RESUMEN
Water immersion to the neck increases central blood volume and evokes a marked diuresis and natriuresis. The present study examined simultaneously effects of water immersion on activities of three endogenous systems thought to participate in sodium homeostasis: the sympathetic nervous system, the atrial natriuretic peptide system, and the renal dopa-dopamine system. Hourly urine collections and antecubital venous blood samples were obtained from 10 normal subjects before, during, and after sitting in a water-immersion tank for 3 h; four control subjects were studied while seated without immersion. Urine volume was increased by more than threefold after 1 h of immersion (from 1.2 +/- 0.2 ml/min at baseline to 5.9 +/- 0.7 ml/min, P less than 0.001) and peaked during the second hour. Urinary sodium excretion increased by more than twofold (from 103 +/- 17 mu eq/min at baseline to 196 +/- 36 mu eq/min at 1 h, P less than 0.001) and peaked during the third hour. Plasma levels and urinary excretion of norepinephrine (NE) and epinephrine were suppressed consistently during immersion (P less than 0.05). There was a marked, prompt, and sustained increase in plasma levels of immunoreactive atrial natriuretic factor (irANF) from 6.9 +/- 1.9 pg/ml baseline to 17.3 +/- 4.3 pg/ml at 1 h (P less than 0.001). Urinary excretion of dopa, dopamine, and 3,4-dihydroxyphenylglycol, a neuronal metabolite of NE, changed in a triphasic pattern, with decreased excretion during the first hour of immersion (P less than 0.01), small but consistent increases during the next 2 h, and decreased excretion, to below baseline, during recovery (P less than 0.01 for dopa and dopamine).(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Glándulas Suprarrenales/fisiología , Dihidroxifenilalanina/metabolismo , Dopamina/metabolismo , Inmersión , Sistema Nervioso Simpático/fisiología , Adulto , Factor Natriurético Atrial/sangre , Líquidos Corporales/metabolismo , Agua Corporal/metabolismo , Catecolaminas/sangre , Catecolaminas/orina , Dihidroxifenilalanina/orina , Dopamina/orina , Electrólitos/metabolismo , Humanos , Riñón/metabolismo , Masculino , Sodio/metabolismoRESUMEN
We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.