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R Katzenschlager

Publications and source records attributed to R Katzenschlager.

43 records · Page 3Linked to original sources
PubMed1992

Detailed evaluation of evoked potentials in Wilson's disease.

Detailed evoked potentials (EPs) were studied in 52 patients (28.7 +/- 11.9 years) with Wilson's disease (WD). Various peak latencies, interpeak latencies and amplitudes of somatosensory, auditory brain-stem and visual EPs were significantly abnormal in the group of 28 neurologically symptomatic patients as compared to controls. Interhemisphere latency and amplitude differences tended to be increased without reaching significance, indicating a symmetrical rather than focal subclinical brain involvement. Selected conduction times of at least 1 EP modality were prolonged in all 4 patients with severe, in 16 of 18 with moderate, in 4 of 6 with mild, and in 4 of 24 patients without neurological symptoms. Auditory brain-stem and somatosensory EPs were more frequently prolonged than visual EPs (more abnormalities with check sizes of 13 than 54 min of arc). Cortical somatosensory EPs correlated well (P much less than 0.01) with either Fz or earlobe reference.

Adolescent↗
PubMed1992

Synergism between PGE1-metabolites(13,14-dihydro-prostaglandin E1, 15-keto prostaglandin E1, 15-keto-13,14-dihydro-prostaglandin E1) and nitric oxide (NO) on platelet aggregation.

A synergistic antiplatelet effect between prostaglandins (PG), cAMP-stimulators and nitric oxide (NO), a cGMP-stimulator, has already been described. Data on a synergism between NO and the metabolites of PGE1, however, are lacking so far. We therefore tested the antiplatelet activity of the metabolites of PGE1 alone and their synergism with NO on human platelets of 8 healthy volunteers in vitro. 13,14-DH-PGE1 (ID 50 = 10.8 ng/ml platelet rich plasma (PRP)) was the only PGE1 metabolite inhibiting the ADP-induced platelet aggregation, its efficacy being 76.4% of the parent compound PGE1 (ID 50 = 8.25 ng/ml PRP). NO (ID 50 = 0.52 microM) also inhibited platelet aggregation. The combined addition of 13,14-dihydro-prostaglandin E1 (13,14-DH-PGE1) and NO caused an additive effect. The other PGE1-metabolites tested, 15-keto prostaglandin (15-K-PGE1) (ID 50 = 16.2. micrograms/ml PRP) and 15-keto-13,14-dihydro-prostaglandin(15-K-13,14-DH-PGE1) (ID 50 = 14.8 micrograms/ml PRP), neither had any relevant antiaggregatory capacity themselves nor a synergistic effect with NO. These findings could be of clinical relevance as a NO-synergism may occur not only with therapeutically administered PGE1 but also with its biologically active metabolite 13,14-DH-PGE1.

Adult↗
PubMed1992

[Risk factors of atherosclerosis--primary examination of Vienna employees].

In the course of an atherosclerosis intervention study, a basic medical check-up of 2105 out of 4800 employees of a Viennese banking house was carried out (37.1 +/- 11.0 years, 54.6% females). Apart from liver and kidney function parameters, an extensive lipid status was determined, the blood pressure was measured, and a cardiovascular-centered case history ascertained. The mean cholesterol level in females was 208.3 +/- 54 mg/dl and that in males was 226.8 +/- 61.1 mg/dl. The HDL-cholesterol level in males was 43.8 +/- 11.9 mg/dl; that in females (54.9 +/- 13.4 mg/dl) was significantly higher. The mean value of LDL-cholesterol in the entire group was 141.6 +/- 51.4 mg/dl and it was significantly higher in males, as well as in participants with known hypertension. 33.4% of the persons stated that they smoked. The obtained data will serve not only to discover potential interrelations between the individual risk factors of atherosclerosis in Austria, but also in particular as a basis for interventional strategies on the part of the company's medical services.

Adolescent↗
PubMed1991

Interaction between prostaglandin E1 and nitric oxide (NO).

A synergistic antiplatelet effect between prostaglandin I2 (PGI2), a cAMP-stimulator, and nitric oxide (NO), a cGMP-stimulator, has been described. Data on a PGE1-NO interaction, however, are lacking so far. We therefore examined the question in healthy volunteers, whether a similar synergism exist between PGE1 and NO on human platelets in vitro. Each of the substances alone caused a dose-dependent inhibition of ADP-induced platelet aggregation, PGE1 (1ng/mlPRP) reduced platelet aggregation by 27.8 +/- 14.6%, NO (0.3%) by 26.7 +/- 25.5%. The combination of these compounds caused an additive effect resulting in a reduction of 40.6 +/- 23.5%. The findings indicate that PGE1 (like PGI2) and NO have a synergistic antiplatelet action. The concomitant treatment with both compounds offers an interesting concept for clinical therapy.

Adult↗
PubMed1991

[Risk factors of atherosclerosis: results of screening in Southern Austria].

In the western industrialized countries atherosclerosis is the leading cause of death. In this investigation serum cholesterol and blood pressure were measured in 4321 (60.9% females) inhabitants of Lower Austria. In addition, a short cardiovascular history was taken and age, sex, body weight, height and smoking habits were recorded. In the various villages the mean serum cholesterol differed considerably (194 +/- 52-244 +/- 49 mg/dl). Overall, women had a slightly, but non-significantly, higher serum cholesterol (224.0 +/- 53.5 mg/dl) than men (218.6 +/- 58.4 mg/dl). Although 2/3 of the participants showed an elevated serum cholesterol, only 6% were taking lipid lowering drugs. An age-dependent increase in cholesterol was found in women, whereas this correlation was present in men only until the age of 40. Approximately 30% of the participants reported a positive family history. A comparison with the mortality register showed a correlation between smoking and bronchogenic cancer. No correlation, however, was demonstrable between smoking and cardiovascular mortality--perhaps due to methodological difficulties. Regional analysis of the results indicates the importance of the role of local general practitioners in the prevention of atherosclerosis.

Adult↗
PubMed1988

Improvement of hepatic encephalopathy treated with flumazenil.

The effects of the benzodiazepine antagonist flumazenil were studied in 20 episodes of hepatic encephalopathy (HE) in 17 patients with acute (n = 9) or chronic (n = 8) liver failure who had not responded to conventional therapy. Patients with a history of benzodiazepine intake were excluded. Changes in HE stage, in Glasgow coma scale, and in somatosensory evoked potentials were measured. In 12 of 20 episodes HE stage improved. The response to treatment occurred rapidly (within 3-60 min). In 8 of these 12 episodes HE worsened 0.5-4 h after treatment. In 5 of the 8 episodes that did not respond to flumazenil patients had clinical evidence of brain oedema. Flumazenil may be valuable in the treatment of HE in acute and chronic liver failure.

Acute Disease↗