Fragments of adult renal tissue were maintained as organ cultures for 7 days in HEPES-buffered medium 199, supplemented with 10% calf serum and antibiotics. Addition of aprotinin (10,000 kallikrein inhibitor units per ml) to the medium resulted in improved survival of the cells of the glomeruli and tubules and preserved the integrity of the glomerular, capsular and tubular basement membranes. Optimal results were obtained when aprotinin was present throughout the period of culturing. Inclusion of aprotinin in the medium for only the first 3 days in vitro slightly increased the numbers of surviving glomerular and tubular cells, but also promoted the growth of connective tissue in the explants and was detrimental to the basement membranes of the tubules. It is suggested that both the antiproteolytic and the carbohydrate-binding properties of aprotinin are involved in the mediation of the observed effects.
Fragments of cerebellar cortex taken from adult rats were maintained for 7 days in organ culture. Inclusion in the medium of aprotinin, a polypeptide proteinase-inhibitor which also has carbohydrate-binding properties, was beneficial to the survival of neurons in the molecular layer, Purkinje cells and axons. This effect of aprotinin was mediated during the first 3 days in vitro. In a discussion of the various actions of aprotinin, it is concluded that the principal effect of the polypeptide on cultured central nervous tissue is to inhibit neuronal lysosomal proteinases activated by the trauma of explantation.
The cutaneous vasodilatation occuring in the early stages of dietary deficiency of magnesium has been investigated in rats. While the time of onset of erythema varies in proportion to the weight of the animal, the duration is not related to weight. In severe states of vasodilatation, the skin is thickened and infiltrated with mononuclear cells, apparently derived from the blood. Intact sympathetic and sensory innervation are not necessary for the development of vasodilatation in the skin. Neither can the genesis of the erythema be attributed to degranulation of mast cells. From consideration of this and other investigations, it is concluded that the cutaneous abnormalities of magnesium-deficient rats cannot be due directly to hypomagnesaemia.
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