Effect of induced metabolic alkalosis in hepatic encephalopathy.
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1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2-5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12-0.94) nmol/l and of adrenaline was 0.15 (0.05-0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2-3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12-0.86) nmol/l] or that of adrenaline [0.16 (0.05-0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6-13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79-2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20-2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.
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To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,
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