Jacob Grossman

STUDIES ON INTRAVENOUS WATER DIURESIS AND NICOTINE AND PITRESSIN ANTIDURESIS IN NORMAL SUBJECTS AND PATIENTS WITH LIVER DISEASE

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

Studies on Water Excretion Following Intravenous Hydration and the Administration of Pitressin or Nicotine in Congestive Heart Failure

The diuretic response to intravenous infusions of 5 per cent glucose in water and the antidiuretic response to intravenous injections of nicotine salicylate and aqueous Pitressin, during maximal water diuresis, were studied in normal subjects and patients in congestive failure of varying severity. Patients in moderately severe congestive failure exhibited normal diuretic responses during the periods of intravenous hydration and normal antidiuretic responses following nicotine or Pitressin injections. Patients in more severe congestive failure failed to achieve comparable diuretic responses, following intravenous hydration; in the course of this, signs of increasing congestive failure developed, which were associated with further decrease in urine flows, at times, without any further decrease in renal hemodynamics. These studies confirm the impression that patients in moderate congestive failure have neither increased sensitivity to, nor reduced ability to, inactivate endogenous or exogenous antidiuretic hormone. In addition, the observation, that patients in more severe failure do not achieve adequate water diuresis during intravenous hydration, suggests that sustained production of antidiuretic production, independent of normal osmoreceptor control, may be contributing to their fluid retention.

Renal extraction and excretion of mercury in man following intravenously administered mercurial diuretics.

Previous studies (1) from this laboratory have indicated that urinary excretion of mercury reaches a maximal value immediately following the intravenous injection of an organic mercurial diuretic and then falls rapidly, presumably as the plasma concentration of mercury decreases. Moreover, the dynamics of mercury excretion during the first four to six hours in a given individual are quite constant on repeated measurement and are not significantly affected by certain factors which either enhance or inhibit diuresis. In the present study the mechanisms by which mercury is removed from the plasma and excreted in the urine and the relationship of this process to mercurial diuresis have been investigated in human subjects with the aid of simultaneous measurements of renal hemodynamics, urinary mercury and electrolyte excretion, and arterial and renal venous plasma mercury concentrations.

Studies on Thiomerin—A Subcutaneously Administerable Mercurial Diuretic

Results of clinical and physiologic studies with Thiomerin, a new subcutaneously administered mercurial diuretic, are presented. The data indicate a clinical diuretic efficacy comparable to that of other mercurials and a negligible systemic toxicity. Renal clearance studies demonstrate that it acts by producing a reversible depression in tubular reabsorption of electrolyte and water. The effects of intravenous and subcutaneous administration are compared.