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Brain myelinolysis could complicate the excessive correction of chronic hyponatremia. Recently it was suggested that hypoxia rather than correction of hyponatremia would be responsible for myelinolysis. We analyzed the incidence and the severity of potentially associated hypoxia and its consequences on survival and on the development of brain damage in rats in which major hyponatremic encephalopathy had developed after either pure acute hyponatremia (serum sodium concentration: -40 mEq/L/3 hr, group I, n = 8) or acute hyponatremia (serum sodium concentration: -30 mEq/L/3 hr, group II, n = 12) superimposed on chronic hyponatremia of 3 days' duration (serum sodium concentration: 113 mEq/L). Our study revealed the following: (1) Despite dramatic hyponatremic encephalopathy (convulsions, coma), hypoxia (PO2 < 70 mm Hg) was present, but the PO2 was not decreased below 40 mm Hg. All of these rats died rapidly if they remained hyponatremic. (2) In the animals rescued by NaCl, the incidence of brain myelinolysis was low (10%), whatever the duration (pure acute or chronic plus acute) of the hyponatremia and despite the combination of hypoxia with major hyponatremic encephalopathy. (3) When acute hyponatremia is superimposed on a chronic preexisting hyponatremic state, the acute component of serum sodium concentration decrease could be rapidly corrected (serum sodium concentration: +35 mEq/L/21 hr) without fear of permanent brain damage. Our results suggest that even in the presence of dramatic hyponatremic encephalopathy and associated hypoxia, neuropathologic sequelae are uncommon. Brain lesions related to post-anoxic encephalopathy probably develop only after respiratory arrest occurs.

DDAVP-related hyponatremia induces a blood volume expansion, but the analysis of fluid distribution in the vascular compartment has given controversial results in previous animal and human studies. In 5 healthy males, hyponatremia was induced by DDAVP and a free water intake during 3 days. Serum sodium concentration decreased from 138 +/- 0.8 mEq/L to 123 +/- 2.7 mEq/L on day 3. The plasma volume measured by dilution of marked albumin rose from 3033 +/- 230 ml to 3320 +/- 295 ml (p < 0.01). The mean corpuscular volume measured by microhematocrit increased slightly from 91.5 +/- 3.8 pl to 92.6 +/- 3.7 pl (p < 0.02). The red blood cell volume calculated with hematocrit and plasma volume did not change significantly (2565 ml to 2567 ml; not significant). In the present work, we demonstrated that in males the expansion of the plasma compartment almost completely amounted for the water retention in the intravascular volume. The erythrocyte volume increased only slightly, a finding that is consistent with an almost perfect adaptation of the erythrocyte cells to the hypoosmolality.

The effects of acute and chronic water intoxication induced by the administration of oral water and arginine vasopressin (AVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) on blood acid-base equilibrium and aldosterone, corticosterone, and thyroxine secretion were studied in rats. Acute hyponatremia (3 hours) was associated with normal bicarbonate and blood acid-base equilibrium and a decrease in aldosterone and thyroxine concentrations, while corticosterone was increased. When similar levels of hyponatremia (serum sodium 110 mEq/L) were maintained for 24 or 72 hours, a normal serum bicarbonate concentration was observed, but blood acid-base equilibrium showed a mixed respiratory and metabolic alkalosis. Blood pH was negatively correlated with serum sodium concentration (R = -0.65; p < 0.001), as was the metabolic alkalosis (base excess; R = -0.64; p < 0.001) and the aldosterone concentration (R = -0.52; p < 0.01), while the PCO2 was positively correlated (R = +0.49; p < 0.01). Hyperaldosteronism was similar whether hyponatremia was induced with AVP or DDAVP and was observed even for mild hyponatremia. When hyponatremia was induced by a high water and salt intake (2.5% D-glucose, 0.45% NaCl; 15% body weight), aldosterone concentration was as high (about three times control values) as in rats with similar levels of hyponatremia but with a salt-free diet. The high salt intake was associated with a more severe metabolic alkalosis (base excess +5,5 mEq/L). In chronic hyponatremia, corticosterone and thyroxine values were normal. In hyponatremia related to syndrome of inappropriate secretion of antidiuretic hormone, the normal serum bicarbonate level is an expected observation; as in acute water intoxication, it stays normal.(ABSTRACT TRUNCATED AT 250 WORDS)