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Biomedical subjects

M Imler

Publications and source records attributed to M Imler.

At least 91 records · Page 5Linked to original sources
PubMed1979

An automated microassay for blood ammonia.

A microassay for blood ammonia has been developed. After dilution, blood is dialyzed by a continuous flow procedure, and the ammonium ions in the dialysate are assayed colorimetrically by the hypochlorite-phenol Berthelot reaction. Concentrations from 1 to 400 mumol/l NH+4 can be measured in a 50 mul whole blood sample. Using slight modifications, concentrations up to 800 mumol/l NH+4 can be determined. The precision, accuracy, sensitivity, and specificity of the method have been studied. In man, the usual values (mean +/- 2 SD) found are 27.4 +/- 10.2 mumol/l NH+4 in arterial blood, 20.9 +/- 9.8 mumol/l in venous blood. The usual values in rats and mice are very close to those given for man.

Amino Acids↗
PubMed1979

[Changes in cephalic and peripheral use of glucose and glutamine under the influence of hyperammonemia in rats].

Arterio-venous differences of glucose and glutamine were determined across the brain and across the hind limb in normal and ammonium salt infused rats, before and during an insulin tolerance test, in an attempt to study the effect of hyperammonemia on cephalic and muscular metabolism. The results demonstrate that 1) hyperammonemia reduces the hind limb uptake of glucose without affect the cephalic uptake of glucose which is lowered during hypoglycemia, 2) the reduction of the cephalic and muscular glutamine output induced by the hypoglycemia is masked in presence of an hyperammonemia. In conclusion, it may be assume that, at the concentration obtained in this study, hyperammonemia does not act directly in the pathogenesis of hepatic coma in which a decrease in cerebral glucose uptake described; on the other hand, ammonium plays an important role in the muscle metabolism.

Ammonia↗
PubMed1979

Effects of biguanides on the intermediate metabolism of glucose in normal and portal-strictured rats.

Phenformin and metformin treatments may be complicated by lactic adidosis. This metabolic complication seems favoured by preexistent hepatic disease. We have therefore compared the metabolic effects of phenformin and metformin on non fasting normal and portal-strictured rats. The latter group is characterized by impaired hepatic passage of these drugs without hepatocellular lesions. Given orally to normal rats over 5 days, phenformin (20 mg/kg/24 h) and metformin (150 mg/kg/24 h) decreased blood glucose levels and increased blood urea and the substrates of gluconeogenesis (alanine, glutamine, lactic and pyruvic acids), effects more apparent with phenformin than metformin. In non-treated portal strictured rats, blood glucose levels were lower and the intermediate metabolites were higher than in noraml rats, suggesting a modification of gluconeogenesis. Treatment of the portal strictured group by phenformin or metformin induced no changes in the studied parameters. This absence of effect of the biguanides in portal strictured rats supports the postulate that, in normal rats, biguanides act principally on hepatic metabolism by reducing gluconeogenesis and that, in the absence of other hepatic damage, the presence of a peri-hepatic shunt, which, by itself, modifies gluconeogenesis, does not further predispose to lactic acidosis during short term administration of biguanides.

Alanine↗
PubMed1979

Hyperammonemia following ureterocolostomy in the rat.

Following ureterosigmoidostomy, encephalopathy with hyperammonemia may occur in the presence of cirrhosis, and the same complication was also observed in a few patients without liver damage. This suggests overloading of normal liver ureagenisis by an increased portal ammonia supply. To test this hypothesis and to try to produce an experimental model of chronic hyperammonemia without portal or hepatic damage, ureterocolostomies were performed in rats. These rats were compared with sham operated upon rats and with rats having chronic uremia induced by subtotal nephrectomy. Rats having a ureterocolostomy had chronic, but moderate, systemic hyperammonemia without any histologic hepatic damage and without gross behavioral modifications and slight uremia with only inconstant pyelonephretic lesions. In these rats, hyperammonemia results from hepatic overloading by the increased portal ammonia supply which is a consequence of both intestinal absorption of some urinary ammonia and increased intestinal ammoniagenesis induced by hydrolysis of urinary and circulating urea.

Ammonia↗
PubMed1979

The effect of chronic uremia on portal and systemic ammonemia in normal and portal-strictured rats.

It is commonly assumed that the uremia occurring in cirrhotic patients leads to hepatic encephalopathy by means of hyperammonemia produced by bacterial hydrolysis of urea in the digestive tract. Therefore the effect of an increase in circulating urea on portal and systemic blood ammonia levels was investigated in normal rats and in rats with a strictured portal vein. It was shown that moderate chronic uremia, produced by subtotal nephrectomy, significantly increases both portal blood ammonia levels in normal rats and the systemic hyperammonemia resulting from portosystemic shunts in portal-strictured rats. In the latter group, despite a prolonged systemic hyperammonemia of around 400 micrograms/dl, no obvious behavioral modification could be observed, but a significant slowing of the growth rate occurred. This slowing, however, was not correlated with the systemic blood ammonia levels.

Ammonia↗
PubMed1978

[Insulin secretion in alcoholic hepatopathy: analysis by measurement of C-peptide (author's transl)].

Basal and reactive peripheral hyperinsulinism recorded in alcoholic hepatic disease may result from decreased hepatic breakdown or pancreatic hypersecretion. C-peptide (CPR) and insulin (IRI) concentrations were measured in 3 groups of 8 alcoholic patients--steatosis, compensated and decompensated cirrhosis--and compared with 8 normal subjects in order to determine the importance of these two possibilities. At basal state, the molar ratio CPR/IRI was near the normal (8.7 +/- 0.9) but is diminished in the 8 hyperinsulinaemic patients (5.9 +/- 0.6). After i.v. glucose tolerance test and tolbutamide stimulations, an hyperreactivity of IRI and CPR may be noted in cirrhotics. A relative insensitivity of the B-cell to glucose appeared after comparison with the effect of tolbutamide. Thus basal hyperinsulinism resulted of decreased hepatic breakdown and stimulated hyperinsulinism resulted of hypersecretion. Glucose intolerance and anomalies of the insulin secretion were more apparent with severe hepatic disease.

Adolescent↗
PubMed1978

The effect of glucose oral administration on hyperammonemia in cirrhotics.

In order to investigate the controverted effect of glucose on hyperammonemia the diet of eight advanced cirrhotics was supplemented hourly, between 9 a.m. and 5 p.m., with 20 g of glucose orally. Plasma insulin and arterial and median cubital venous ammonia levels were measured hourly and the results were compared to those of a control test performed in the same patients without glucose supplementation. In the control test the lunch (protein meal) induced an identical rise in arterial and venous ammonia levels (+40 +/- 3 and +36 +/- 5 microgram/100 ml, respectively). With glucose supplementation plasma insulin rose significantly and the arterial ammonia increase produced by lunch (+42 +/- 3 microgram/100 ml) did not differ from that observed in the control test; but the rise in venous ammonemia was lower (+12 +/- 4 microgram/100 ml; p less than 0.01) with a significant increase in arterio-venous ammonia difference. These results suggest that oral glucose administration increases the peripheral muscular ammonia uptake through a mechanism which remains to be elucidated but which is inefficient for arterial hyperammonemia.

Ammonia↗
PubMed1978

[Effect of protein deprivation on ammonia metabolism in the rat].

In order to investigate the mechanisms of the hyperammonemia previously described in protein deprivation, the effects of sucrose and fasting on the ammonia metabolism were studied in control, streptozotocine-induced diabetics and colectomized rats. Hyperammonemia, hyperglutaminemia, hypouremia and intolerance to an ammonium load were observed in the control group after a 5 days sucrose-feeding. Any of these abnormalities were found in the diabetic animals whereas hyperglutaminemia did not occur in colectomized animals. It is concluded that protein deprivation obtained by sucrose feeding involves an hyperammonemia by a reduction of ureogenesis (which seemed to be related to an elevation of the ratio insulin/glucagon) and an hyperglutamininemia of colic origin.

Ammonia↗
PubMed1978

[Prolonged fever revealing acquired toxoplasmosis in an adult].

Two cases of acquired toxoplasmosis are reported in 16 and 44 year old patients; prolonged fever was the dominating sign in both cases. It follows from these observations that toxoplasmosis has to be systematically considered as a possible etiology of prolonged fever of undetermined origin.

Adolescent↗
PubMed1978

[Alterations in thyroid hormones and thyrotropin response to TRH in cirrhotic patients with or without hyperammonemia (author's transl)].

Serum concentrations of thyroid hormones and TSH response to TRH are studied in normal controls and in patients with liver cirrhosis. T3 levels are significantly diminished in the cirrhotic group while the mean total T4 concentration, the basal TSH and the magnitude of the peak response to TRH are similar in cirrhotic and control patients. However when the cirrhotic patients are separated in two groups according to the level of arterial ammonemia, it appears that the group with hyperammonemia (n = 10) has a significantly higher peak response than the control group. Since hyperammonemia is a wittness of hepatic encephalopathy it is suggested that TSH release or synthesis may be modified by this situation resulting from a cerebral accumulation of false neurotransmitters and a depletion of aminergic mediators.

Ammonia↗
PubMed1978

Enzymic micro-assay for blood glutamine.

Blood glutamine is hydrolyzed by glutaminase; the resulting ammonia is dialyzed out and measured by use of a continuous-flow colorimetric microassay. Concentrations in the range of 10 to 1300 micromol of glutamine per liter can be determined in a 40-microliter sample. With slight modifications, higher concentrations, up to 5 mmol/liter, can be measured. Assay conditions and the qualities of the microtechnique were made optimal. Usual values obtained with this method for arterial and venous blood in man are, respectively, 443 +/- 140 and 466 +/- 142 micromol/liter (mean +/- 2 SD). Corresponding values for rats are 320 +/- 92 and 340 +/- 108 micromol/liter. Fasting causes a decreased blood glutamine.

Adult↗
PubMed1977

[Hyperammonemia and hepatic encephalopathy in cirrhotics receiving spironolactone (author's transl)].

The aim of this study was to specify the mechanism of hepatic encephalopathy which may occur in some cirrhotics treated by Spironolactone. In 31 cirrhotics with ascite, this diuretic induced a significant increase in arterial ammonemia; 8 patients developed an impending hepatic coma which was associated with ammonemia levels significantly higher than those observed in the patients without encephalopathy at the end of the treatment. Hyperammonemia induced by Spironolactone does not result from a muscular, renal or hepatic ammonia production but seems related to an increased intestinal ammoniagenesis which which is secondary to the bacterial hydrolysis of urea in the colon; indeed, there is a significant correlation between the ammonemia increase and the simultaneous rise in blood urea during treatment.

Adult↗
PubMed1977

Hepatic origin of hyperammonemia induced by shock in normal rats.

This study was undertaken in order to see whether instability in blood ammonia levels frequently observed in the anaesthesized rat could be explained by variations in blood pressure. In normal Wistar rats, anaesthesized with sodium pentobarbital, a bleeding of 1 ml/100 g body weigth produced in a few minutes a significant decrease in blood pressure and a significant increase in arterial blood ammonia level. With the blood pressure normalization following the blood reinfusion this hyperammonemia decreased but reappeared at high levels after a second and a third bleeding. The shock produced by an occlusion of the inferior vena cava above the renal veins gave similar results. The arterial hyperammonemia induced by shock did not result from muscle or renal ammonia production but is related to impaired hepatic uptake of portal ammonia. These results indicate that in the rat the blood pressure stability is a necessary precondition in any experiment on ammonia metabolism.

Ammonia↗