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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 289 records · Page 16Linked to original sources
PubMed1990

[Risk factors of atherosclerosis and awareness of risk in employees of a Viennese insurance company].

In Austria still more than 50% of overall mortality are due to cardiovascular diseases. An efficient prevention via change of life-style has been proven. We started with an intervention-trial in a Viennese insurance company. 667 persons (50.7% m, 49.1% f, 0.1% no declaration) participated in the basic examination. The mean cholesterol level was 221.85 +/- 43.87 mg/dl, being clearly above the threshold value of 200 mg/dl. In spite of the fact, that 69.7% of the female and 65.5% of the male had elevated serum cholesterol only 1.8% already took lipid lowering drugs. Participants with a positive family history (myocardial infarction) had significantly elevated cholesterol (228.2 +/- 49.4 mg/dl vs 219.7 +/- 50.4 mg/dl). Another point we were drawing special attention to was the knowledge of the participants about the risk factors of atherosclerosis. Only 13% of the males and 13.8% of the females knew their cholesterol level. 11.5% of the males and 15.9% of the females were aware of the threshold value of cholesterol. Intervention strategies (information campaign, works kitchen) have been initiated. A possible beneficial effect will be examined in biannual follow-up examinations.

Adult↗
PubMed1989

[Prostaglandin interaction in the human liver].

The binding of prostaglandin (PG) E1 and Iloprost, a chemically stable PGI2-analogue, to purified plasma cell membranes (LPZM) from liver tissue samples obtained at surgery revealed heterogeneity of the binding sites identifying high and low affinity subpopulations. In contrast to these findings only high affinity binding sites were characterized for PGE2. Displacement studies exhibited the highest competition for the PGE1-sites by PGE1 and subsequently by PGE2, Iloprost, PGD2 and PGF2 alpha. The binding of PGE2 to the hepatic receptor could be best displaced by PGE2 and subsequently by PGE1 and Iloprost, PGD2 and PGF2 alpha. In addition, PGE1, PGE2 and Iloprost enhanced cAMP-production dose-dependently over baseline. Clinical studies revealed a remarkably lower binding capacity for PGE1 in hepatocellular cancer tissue than in normal liver parenchyma. The different binding behaviour of PGE1 (Iloprost) and PGE2 for the first time provides evidence that PGE1 and PGI2 like at platelet membranes occupate the same receptor also at human LPZM. Since a reasonable number of binding sites for these substances and an enhanced cAMP-production were shown in the liver, the study indicates a regulatory role of PGs in hepatic function.

Alprostadil↗
PubMed1989

[In vivo flow of autologous radioactively labeled low-density lipoproteins (LDL) in human blood vessels].

Following 123I-labelling and reinjection of autologous low-density lipoproteins (LDL) to patients with clinically manifest atherosclerosis and/or hyperlipoproteinaemia (HLP), an investigation was carried out of whole body kinetics and local kinetics over atherosclerotic lesions and areas of increased LDL entry identified by "hot spots" in the 123I-LDL scintigram. In patients with HLP the number and frequency of "hot spots" was higher than in normolipaemics. The time course of 123I-LDL influx into atherosclerotic lesion sites until scintigraphic visualization of "hot spots" exhibited three different types of LDL uptake among the patients. In the majority of patients LDL kinetics was characterized by entry into the vessels with the maximal radioactivity measured as early as within 60 minutes after reinjection. In some patients maximal radioactivity over lesion sites was discovered after 20 hours or even later. Morphological evaluation revealed that in comparison to control tissue, fatty streaks and lipid lesions show by far the highest 123I-LDL accumulation. Ex vivo measurement of the deposition of 125I-LDL in de- and re-endothelialized rabbit aortic segments exhibited a significantly (p less than 0.01 - p less than 0.001) higher 125I-LDL retention as compared with endothelialized segments (after i.v.-injection).

Adult↗
PubMed1989

[Do passive smokers have an increased risk of thrombosis?].

In contrast to the proven association between active smoking and vascular injury, as well as hemostatic imbalance, such a relation is not jet proven for passive smoking. Vascular damage induced by smoking, however, can be seen in the materno-fetal circulation of smoking mothers, being much more pronounced in the umbilical system than in fetal vessels. These lesions show fast recovery after birth. In non-smokers acute exposure to passive smoke induces a short-lasting activation of platelet function and the prostaglandin system, followed by a quick recovery. Chronic exposure of non-smokers to passive smoke, however, results in changes of these parameters comparable to those seen in smokers, characterized by an activation of platelet function and a decrease in platelet sensitivity to the antiaggregatory prostaglandin I2. These results suggest that in non-smokers with atherogenic risk factors passive smoking may contribute to the incidence of atherosclerosis, as well as acute complications (thrombosis).

Adult↗
PubMed1989

Effects of Hydergine on platelet deposition on "active" human carotid artery lesions and platelet function.

Effects of co-dergocrine mesylate (Hydergine), a drug widely used for the therapy of cerebral vascular disease on local platelet accumulation in the carotid artery region was studied by means of the platelet uptake ratio (PUR) and on the systemic platelet-vascular wall interaction as calculated from platelet half-life were investigated. A placebo controlled, double blind, randomised protocol was used, 18 patients were treated with co-dergocrine and compared to placebo (n = 18). Co-dergocrine treatment resulted in a significant decrease in platelet deposition, PUR decreased from 1.28 +/- 0.05 before treatment to 1.25 +/- 0.06 on day 5 of therapy with a statistically significant (p less than 0.001) in the paired comparison. In the control group the corresponding changes from 1.29 +/- 0.04 before to 1.28 +/- 0.04 did not show a p-value of less than 0.05 in paired comparison. Platelet half-life (72 +/- 11 before vs. 76 +/- 11 hours after 5 days of co-dergocrine treatment) showed a statistically significant (p less than 0.001) prolongation, whereas in the placebo group no relevant change of T/2 was observed (71 +/- 10 before vs. 72 +/- 10 hours on day 5, p greater than 0.10). No relevant effects on ADP-induced platelet aggregation, platelet-release reaction, platelet aggregate ratio, TXB2 plasma levels and thrombin-induced MDA-formation could be detected. These results indicate that co-dergocrine decreased in-vivo platelet residence time to atherosclerotic lesions of the carotid artery. Co-dergocrine may thereby be of benefit in prevention of mural thrombus formation and prevention of transient ischemic attacks, but also of atherosclerosis in man.

Aged↗
PubMed1989

[Cholesterol 87--status of knowledge of the Vienna public].

A representative survey on cholesterol was carried out in June 1987 in Vienna on the basis of a personal interview. 93% of 1471 interviewees knew the term cholesterol, but only 65% knew its meaning. 46% associated it with myocardial infarction, 11% with cardiovascular disease. The cholesterol level had already been measured in 61% of the interviewees; out of these 16% had an elevated value, 68% a normal one; 16% did not know their own cholesterol. 70% were prepared to submit to an annual check up on their cholesterol or at even more frequent intervals. 94% would be willing to undertake counteractive measures in case of elevated cholesterol, 71% to stick to a diet, 56% to alter their lifestyle and 35% even to take medication.

Adolescent↗
PubMed1989

[The cholesterol risk factor--initial results of a screening study in industries].

After the distribution of suitably informative leaflets all the employees of 2 companies were invited to participate in a screening programme with the aim of detecting elevated cholesterol levels. 238 out of 510 employees participated in the screening. Related to the age-adjusted Austrian recommendations for the upper limit of normal values, cholesterol was elevated in 73 people (30.7%). The percentage of smokers was slightly below the Austrian rate with 26% in company M and 30% in company H. All the participants were informed of their laboratory results within one week. Participants with a moderately or extremely increased risk were invited to a personal talk. Furthermore, a number of other previously undetected abnormalities were detected in 41 cases (17.2%), leading to subsequent clinical diagnosis and treatment. In addition, 3 plasma factor defects were discovered. These investigations served as a foundation for a more intensive planned programme. A continuation of this screening procedure is planned involving about 10,000 people per year.

Adult↗
PubMed1989

[Cholesterol screening in a bank for the detection of a risk population].

In October 1987 voluntary screening for cholesterol war performed in a bank. After preceding information had been issued to the participants 25 ml blood were drawn on 4 days from 667 employees (48.9% males, 51.1% females) for determination of the blood lipids and other parameters. The mean age (range 19 to 60) was 39 +/- 9 years; 29.2% were smokers. The mean cholesterol level amounted to 212 mg/dl. According to age- and sex-related normal values 42% exhibited an increased risk, whereby the percentage was particularly high (55%) in the age group under 30 years.

Adult↗
PubMed1989

Isradipine: a potent calcium blocker with beneficial effects on platelet function and vascular prostacyclin production.

Calcium blockers inhibit platelet aggregation induced in vitro by various stimuli, such as ADP and collagen. In this study the in vitro effects of isradipine, a new dihydropyridine-derivative, and of nifedipine on platelet aggregation and malondialdehyde-production were tested. The lowest concentrations affecting ADP-induced platelet aggregation were 1.0 micrograms/ml isradipine and 12.5 micrograms/ml nifedipine. Both drugs exhibited an inhibitory action on malondialdehyde-production in concentrations 2 to 3 times lower than those affecting platelet aggregation. In vitro, PGI2-formation by rat aortic rings incubated with calcium blockers was increased in a dose-dependent manner. The lowest concentration of isradipine which increased PGI2-generation amounted 0.5 micrograms/ml. The corresponding value for nifedipine was 10 micrograms/ml. The findings demonstrate isradipine to be more potent than nifedipine in affecting in vitro platelet aggregation and enhancing PGI2-formation.

Adenosine Diphosphate↗
PubMed1989

[Effects of omega-3-fatty acids on the prostaglandin system in healthy probands].

Epidemiological comparisons of Greenland Eskimos and mainland Danes suggested that a diet rich in marine lipids mainly containing polyunsaturated fatty acids may be associated with a reduction in the incidence of occlusive vascular disease. Fish oils contain the Omega-3 polyunsaturated fatty acid eicosapentaenoate (timnodonic acid, EPA, 20:5n-3), which is incorporated into the platelet membrane after dietary intake instead of arachidonic acid (20:4n-6), the main substrate for prostaglandin synthesis. After incorporation of the fatty acids into the platelet membrane the overall effect of prostanoids with three double bonds derived from EPA proves to be less atherogenic. Since only TxA2 is a potent vasoconstrictor and platelet agonist whilst TxA3 is virtually biologically inert.

Adult↗
PubMed1989

Response of thromboxane B2, malondialdehyde and platelet sensitivity to 3 weeks low-dose aspirin (ASA) in healthy volunteers.

To examine the effects of low-dose aspirin thromboxane B2 (TXB2), malondialdehyde (MDA) and platelet sensitivity to prostaglandin I2 (PGI2) have been measured in a total of 18 healthy volunteers. They were randomly assigned to 3 groups, 6 volunteers each, receiving either 1, 10 or 20 mg ASA orally a day for 3 weeks in a double-blind fashion. In order to assess the time course of ASA-induced changes, blood was drawn before, 1 hour and 2, 3, 5, 7, 9, 12, 14, 16 and 21 days after the first drug-intake. Serum-TXB2 was depressed time- and dose-dependently, after 1 mg daily to about 60%, after 10 mg to about 30%, after 20 mg to about 5% of controls. MDA-formation and conversion of exogenously added arachidonic acid (AA) to TXB2 also dropped significantly, (p less than 0.01), the extent depending on the ASA-dosage administered. The drop in MDA- and TXB2-values in the 3 groups correlated with r = 0.98, 0.94, 0.98, respectively. The platelet sensitivity during 20 and 10 mg ASA-administration did not change at all, whereas a significant increase (p less than 0.01) in platelet sensitivity during treatment with 1 mg ASA was observed.

Adult↗
PubMed1989

Early-onset thrombocytopenia during combination chemotherapy in testicular cancer is induced by vinblastine.

Platelet kinetics were studied in 70 patients with testicular cancer to elicit the agent responsible for chemotherapy-induced transient early-onset thrombocytopenia; 204 treatment courses were analyzed using three different therapy protocols, which contained vinblastine and bleomycin either alone or in combination with cisplatin. Platelet count decreased significantly from the start of vinblastine administration reaching its nadir on the third day of therapy in each of the three treatment groups. Between day 4 and day 10 of the treatment cycle, platelet counts steadily increased even in patients still receiving continuous bleomycin infusions. The conclusion that the observed early-onset thrombocytopenia was caused by vinblastine was substantiated by the outcome of two additional examinations. Platelet half-life was significantly shortened 24 hours after vinblastine administration and electron microscopy revealed a dissolution of cytoplasmatic microtubules with loss of the typical discoid shape of platelets within 15 minutes after the start of therapy. Both findings occurred irrespective of the specific treatment protocol, i.e., even after nothing but vinblastine had been given. These results strongly suggest that vinblastine is the main cytostatic agent responsible for the transient early-onset thrombocytopenia observed during chemotherapy of testicular cancer.

Adolescent↗