<i>Respiratory Alkalosis Accompanying Ammonium Toxicity</i>

Roberts, Kate; Thompson, F. Gregg; Poppell, J. William; Vanamee, Parker

doi:10.1152/jappl.1956.9.3.367

Cited by 43 publications

(6 citation statements)

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“…The possible clinical relevance of this adverse response to exogenous CO, is that cerebral function may be similarly impaired when a patient with liver failure is exposed to respiratory depressants, such as narcotic drugs (Loeschke, Sweel, Kough & Lambertsen, 19531, tranquilizers (Renzetti & Padget, 1957), certain diuretics (Goldring, Cannon, Heinemann & Fishman, 1968) and anaesthetic agents (Dripps & Severinghaus, 1955). These observations on the deleterious effects of increased cerebral PcoZ cast doubt on earlier suggestions that correction of alkalosis might be useful in treating liver disease (Roberts, Thompson, Poppell & Vanamee, 1956;Warren, 1958). On the contrary, the demonstration that artificially increasing the arterial pH in hepatic coma may be accompanied by clinical improvement as well as increases in cerebral blood flow and metabolic rate indicates that the extracellular alkalosis is probably beneficial.…”

Section: Discussionmentioning

confidence: 80%

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

et al. 1975

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1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.

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Section: Discussionmentioning

confidence: 80%

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

et al. 1975

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“…We also noted a slight elevation in arterial pH (7.44 _+ 0.01 before the infusion; 7.47 _+ 0.03 at the 60th min; 7.48 _+ 0.02 at the end). This last modification was seemingly linked to the hyperpnea which may have resulted from stimulation of the respiratory centre by the ammonium infusion [27].…”

Section: Arterial Blood Ammoniamentioning

confidence: 99%

Diabetogenic effect and inhibition of insulin secretion induced in normal rats by ammonium infusions

Schlienger¹,

Imler²,

Stahl³

1975

Diabetologia

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Summary. In order to explain the abnormalities of glucose metabolism previously observed in patients with blood ammonia elevation, the effect of a transitory hyperammonemia on I. V. glucose tolerance was investigated in rats. An I. V. glucose tolerance test was performed in 3 groups of 15 rats 60 min after the beginning of a 95 rain infusion of either a 2 ml isotonic NaC1 solution (control group) or ammonium acetate solutions at low (0.50 gmol/kg/min. NI-I4+ ) or high doses (1.70 ~tmol/kg/min NH4+ ). The "high" NH4+ infusion produced an increase of blood ammonia to levels near 1000 ~tg/100 ml, a significant decrease in the K coefficient for glucose disappearance (2.53 x 10-24-0.20 compared to 4.92 x 10 -a 4-0.13 in control group) and a suppression of the radioimmunological plasma insulin (I. R. I.) response to glucose.With the "low" NH 4 -/-infusion the hyperammonemia was less pronounced (200-300 gg/100 ml), but the decrease in K(3.02 x 10 -2 4-0.15) and in the first phase of I.R.I. release remained significant. The decrease in glucose disappearance rate could be accounted for by the proportional decrease in insulin secretion. Thus glucose intolerance induced by ammonium acetate infusions may be due to a direct effect of NI"I 4 "1-on the pancreas. These abnormalities in glucose metabolism depend on the quantity of infused ammonium.Key words: Rat, ammonium infusion, blood ammonia, glucose metabolism, plasma immunoreactive insulin.In 1955 Bessman et al [4] suggested that the neurotoxicity of hyperammonemia in porto-systemic encephalopathy results from a disturbance in cerebral glucose utilization. The observation, in hepatic coma, of a decrease in cerebral oxygen consumption [12,22] and an increase in some intermediates of glucose metabolism [11,35] supports this hypothesis. However the influence of variations in ammonium metabolism on the regulation of carbohydrate metabolism is still debated [10,34]. Recently, we noted that I. V. glucose tolerance was worse in cirrhotic patients with hepatic coma than in those without porto-systemic encephalopathy [30]. One factor which could explain this observation, was the increase in arterial blood ammonia which was consistently observed during hepatic coma. Thus we noted in both normal and cirrhotic subjects, infused with ammonium chloride or acetate, that a transitory elevation in arterial blood ammonia invariably brought about a very significant diminution in I. V. glucose tolerance [31] and an inhibition of the insulin secretion induced by the glucose load [32]. However, in these studies, we were unable to show any correlation between these anomalies and the blood ammonia levels. The aim of * Presented at the 9th Meeting of the European Association for the Study of the Liver. Hemsedal, Norway, september [6][7] 1974 the present study was to compare in normal rats the action of a moderate or gross hyperammonemia on glucose tolerance and insulin secretion. Material and MethodsThree groups of 15 male Wistar rats, weighing 250-300 g and fasted for 20 hours, were used. Afte...

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“…Peripheral reflexes from the lungs stimulating the respiration (34) have not been examined. Lacking evidence for other mechanisms, most workers who have studied the problem (11,32,35) speculate that the hyperventilation of cirrhosis arises centrally, presumably from biochemical stimulation of respiratory center neurons.…”

Section: Normal Valuesmentioning

confidence: 99%

The Toxic Effects of Carbon Dioxide and Acetazolamide in Hepatic Encephalopathy *

Posner¹,

Plum²

1960

J. Clin. Invest.

173

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Respiratory Alkalosis Accompanying Ammonium Toxicity

Cited by 43 publications

References 0 publications

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

Diabetogenic effect and inhibition of insulin secretion induced in normal rats by ammonium infusions

The Toxic Effects of Carbon Dioxide and Acetazolamide in Hepatic Encephalopathy *

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