Studies on the antidiuretic effect of cyclophosphamide: Vasopressin release and sodium excretion
β Scribed by Bode, U. ;Seif, S. M. ;Levine, A. S.
- Publisher
- John Wiley and Sons
- Year
- 1980
- Tongue
- English
- Weight
- 512 KB
- Volume
- 8
- Category
- Article
- ISSN
- 0098-1532
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β¦ Synopsis
Abstract
To elucidate the mechanism of cyclophosphamide (CTX)βinduced antidiuresis, plasma and urine volume as well as serum electrolytes, creatinine, osmolality, and appropriate hormones were monitored serially during 19 courses of chemotherapy. In spite of plasma hypotonicity and urinary hypertonicity, the plasma vasopressin concentrations were unaltered. Intravenous isotonic hydration did not prevent water retention, but did not lead to plasma hypotonicity, and compensated for modest urinary sodium losses. Furosemide diuresis did not prevent the development of hyponatremia in patients receiving hypotonic hydration. The results indicate that the origin of this selfβlimited syndrome is a direct effect of CTX on the renal tubule, permitting increased water reabsorption and sodium loss. The likelihood that water and salt imbalance will develop after CTX administration can be reduced by vigorous isotonic hydration, and pharmacological diuresis.
π SIMILAR VOLUMES
The acetates of ursolic acid, oleanolic acid, glycyrrhetinic acid, lu eol, and lurenol were administered subcutaneously to adrenalectomized rats and tgeir effect on the excretion of sodium and potassium determined. Ursolic acid acetate induced significant sodiun retention at 3 mg. per rat. Potassium