destroyed bilaterally in at least one animal. Seven of the 10 dogs survived the subacute 3-day period; two dogs died after 6 days but five animals lived for 2 weeks or longer. In these seven animals, aldosterone excretion in urine remained elevated above normal although in three animals a progressive decline occurred; sodium excretion remained low in all seven dogs surviving the subacute period. In the three animals in which aldosterone output declined, there was bilateral injury of the median eminence and adrenal atrophy. The data show that chronic hypothalamic lesions were without effect unless the median eminence was injured.

Acute effects of hypophysectomy and of diencephalic lesions on aldosterone and corticosterone secretion were studied in 10 dogs with chronic experimental ascites. During preliminary observations, diencephalic lesions were made by the oral approach but the pituitary gland was damaged; in two dogs aldosterone and corticosterone secretion fell markedly. In the third animal, ACTH was given following the lesion; aldosterone failed to fall while corticosterone declined slightly. In the definitive study (7 dogs), hypophysectomy was performed before the diencephalic lesion was made. Following hypophysectomy, a 76–97% decrease in aldosterone secretion occurred within 2 hours. The effects of diencephalic lesions were variable; aldosterone output was unchanged, increased, decreased and increased during the 1st hour but declined thereafter. Corticosterone secretion fell 81–99% after hypophysectomy. These acute observations show a striking dependence of aldosterone and corticosterone secretion upon intact pituitary function. The evidence on the relation of the diencephalon to aldosterone secretion was inconclusive but an intact middle and posterior hypothalamus was not essential for normal or elevated rates of aldosterone secretion.

Calcific emboli were observed in 38 of 62 patients (61 per cent) who died at varying intervals following aortic valvotomy for calcific aortic stenosis. Major coronary embolization occurred in 10 patients (16 per cent) and was considered to be a major cause of death of four patients. Minor coronary embolization occurred in 33 patients (53 per cent) and was not directly implicated as a cause of death in any patient. Calcific emboli occurred to other organs in eight patients (13 per cent). The technics instituted for reducing the incidence of embolization—occlusion of coronary ostia, diligence in detection and removal of any debris, and final aspiration of the left ventricle—appeared to have had a favorable effect.

The problem of spontaneous calcific embolization was investigated at necropsy in 165 patients with calcific aortic stenosis. Minor coronary arteries contained calcific emboli in 18 patients (11 per cent), and major coronary arteries contained calcific emboli in 10 (6 per cent). Examination of the brain, kidney, and eye also disclosed spontaneous calcific emboli. In three instances of major coronary artery embolization, there was evidence of old silent infarction but no associated clinical disorder. Calcific embolization is apparently not rare in cases of calcific aortic stenosis, but this phenomenon does not appear to lead very often to extensive infarction or to clinically obvious disorders.