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M Imler

Publications and source records attributed to M Imler.

At least 109 records · Page 6Linked to original sources

[Present-day therapy of hepatic encephalopathy (author's transl)].

The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia formation in the intestinal tract. Equally important is the correction of the hypopotassemia, which may lead to a renally induced hyperammonemia. At the same time, disorders which favor the cerebral toxicity of ammonia, especially anemia and hypoxias, must be compensated. These various measures have improved the prognosis for hepatic encephalopathy of the cirrhosis patient, but were without effect on the course of the coma in severe toxic hepatitis. During the last toxic hepatitis. During the last 10 years, many treatment methods have been reported whose efficacy, however, could not be proved.

Acid-Base Imbalance↗

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

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 min infusion of either a 2 ml isotonic NaCl solution (control group) or ammonium acetate solutions at low (0.50 mumol/kg/min. NH4+) or high doses (1.70 mumol/kg/min NH4+). The "high" NH4+ infusion produced an increase of blood ammonia to levels near 1000 mug/100 ml, a significant decrease in the K coefficient for glucose disappearance (2.53 X 10(-2) +/- 0.20 compared to 4.92 X 10(-2) +/- 0.13 in control group) and a suppression of the radioimmunological plasma insulin (I.R.I.) response to glucose. With the "low" NH4+ infusion the hyperammonemia was less pronounced (200-300) mug/100 ml), but the decrease in K(3.02 X 10(-2) +/- 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 NH4 + on the pancreas. These abnormalities in glucose metabolism depend on the quantity of infused ammonium.

Acetates↗