Myocardial necrosis due to vitamin D3 overdose -- scanning electron microscopic observations.

Our studies were carried out on the hearts of virgin female Wistar rats treated with 100,000 i.u. of vitamin D3 (calciol) per os for 3 consecutive days. Multifocal cardionecrosis was established macroscopically in 70% of the vitamin D-treated rats on the 7th day of the experiment when the rats were in the acute phase of intoxication. Using a scanning electron microscopy (SEM), we received three-dimensional information about the structural changes to the rat myocardium damaged by high doses of vitamin D3. The images of necrotic hearts revealed significant disruption of the structural integrity of the myocardium linked to fragmentation of the cardiac muscle bundles and a visible disruption of the extracellular matrix (ECM) components. In healthy hearts, the structural integrity of the myocardium and the dense network of the extracellular matrix were well preserved. In parallel, the effect of an increasing concentration of free Ca2+ on the total proteolytic activity of the heart muscle homogenate of the healthy and necrotic rats was investigated at neutral pH. These data showed that following vitamin D3 intoxication, the proteolytic processes in the rat hearts occurred in Ca2+ overload or saturation. On the basis of our morphological and biochemical results we can suggest that calcium-activated neutral proteinases may have contributed to the structural alteration of the extracellular matrix components and were in this way involved in vitamin D-induced cardionecrosis.

The effect of fasting and refeeding on the ultrastructure of the hypothalamic paraventricular nucleus in young and old rats.

In order to explore the morphological basis of the altered feeding behaviour of old rats, an ultrastructural investigation of the magnocellular neurons of the hypothalamic paraventricular nucleus (PVN) was performed. Young and old male Wistar rats, 5 and 24 months old, respectively, and with each age group comprising 12 animals, were divided into 3 groups. The rats in Group I were used as controls (normally fed), the rats of Group II were fasted for 48 hours and in Group III the rats were fasted for 48 hours and then refed for 24 hours. The brains were fixed by perfusion and histological and ultrathin sections were obtained by routine methods. Common features of the magnocellular PVN neurons of young and old rats were abundant Golgi complexes and short fragments of RER localised at the cell periphery. In contrast to young rats, the PVN neurons of old animals showed deep indentations of the nuclear envelope and age-related residual bodies. In both age groups fasting for 48 hours led to the expansion of the Golgi complexes and dilatation of RER cisternae. In contrast to those in fed rats, RER cisternae in the neurons of old fasted animals were situated between the nuclear envelope and the Golgi zone. Prolonged RER cisternae were distributed in the peripheral cytoplasm of refed old rats. Our observations suggest that at the ultrastructural level the process of ageing does not change the responsiveness of magnocellular PVN neurons to fasting-refeeding.