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Biomedical subjects

D Brachtel

Publications and source records attributed to D Brachtel.

At least 19 recordsLinked to original sources
PubMed1993

Caffeine elimination in cirrhotic and non-cirrhotic liver disease of different etiology.

Caffeine elimination was studied in 419 patients with cirrhotic and noncirrhotic liver disease of different etiology (hepatitis B virus infection n = 79; hepatitis NANB virus infection n = 74; ethanol-induced liver damage n = 143; primary biliary cirrhosis I-IV n = 63; cryptogenic liver cirrhosis n = 60) following oral administration of 366 mg caffeine. Caffeine clearance in the control group was 69 +/- 33 ml/min (age-matched healthy volunteers and patients without liver disease). Caffeine clearance in acute hepatitis B (70 +/- 60 ml/min) chronic persistent hepatitis B (81 +/- 56 ml/min), chronic aggressive hepatitis B (107 +/- 66 ml/min), posthepatitic liver cirrhosis B (84 +/- 62 ml/min), acute hepatitis NANB (94 +/- 69 ml/min), chronic persistent hepatitis NANB (122 +/- 60 ml/min), chronic aggressive hepatitis NANB (87 +/- 52 ml/min) and posthepatitic cirrhosis NANB (59 +/- 26 ml/min) is not reduced in comparison with controls. In patients with alcoholic fatty liver (127 +/- 71 ml/min, p < 0.05) caffeine clearance is enhanced, in alcoholic hepatitis (57 +/- 72 ml/min) comparable to controls and in alcoholic cirrhosis reduced (36 +/- 44 ml/min, p < 0.05). In primary biliary cirrhosis I-IV caffeine clearance is higher than in controls (117 +/- 59 ml/min, p < 0.05). In cirrhotic liver disease of different origin caffeine clearance is inversely related to the serum bilirubin level. However, the absolute value is determined in addition by the underlying disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Renin-angiotensin system, blood pressure homeostasis and renal function in galactosamine-induced fulminant hepatic failure in the guinea pig.

Arterial blood pressure, renal function and plasma concentrations of renin and renin substrate (angiotensinogen) were investigated in guinea pigs subjected to galactosamine-induced (1 g/kg i.v.) liver cell necrosis. Blood pressure declined continuously by 50% during a follow-up period of 72 h which was associated with a decrease in diuresis and natriuresis to 36 and 31%, respectively. Simultaneously, plasma renin concentration increased 30-fold indicating marked reduction of renal perfusion, while plasma renin substrate concentration fell to 6% of the baseline level. There was microscopic evidence of oligemic circulatory renal damage characterized by acute proximal tubular necrosis with concomitant tubular dilatation. Short-term infusion of homologous renin substrate-enriched plasma, derived from nephrectomized animals, was followed by marked increase in mean arterial blood pressure from 34 +/- 9 to 77 +/- 7 mm Hg accompanied by marked diuresis and natriuresis. Renin substrate depletion following galactosamine-induced fulminant liver failure may represent impaired hepatic biosynthesis as well as increased renin substrate consumption due to excessive renin secretion. Angiotensinogen repletion has a beneficial effect on both renal function and blood pressure probably due to marked generation of the potent vasoconstrictor angiotensin II which consequently inhibits renin secretion. These observations strongly support the suggestion that the renin-angiotensin system is of major importance to cardiovascular homeostasis in acute liver failure.

Angiotensinogen↗
PubMed1988

[One point determination of oral caffeine clearance in patients with liver diseases].

Caffeine clearance has been determined in 117 volunteers and patients (including 27 patients with liver cirrhosis) after oral application of 366.1 mg caffeine according to conventional pharmacokinetic methods (Cl = D/AUC). The resulting clearance values can be estimated with adequate accuracy from the plasma concentration at 12h for a concentration range of 2.0 to 6.5 mg/l according to Cl max = Doses/C 12h x t 12h x e and for concentrations higher than 6.5 mg/l according to Cl = Vd x (1n (D/Vd) - 1n C 12h/t 12h Vd is estimated from body weight as Vd = 0.42 x BW. "One - point" - estimation does not provide reliable data for plasma concentrations below 2.0 mg/l.

Administration, Oral↗
PubMed1988

Effect of altered gastric emptying on caffeine absorption.

The effect of altered gastric emptying on caffeine absorption (tablets; 366.1 mg) was studied in patients with gastric stasis or after Billroth II partial gastrectomy with adequate gastric emptying and in healthy subjects with slowed gastric emptying due to a fibre-free and a fibre-rich liquid test meal of an elemental diet, respectively. Compared with controls (n = 15), a significantly slowed caffeine absorption was found in gastric stasis (n = 8) by means of a lower absorption rate constant KA (0.018 +/- 0.007 vs. 0.122 +/- 0.110 min-1 in controls) and a prolonged peak time tmax (160 +/- 77 vs. 46 +/- 19 min). Similar results were obtained after a fibre-free and a fibre-rich liquid test meal, respectively (n = 8 and n = 8, respectively; KA 0.035 +/- 0.01 and 0.035 +/- 0.023 min-1, respectively; tmax 91 +/- 24 and 93 +/- 23 min, respectively vs. KA 0.10 +/- 0.06 min-1 and tmax 50 +/- 14 min in controls; n = 7). After B II with adequate gastric emptying (n = 11) the absorption rate was within the normal range. The significantly lower average of the peak concentration cmax and of the area under the serum concentration-time curve x elimination rate constant (AUC x KE) in gastric stasis (5.9 +/- 1.8 micrograms/ml and 8.9 +/- 3.2 mg/l, respectively) and after B II partial gastrectomy (8.8 +/- 2.6 micrograms/ml and 10.8 +/- 3.0 mg/l, respectively) compared with controls (17.7 +/- 9.4 micrograms/ml and 20.8 +/- 10.7 mg/l respectively) probably reflect reduced bioavailability, which is apparently unchanged after a liquid test meal.

Caffeine↗
PubMed1986

[Galactosamine-induced acute liver failure in the guinea pig--spontaneous course and controlled study conditions].

The spontaneous course of the galactosamine-hepatitis in the guinea-pig (750 and 1000 mg/kg GalN iv respectively) is characterized by a terminal hypoglycemia together with hypothermia and arterial hypotension fifty-nine hours on average after GalN-application. Preventing hypoglycemia and hypothermia by continuous intravenous infusion of a glucose solution and by increasing room temperature, the animals do not develop hepatic coma, but show an increasing disturbance of the righting reflex and survive at least seventy-two hours. Plasma biochemical tests and liver histology reflect severe hepatic damage. A twofold increase of the liver weight is caused by raised water and lipid content combined with a concomitant depletion of liver glycogen. Pharmacological studies with 14C-Pentobarbital result in a distinctly diminished clearance and in a prolonged half life while the cytochrome P-450 content of the liver shows a moderate decrease. In animal models of acute liver failure the possible incidence of hypoglycemia, arterial hypotension and hypothermia should be considered.

Acute Disease↗
PubMed1977

[Metabolism of hexobarbital in patients with acute hepatitis and cirrhosis (author's transl)].

16 patients with acute hepatitis, 18 patients with cirrhosis and a total of 21 volunteers and patients with normal liver function received 7.32 mg/kg hexobarbital by linear intravenous infusion within 60 min. Hexobarbital was determined gaschromatographically in serial blood samples and the hexobarbital-clearance was calculated from the plasma concentration curve versus time. Additional experiments were performed in rats suffering from so called "galactosamine hepatitis". In half of the patients with acute hepatitis a normal hexobarbital clearance could be found. In the other patients this was distinctly reduced but not correlation was found to other liver function tests. Patients with cirrhosis were subdivided into two groups. The patients in group 1 were well compensated. The patients in group 2 had a decompensated state with ascites and oesophageal varices. In nearly all patients with cirrhosis the hexobarbital-clearance was diminished. This was more pronounced in group 2. Ketohexobarbital excretion in healthy subjects was in the range of 40-60% of dose. Patients with acute hepatitis excreted only 10-20% of dose and patients with liver cirrhosis only about 5% of dose. In rats with "galactosamine hepatitis" hexobarbital clearance in vivo was distinctly reduced and this could be explained by diminished microsomal cytochrome p 45- and hexobarbital oxidation rate.

Acute Disease↗
PubMed1977

[Hexobarbital-oxidation in vivo and in vitro in rats after phenobarbital-pretreatment or after portacaval anastomosis (author's transl)].

Male rats were pretreated with phenobarbital for 5 days or received portacaval anastomosis 3 weeks before. Hexobarbital was applicated intravenously and hexobarbital plasma concentrations were followed up gaschromatographically in arterial blood samples. Hexobarbital clearance was calculated from the plasma concentration curve versus time. Liver microsomes were prepared and cytochrome P 450 and the hexobarbital oxidation rate was determined. After portacaval shunt the animals showed a small liver, a reduced cytochrome P 450 and diminished hexobarbital oxidation rate. Hexobarbital clearance in vivo was reduced, too. After phenobarbital pretreatment liver weight increased and cytochrome P 450 and hexobarbital oxidation rate were distinctly enhanced. The hexobarbital clearance in vivo were increased. Since the plot of hexobarbital clearance in vivo versus cytochrome P 450 or versus hexobarbital oxidation rate in vitro gave a good correlation, it is concluded that hexobarbital clearance in vivo may be a good estimate for hepatic cytochrome P 450 and hepatic hexobarbital oxidation rate.

Animals↗
PubMed1976

Influence of d-galactosamine hydrochloride on lipids and their fatty acid composition in plasma and liver of guinea pigs.

48 hrs after i.v. applications of 1 g/kg b.w. galactosamine hydrochloride to guinea pigs the total lipids of plasma, liver homogenate and isolated liver microsomes were extracted and separated by dialysis and thin-layer chromatography. The fatty acid fractions of total lipids (plasma), neutral lipids and total phospholipids (liver homogenate) as well as phosphatidylcholines and remaining phospholipids (liver microsomes) were analyzed by gaschromatography. In plasma the concentration of total lipids was unchanged in the galactosamine group. A slight decrease of the C16- and an increase of the C161- fatty acids were observed. In total liver homogenate neutral lipids increased 9-fold, and phospholipids 2.5 fold after galactosamine application. Specially there was a relative and absolute increase of the C16-, C16(1)-, C18(1)-, and C18(3)-fatty acids in the neutral lipids, whereas the C18- and C18(2)-Fatty acids were relatively diminished. Similar changes within the fatty acid fractions could be found to a minor degree in the phospholipids. 48 hours after application of galactosamine the phospholipid content in isolated liver microsomes increased about 2-fold. Likewise there was an absolute increase of nearly all fatty acid fractions as well in phosphatidylcholines as in the other phospholipids. In both phospholipid fractions the percentage of the C18-fatty acids decreased and a relative increase in C16-fatty acids was observed. Contrary to the findings in total liver, in the isolated microsomes predominantly saturated fatty acids (C16, C18) were found.

Animals↗
PubMed1976

[Continuous EEG monitoring and clinical chemical findings in poisoning from Death cap (Amanita phalloides) (author's transl)].

The changes in the EEG were put in relation to the clinical course and liver function tests in 3 cases of acute poisoning by Amanita phalloides. Within discrete disturbances of liver function, distinct paroxysmal changes and increased interspersion of epsilon waves in the EEG are already found on the second day after taking the fungi. The liver dystrophy developing in the later course, recognisable by Quick values below 2%, at first only produces a small increase in the EEG changes. On the 5th or 6th day, severe general changes in the EEG appear along with symptoms of confusion to delirium. At this time, no further deterioration of the laboratory findings were demonstrable, but on the contrary we already even found a distinct improvement in the liver function. With further continuous increase in the clotting factors, the EEG becomes increasing slower in the next 4 days and after surviving this stage, improves very quickly thereafter. Our findings show that in poisoning with Amanita phalloides, EEG changes may become manifest even before the appearance of psycho-pathological changes and do not correlate directly with the tangible technical liver function tests of the laboratory.

Adult↗