Biochemical Observations on the Use of L-Glutamic Acid in the Treatment of Hepatic Coma

Iber, Frank L.; Chalmers, Thomas C.; Stowers, Barbara; Fryar, Albert; Link, Anna Marie

doi:10.1172/jci103473

Cited by 26 publications

(3 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, if an increased ammonium load to the systemic circulation were to initiate NH4-N removal in the extremities only by increasing the arterial NH4-N concentration, one would expect large arteriovenous NH4-N differences across the extremities and brains of all patients having markedly ele- trasted to venous) might affect the amount of ammonium recovered during analysis. For instance, some investigators suggest that the ammonium concentration in blood is proportional to its oxygen content (35,36). However, a patient with cor pulmonale studied in this laboratory did not demonstrate significant fluctuations in arterial blood NH4-N concentrations when his arterial oxygen saturation was increased in vivo from 28 to 88 per cent (Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Ammonium Uptake by the Extremities and Brain in Hepatic Coma, 12

Webster¹,

Gabuzda²

1958

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Ammonium Uptake by the Extremities and Brain in Hepatic Coma, 12

Webster¹,

Gabuzda²

1958

J. Clin. Invest.

View full text Add to dashboard Cite

“…Various investigators have used glutamate in the therapy of hepatic coma with varying reports as to its success or failure (21)(22)(23)(24). However, even in those instances in which the patient did not respond clinically, the blood ammonia levels usually fell during or shortly after glutamate administration.…”

Section: Discussionmentioning

confidence: 99%

Blood Ammonia Levels Following the Ingestion of Casein and Whole Blood1

Bessman¹,

Mirick²

1958

J. Clin. Invest.

View full text Add to dashboard Cite

In the recent past, much attention has been focused on the role of ammonia in hepatic coma. A relation between gastrointestinal bleeding and the precipitation of hepatic coma has been noted (1, 2). Various substances have been administered into the gastrointestinal tract, such as urea, ammonium chloride, exchange resins of the ammonia cycle, high protein feedings, and blood (3-7), all of which can produce elevated blood ammonia levels and precipitate hepatic coma in susceptible individuals. The implicit assumption, if not explicit expression, in these various studies, has been that all of these substances are more or less equally noxious agents in regard to elevating blood ammonia and causing the concomitant neurological changes. The problem of irreversible coma in patients with liver disease following gastrointestinal bleeding is frequently found; yet high protein diets are standard fare in the treatment of cirrhosis, and relatively infrequent catastrophies result. We have compared the relative effect of the ingestion of protein derived from blood as compared to protein derived from casein and milk solids (Protenum®) on the blood ammonia and nonprotein nitrogen (NPN). METHODS

show abstract

“…The lack of correlation between venous ammonia values and the presence and severity of symptoms,'l7 [32][33][34][35][36] be related to muscle uptake, pH change or to enzyme alteration and adaptation.…”

Section: Patient Niaterial and Methodsmentioning

confidence: 99%