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Biomedical subjects

A Steuer

Publications and source records attributed to A Steuer.

31 records · Page 2Linked to original sources
PubMed1992

Oxidative modification of low-density lipoproteins and the inhibition of relaxations mediated by endothelium-derived nitric oxide in rabbit aorta.

1. The mechanism by which Cu(2+)-oxidized low-density lipoproteins (oxLDL) inhibit acetylcholine (ACh)-evoked relaxations mediated by endothelium-derived nitric oxide (EDRF) in rabbit aortic rings was investigated. The proposed role of lysophosphatidylcholine (LPC) in the inhibition was also studied. 2. The kinetics of lipid peroxidation of native low-density lipoproteins (LDL) from individual donors, as measured by changes in conjugated diene concentration, were related to the inhibitory effects of the resultant oxLDL. It was found that the more susceptible LDL was to oxidation, the greater the inhibition. 3. No correlation was found between the inhibitory effects of oxLDL and LPC content. 4. Synthetic 1-palmitoyl LPC produced an inhibition of ACh-induced relaxations and when added to precontracted rings evoked nitric oxide-mediated endothelium-dependent relaxation. This latter effect was not elicited by oxLDL. 5. Synthetic 1-palmitoyl (10 microM) had no effect on relaxations evoked by glyceryl trinitrate in endothelium-denuded aortic rings in contrast to the inhibition found previously for oxLDL. 6. Concentrations of oxLDL and phospholipase A2-treated LDL which inhibited relaxation contained very different LPC concentrations. Unlike oxLDL, the inhibitory effects of phospholipase A2-treated LDL preparations were independent of the donors and showed no lag period. 7. We suggest that there are differences in the mechanisms by which oxLDL and 1-palmitoyl LPC exert their inhibitory effects on relaxation. 8. The inhibition of relaxation by oxLDL (1-2 mg protein ml-1) was prevented by the presence of high-density lipoproteins (HDL; 1-2 mg protein ml-1).9. It is proposed that prevention of the inhibition of relaxation by HDL is consistent with the inhibitory factor(s) being lipophilic constituents of oxLDL. However, variations in the inhibitory effects of oxLDL preparations are not due to differences in their LPC content and factors other than LPC must contribute to the inhibition.

Animals↗
PubMed1991

[Thiamine deficiency as a cause of life threatening lactic acidosis in total parenteral nutrition].

Two patients aged 37 and 44 years developed life-threatening lactic acidosis following abdominal surgery and a period of about 3 weeks of total parenteral nutrition. Septicaemia and hypoxia were excluded as possible causes. Conventional treatment including high doses of buffer agents was unsuccessful. Thiamine (vitamin B1) depletion was suspected as the cause of the metabolic acidosis, and two doses of 400 mg thiamine were given. In both patients, the lactic acidosis improved immediately, and it disappeared following the second dose of thiamine. Both patients were subsequently discharged as symptom-free. As part of the pyruvate-dehydrogenase (PDH) complex, thiamine was capable of improving the life-threatening situation.

Acid-Base Equilibrium↗
PubMed1987

[Continuous Midazolam infusion for sedation of respirator patients].

UNLABELLED: Most intensive care (ICU) patients need pharmacological sedation during ventilatory support. The short-acting drug midazolam might be preferable to neuroleptic agents and opiates because of its anxiolytic and sedative properties. The dosage of a drug given in a continuous infusion is based upon knowledge of its clearance and of the function of concentration and effect. METHOD: A midazolam infusion (7.5 or 15 mg/h) was given to 16 patients receiving ventilatory support for 24 h. Clearance was estimated using the rule Cl = R/C (R = rate of infusion, C = concentration in steady state). To estimate the concentration of midazolam necessary for good sedation, the amount of supplementary injected neuroleptic during midazolam infusion was compared with that of the day before. Plasma cortisol and parameters of energy metabolism, electrolytes, and liver and kidney function were measured. RESULTS: Patients with disease of abdominal organs showed the lowest values for clearance (1.0-2.92 ml/min/kg). Some of the injured patients showed elevated values for clearance (3.0-21.36 ml/min/kg). Elimination half-life ranged from 1.5-50 h. Changes in intestinal perfusion or cardiac output might be responsible for the wide range. For good sedation, plasma midazolam concentrations had to be above 600 ng/ml. Plasma cortisol levels were not affected by midazolam, nor were metabolism, electrolytes, or liver and kidney function. CONCLUSION: Continuous infusion of midazolam is a useful way of sedation for ICU patients, but the wide range of clearance values must be considered.

Adult↗
PubMed1987

[Use of a computer program for statistical calculation of various research data in anesthesia].

A software package for statistical data analysis will be discussed. The program "Test" help also in the computer entry and storage of data. This database package is available for small Personal Computer with a capacity of 512 kB, working with a Disk Operating System (DOS). "Test" is a very simple and very fast working statistical package. The most important advantages of this system are: (1) Simple to work and to learn, (2) Simple data collection and processing, (3) Very fast data analysis and calculation, (4) Checking of test assumptions, (5) Detailed demonstrations of results both with a matrix printer and computer display.

Algorithms↗
PubMed1980

[The question of "lactate alkalosis": animal experiments and a case report].

The intravenous infusion of sodium bicarbonate causes an alkalosis and an increase of lactate concentration in excess of 10 mmol/l in the experimental animal. The causal relation of alkalosis and lactic acidemia is also found in patients. A case of a therapy resistant alkalosis is demonstrated where a blood pH of 7.5 to 7.6 was correlated to a blood lactate concentration of 5 to 10 mmol/l. The normalisation of alkalosis was accompanied by a normalisation of lactate concentration to values of 1 to 2 mmol/l. The causal relation of alkalosis and increased blood lactate concentration seems to be obvious. We conclude that alkalosis is counteracted by a metabolic compensation due to the non volatile and lactic acid. Hyperlacticacidemia, therefore, is not identical with acidosis.

Alkalosis↗
PubMed1978

[Insulin concentration in polytraumatized patients during infusion of glucose, fructose and sorbitol].

Serum insulin concentration was measured during infusion of glucose, fructose or sorbitol for several days in polytraumatized patients. The patients are divided in two groups, one group with normal glucose tolerance and a second group, where an extreme disturbance of the glucose utilization was found. In patients with normal glucose tolerance the glucose substitutes had the same metabolic effects as in metabolically healthy volunteers. In patients with disturbed glucose tolerance the glucose substitutes (fructose as well as sorbitol) effected an increase in blood glucose concentration and in serum insulin concentration. It is concluded that the increase in blood glucose concentration causes the increase in serum insulin concentration. Obviously, in a certain group of polytraumatized patients a "metabolic insulin resistence" exists. Therefore, glucose utilization is decreased despite an increase in serum insulin. In most cases the metabolic disturbance in these patients is mastered, if glucose substitutes are used instead of glucose as energy source. However, in many cases glucose can be administered only if insulin is given additionally.

Dietary Carbohydrates↗
PubMed1976

[Effect of amino acid infusions on fructose-induced chemical blood changes in intensive care patients].

Influence of the infusion of amino acid solutions on metabolic changes caused by parenteral nutrition with fructose. In eleven unconscious polytraumatized patients of the intensive care station, intravenous infusions with fructose (0.5 g/kg bodyweight and hour) were performed. During the last 24 hours of the 72 hours infusion period, amino acid solutions (1.0 g/kg bodyweight and 24 hours) were given in addition to fructose. The investigations were initiated after an eight hour "starvation period" preinfusion. During this time only electrolytes were given. For comparison 48 hours intravenous infusions with fructose (0.5 g/kg B.W. and hour) were performed with six healthy volunteers. In both groups of subjects the intravenous fructose was metabolized very well, renal losses were less than 2% of the whole amount given. Considering the metabolic healthy volunteers, the blood glucose concentration remained unaltered despite the high dosage carbohydrate infusion. The patients of the intensive care station showed a slight increase of blood glucose values which were elevated already before infusion. Additionally, during fructose infusions, the increase in blood lactate concentration was more pronounced in the intensive care patients than in healthy volunteers. However, in contrast to the healthy volunteers, no increase in serum bilirubin concentration and only a slight increase in serum uric acid concentration was observed in the intensive care patients, despite the high-dose fructose infusion for 72 hours. Additionally, the fructose-induced hypertriglyceridemia was of a minor degree in the intensive care patients. In volunteers the increase in triglyceride concentration was 200% in 48 hours, whereas only a 50% increase was observed in intensive care patients during 72 hours. The pronounced nitrogen sparing effect of fructose in healthy volunteers was not seen in the intensive care patients to the same degree. The most prominent side effect of the fructose infusions in intensive care patients was the strong decrease in serum phosphate concentration seen in some patients. The additional infusion of amino acid solutions lead to a further diminution of the slight alterations caused by fructose infusions. In conclusion, it can be stated that total parenteral nutrition with fructose and amino acid solutions is possible in intensive care patients without danger of side effects. However, it should be mnetioned that hyperalimentation can cause fatty liver.

Amino Acids↗