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The fluid retention of patients with liver disease, leading to edema and ascites, has generally been attributed to primary sodium retention with secondary, obligatory water retention. However, because of the impaired water diuresis following oral hydration and the increased amounts of urinary antidiuretic activity observed in such patients, several investigators (1-4) have postulated some primary change in mechanisms influencing the release, physiological effect or inactivation of the -neurohypophyseal antidiuretic hormone. White, Rubin and Leiter (5) observed that, on the average, the maximal urine flows and periods of time required to achieve peak diuresis, during infusions of 10 ml. of intravenous glucose in water per minute, were the same in patients with liver disease and subjects with normal liver function. Furthermore, intravenous administration of 0.57 mU of Pitressin per Kg., during such wa |
