Normal and iron-deficient rats were exposed to cold at 4°C for 1 hr or 5 hrs and the serum TSH, T3 and T4 levels were compared with those in rats kept at room temperature (20°C). There was a rise in serum TSH, T3 and T4 levels in response to 1 hr and 5 hrs of cold exposure in normal, but not in iron-deficient rats. Although pituitary TSH contents were lower in iron-deficient rats, the increases in serum levels of TSH following administration of TRH were similar in both normal and iron-deficient rats. The results suggest that the inability to respond to cold in iron-deficient rats may be due to a reduction in the release of TRH from the hypothalamus.
Summary. In acute carbon tetrachloride-induced liver damage in rats, plasma iron and total iron-building capacity were enormously elevated. This was coupled with an increase in the weight of livers and spleens as well as spleen iron concentrations when compared with control values. On the other hand, the haematocrit and liver iron concentrations were low. In chronic liver injury there were no changes in plasma iron or total iron-binding capacity. The gains in weight of both liver and spleen were dependent upon the dose of hepatic poison. Liver iron stores were also increased; however, this increase was attributable to the expansion of haemosiderin iron. In Grade III cirrhosis, the rate of iron absorption dropped significantly, possibly as a result of increased liver stores.
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