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Biomedical subjects

K Silberbauer

Publications and source records attributed to K Silberbauer.

At least 19 recordsLinked to original sources
PubMed1992

Efficacy, safety and tolerability of lovastatin and bezafibrate retard in patients with hypercholesterolemia.

Hyperlipidemia has turned out to be the most important risk factor for coronary heart disease and necessitates frequently lipid lowering long-term treatment. Therefore, efficacy and tolerability of hypolipemic drugs are of great interest. The objective of the present study was to compare the safety, tolerability and effect on plasma lipids of Lovastatin and Bezafibrate retard in patients with hypercholesterolemia. 99 patients with total cholesterol of > or = 250 mg/dl after a 4 week standard lipid-lowering diet were treated another 4 weeks with placebo and then randomized to 400 mg Bezafibrate retard or 20 to 80 mg Lovastatin given once a day for 12 weeks. Mean changes from baseline in total cholesterol, LDL cholesterol and triglycerides were significantly reduced, in HDL cholesterol increased in both treatment-groups (p < or = 0.01). The effects of Lovastatin on total cholesterol and LDL cholesterol were more pronounced than those of Bezafibrate retard (p < or = 0.01), while Bezafibrate had a larger effect on triglycerides (p < or = 0.05). The frequency of clinical adverse experiences was low and similar among treatment groups, the frequency of laboratory adverse experiences was higher in the Lovastatin group. One patient in the Bezafibrate group was withdrawn because of nausea, one patient in the Lovastatin group because of GGT elevation.

Adult↗
PubMed1992

[Acute management of myocardial infarct patients in Austria (cross-sectional study of 8 intensive care units)].

8 Austrian Intensive Care Units provided data from 6,317 cases (including 1,667 cases with acute myocardial infarction) admitted during 1990 and 1991 for a documentation system offered by the Austrian Heart Foundation. Significant differences were observed between the units concerning admission policies and the use of diagnostic methods. 71% of the AMI cases were first infarctions, 10% were Non-Q-infarcts. The median of the prehospital period varied between 2.5 and 6.5 hours. The evaluation of the admission mode showed that on average 42% of the AMI cases had contact to their G.P. before hospital admission, this figure varying, however, between 24 and 90% in different areas. It seems that this contact takes place to a much lower extent in big cities. On average G.P. contact before hospital admission in AMI resulted in doubling of the duration of the prehospital period. Thrombolytic treatment was applied in 24.7% of AMI cases with a variation between 13.9 and 48.4% in the different centers. It is suggested that regular use of this kind of quality control should offer means for optimizing the acute care of infarct patients on a regional and on a national level.

Adult↗
PubMed1979

[Monoclonal gammopathy and platelet function (author's transl)].

This study of 20 patients with monoclonal gammopathy (17 patients with multiple myeloma and 3 patients with Waldenström's syndrome) showed a decreased platlet aggregation induced by ADP and collagen, a reduced platlet retention and a prolonged bleeding time in 25% of the cases in comparison with 30 age- and sex-matched healthy controls. Using Wu and Hoak's technique as increased number of reversible platelet aggregates was observed. There was no relationship between the parameters of primary haemostasis and protein analysis. A disturbed mechanism of primary haemostasis is the main factor responsible for the bleeding diathesis in patients with monoclonal gammopathy.

Aged↗
PubMed1979

Platelet adhesion and platelet thrombus formation on subendothelium of human arteries and veins exposed to flowing blood in vitro. A comparison with rabbit aorta.

Subendothelium of blood vessel segments from elderly patients was exposed in a perfusion chamber to citrated blood under arterial blood flow conditions. The resulting platelet adhesion and thrombus formation was assessed morphometrically. The results show that the time course and the extent of platelet adhesion and aggregation were similar to the results obtained previously with subendothelium from rabbit arteries. The extent of surface-induced platelet aggregation was furthermore governed by both the properties of the exposed surface as well as those of the blood perfusate. No significant differences with regard to platelet reactivity were found between veins and arteries and the extent of surface-induced platelet aggregation was rather low.

Animals↗
PubMed1979

[Physiopathology of prostaglandin I2 synthesis in the human gastrointestinal mucosa].

1. PGI2 is synthetized in human gastrointestinal mucosa. 2. PGI2 seems to be responsible for pathophysiological conditions. 3. Disorders caused by an enhanced or diminished PGI2-synthesis could be treated in the future by inhibition of prostacyclin synthetase or exogenous synthetic PGI2 respectively. 4. In order to remove the problems with the unstable PGI2, synthetic analogs could be used for the treatment.

Adult↗
PubMed1979

Prostacyclin activity in rat kidney stimulated by angiotensin II.

Prostacyclin (PGx, PG12) activity can be found in renal tissue as indicated by platelet aggregation inhibition. The activity of the medullary tissue in terms of wet weight is significantly higher (P less than 0.01) than that of cortex. The activity decreases with time and has almost entirely gone within 1 h. Boiling for 30 s destroys the inhibitory effect of the prostacyclin on platelet aggregation. Angiotensin II is able to stimulate the prostacyclin availability of the tissue after incubation for 3 min. Addition of angiotensin II to platelet-rich plasma (PRP) has no significant effect on ADP-induced platelet aggregation. The spontaneous generation of prostacyclin as well as that stimulated by angiotensin II can be suppressed by previous incubation of the tissue with a prostaglandin synthetase inhibitor such as ketoprofen. Tissues which have only a small amount of basal release in buffer show an increased platelet aggregation inhibitory effect after addition to PRP. The difference between medulla and cortex is statistically significant. This different release of prostacyclin cannot be related to different endothelial surface area, because the endothelial surface in medulla and cortex is quite similar. It is suggested that prostacyclin has an important influence on the renal function. The different capacity of renal medulla and cortex in generation of prostacyclin could be of great importance for a fuller understanding of the physiology of renal function.

Angiotensin II↗