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. E VIDENCE has accumulated that under certain circumstances in congestive failure mechanisms leading to the retention of water in excess of sodium may be activated. Metabolic studies from several laboratories1' 2 have established that in cardiac patients the weight changes during the accumulation or removal of edema fluid are often greater than anticipated on the basis of the observed sodium balances. In addition, there have been reports that urine of edematous cardiac patients may contain increased amounts of antidiuretic material.' 4 More recently, it has been demonstrated that, in patients on low salt diets, retention of water without sodium, leading to increasing edema, hyponatremia and hypochloremia, may occur when chronic con-gestive failure is acutely intensified by the development of severe respiratory infection, digitalis toxicity or escape from adequate digitalization.5 However, patients in congestive failure ordinarily can achieve water diuresis in response to intravenous hydration and exhibit no increased sensitivity to aqueous Pitressin.6 Therefore, it was suggested that this water retention , occurring despite extracellular hypo-tonicity, may reflect sustained posterior pituitary antidiuretic hormone production,5 presumably independent of osmoreceptor control and induced by the inadequacy of the cardiac output relative to the body's metabolic requirements.5' 7-9 The present study is a comparison of the diuretic and antidiuretic responses of subjects without heart disease and patients in con-gestive failure of varying severity, who were given intravenous …