The bones of adult (26 weeks old) spontaneously hypertensive rats (SHR) were examined chemically and histologically by comparing them with those of the corresponding normotensive Wistar-Kyoto (WKY) rats. The mean cortical thickness, the mean ash weight per unit bone volume, and the ash as percentage of dry weight of femur were significantly lower in SHR than in WKY. Besides, the percent cortical area measured on tibial cross-section was also reduced in SHR compared with WKY. These findings strongly suggest that the development of osteoporotic bone disorders exists in adult spontaneously hypertensive rats.

Using food-deprived rabbits we investigated the effects of nutritional deficiency on the development of pressure sores. The body weight of these animals was decreased significantly from normal. Organ weights of liver, heart, spleen, kidney, and testis were significantly decreased from normal as well. Protein deficiency in these animals was indicated by serum tests, as well as by histologic features of liver and testis and ultrastructural findings on fibroblasts. We produced lesions in malnourished as well as normal rabbits by exposing their skin to a balloon-produced compressive force of 120 +/- 10 mmHg for 4 hours. Biopsies were taken 1, 2, and 3 days after the pressure application. Histologic findings at each time were as follows: At day one, the degree of ischemic skin destruction in the malnourished animals was more severe than that in the normal ones, and thrombi were occasionally seen in the malnourished cases. At day two, proliferation of fibroblasts and macrophage infiltration were evidenced in the normal animals, whereas signs of collagen fiber degeneration as well as microthrombi were seen in the malnourished ones. At three days, epidermal cells covered the lesions in the case of normal animals; however, massive necrosis of the epidermis was still recognized in the malnourished rabbits. Thus, the healing process of pressure sores was strongly suppressed in the malnourished animals. This suppression was attributed to the reduction in fibroblast proliferation, capillary formation, macrophage infiltration, and also to the low level of epidermal cell proliferation.

The therapeutic effects of vitamin D analogs, 1,24(R)-dihydroxycholecalciferol [1,24(R)-(OH)2D3], 1,24(S)-dihydroxycholecalciferol [1,24-(S)(OH)2D3], and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] on immobilization osteoporosis were studied in rats. The right hind limb was immobilized through application of a plaster cast following the section of the sciatic nerve. The left hind limb was intact. Vitamin D analogs were orally administered for 6 weeks at dose levels of 0.02 and 0.10 micrograms/kg/day, respectively. The mean lengths of the immobilized femurs were not significantly different from those of the intact femurs in all the experimental groups. In the immobilized femur of animals treated with 1,24(R)(OH)2D3, 0.10 micrograms/kg, dry and ash weights were heavier and calcium and phosphorus contents greater than those in the nontreated group. Furthermore, the amount of calcified bone mass and the cortical thickness of the femurs of the immobilized limb in 1,24(OH)2D3-treated animals were greater than those in the nontreated animals. Treatment with 1,25(OH)2D3 at 0.10 micrograms/kg caused an increase of the bone mass in both immobilized and intact femurs when compared with those of the control group. It was concluded that the administration of 1,24(R)(OH)2D3 diminished the effect of immobilization in the development of osteoporosis without any side effects.

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Disorders of bone metabolism caused by resection of three quarters of the small bowel in rats were investigated biochemically and histomorphologically. Metabolic bone disorders developing 90 days after in 75%-distal-small-bowel resected rats were characterized by reduction in ash content of the femur and by the disappearance of the trabecular bone in tibial metaphysis. Biochemical studies showed significant decrease in serum Ca and 1,25-dihydroxyvitamin D concentrations in 75% distal small bowel resected rats. These data suggest that 75% distal small bowel resection impairs intestinal absorption of calcium and results in a negative calcium balance, which may contribute to the development of bone metabolic disorder in rats. On the other hand, 75% proximal small bowel resection causes no obvious metabolic bone disorders in rats, possibly because of the adaptation by the remaining part of the intestine.