Studies on Renal ammonia metabolism in Hypoxia.I. Urinary acidification in hypoxia

Abstract

Many reports are available concerning to the effects of hypercapnea on acid-base disorder complicated with neonatal respiratory distress syndrome, severe bronchial asthma, cardiac failure and so on. But little was known as to the effects of hypoxia on these states, especially in respect to the renal buffer action. According to the study reports of AkashP of our labolatory, urinary hydrogen ion excretionn was delayed as a result of the decreased renal and cellular buffer action which probablly causedd by the intracellular accumulation of lactate in hypoxiad This study was undertaken to investigate the mechanism of the impaired renal buffer action in hypoxia. In the present study, the urinary acidification in response to oral ammonium chloride (NH4C1) load was examined in the patients with cyanotic or non-cyanotic heart disease The increment of urinary net acid excretion was decreased in cyanotic patients, The total urinary ammonia excretion in 42 hours after acid load was decreased by 28e 9 mmoles in cyanotic patients compared with 39.0 mmoles in non-cyanotic patients, although titratable acid. (TA), total CO₂ content and pH were not significantly different between the two groups. Following these studies, the urinary acidification was examined in rats with control, hypoxia (10% 02+90% N₂ gas inhalation), metabolic acidosis (HC1 administration iv.) and metabolic acidosis+hypoxia. In metabolic acidosis, ammonia and TA excretion increased and total CO₂ content decreased soon after HCl administration, while ammonia excretion was not sufficiently increased in metabolic acidosis 1- hypoxia Changes of pH and electrolytes of these 4 groups showed decreased pH, potassium con-centration (K) and increased sodium concentration (Na) in tissue level, while pH, Na decreasedd and K increased in blood level, and urinary Na reabsorption, K excretion decreased in hypoxiaa and metabolic acidosis+ hypoxia, as most likely in decreased activity of aldosterone. We concluded that impaired urinary acidification in hypoxia was due to the inability of the kidney to excrete sufficient amount of ammonia into the urine.