J.Jpn. Surg. Soc.. 58(12): 1882-1902, 1958
THE RELATION BETWEEN THE ANTIDIURETIC SUBSTANCE AND ASCITES IN PORTAL HYPERTNSION
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Second Dept. of Surgery, Nagoya University School of Medicine (Director: Prof. Hajime IMANAGA) Isamu MORI |
1) By the Jeffers's method the antidiuretic activity of serum, tissue extracts and urine is measured. In portal hypertension, the antidiuretic substance increases both in serum and urine, in proportion to the retention of ascites.
2) The antidiuretic substance decreases the urine volume and the excretion of chloride in the urine. The effect of the antidiuretic substance on the metabolism of sodium and potassium is equivocal, but tends to diminish the excretion of sodium.
3) In portal hypertension, the mechanism of the secretion of the antidiuretic substance seems to be possible through volume receptor rather than through osmoreceptor. But significancy of this mechanism is not observed.
4) From the relationship between the antidiuretic activity of serum and liver function test, and from the experiments in vivo and in vitro, it is apparent that antidiuretic hormone is inactivated in the liver, but, in portal hypertension, the inactivation of antidiuretic hormon declines with the liver degeneration and liver circulatory insufficiency, consequently the antidiuretic activity in serum and urine increases.
5) The liver can inactivate the antibiuretic hormone in the presence of the adrenocortical hormone, but, in portal hypertension, adreno-cortical insufficiency disturbs this inactivation of antidiuretic hormone in the liver.
6) Portal venous hypertension which should affect the pressoreceptor, is not an essential factor to the metabolism of antidiuretic substance.
7) Hypoproteinemia and adreno-cortical insufficiency play some roles for the retention of ascites which did not affect the antidiuretic substance.
(author's abstract)
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