During the winter and spring of 1952-53 a survey of hemoglobin values was made in Halifax among 1308 male subjects 6 to 98 years of age, and 1424 female subjects 6 to 94 years of age. Among children 6 to 14 years old the values increased from about 13 to about 14 Gm. per 100 ml. of blood, and there were essentially no differences between the sexes. The average value for both the boys and the girls was 13.5 Gm. In girls between 14 and 20 years of age the hemoglobin values decreased slightly, reaching about 13 Gm. per 100 ml. In boys of corresponding ages there was an increase to about 15 Gm. In both sexes these values were attained at about 20 years of age, and remained characteristic of the third decade of life. They were essentially the lowest and the highest shown respectively by the female and the male subjects of any age group. Hemoglobin values in men between 20 and 60 years of age were typically 14.5 to 15 Gm. per 100 ml., the higher values tending to occur among the younger men. After the fifth decade there were progressive and marked decreases to an average of 12.4 in men between 80 and 90 years of age. In women from 20 years of age onward the average hemoglobin values remained near 13 Gm. per 100 ml.

SUMMARYThe pathogenesis of the vasodilatation associated with liver cirrhosis is not fully understood, but it has recently been postulated that it may be related to an increase in nitric oxide production. The aim of this study was to compare the response of isolated aortic rings from normal and cirrhotic rats to two vasoconstrictors, phenylephrine and U46619, a thromboxane analogue. Biliary cirrhosis was induced by ligation of the common bile duct; a sham operation was performed in control animals. Five weeks later, the aorta was removed and dissected into rings for study in organ chambers. Concentration-response curves were obtained for the two vasoconstrictors from rings with intact endothelium and from rings denuded of endothelium. We found that the vasoconstriction produced by phenylephrine was decreased in cirrhotic vessels both with and without endothelium, but the response to U46619 was not modified by cirrhosis. Concentration-response curves for phenylephrine were also obtained from rings in which the synthesis of nitric oxide and prostaglandins was inhibited by NG-monomethyl-L-arginine and indomethacin, respectively. Nitric oxide synthase inhibition restored normal contractility of the rings with and without endothelium. This beneficial effect was not observed when cyclo-oxygenase activity was blocked with indomethacin. This study suggests that cirrhotic vessels are hyporeactive to vasoconstrictors and that this effect is mediated through increased nitric oxide production. The improvement observed after inhibition of the nitric oxide pathway in denuded rings led us to suggest that cirrhosis also induces nitric oxide synthase in smooth muscle cells, as previously observed by others in septic animals.

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Young rats were maintained for 84 days on a diet which supplied to each 0.15 mg of iron and 4.26 mg of calcium per day. The Ca:P ratio of the diet was 1.4. For some of the animals the dihydrate of disodium ethylenediaminetetraacetic acid (EDTA) was added at a level of 0.01%, which supplied 1 mg per rat per day. The molar ratio of EDTA:Ca:Fe was 1:37.9:1.The EDTA did not affect the growth of the rats. It did not affect the excretion of calcium, or its concentration in blood serum or femur. Since the faecal excretion was not affected, apparently the absorption was not impaired. The growth of the femur was not affected. EDTA was associated with generally higher levels of iron in the serum, but the average difference was not statistically significant. There was no effect upon the liver iron or the haemoglobin level in the blood.Small amounts of EDTA in the diet apparently did not interfere with the utilization of low and probably inadequate dietary levels of calcium and iron.