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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 145 records · Page 8Linked to original sources
PubMed1997

[Imaging of early carotid artery atherosclerotic lesions with 111In-labeled polyelonalhuman IgG (HIG)].

AIM: To assess the value of scintigraphy with 111In-HIG for diagnosis and evaluation of the stage and the clinical extent of carotid artery disease in humans a prospective clinical comparative trial of scintigraphy vs. sonography was performed. METHODS: 58 patients (38 male, 20 female; mean age 60 +/- 7 years) with hyperlipidemia and ultrasonographically detectable carotid artery lesions were studied. After i.v. injection of 18.5 MBq 111In-HIG, anterior scintigraphic images of the neck were acquired. Real time two-dimensional B-mode ultrasonography of the left and the right carotid arteries was performed. RESULTS: 111In-HIG-scintigraphy as compared to the morphological gold standard (ultrasonography) had a sensitivity of 70-73%, specificity of 33-41% and a positive predictive value of 77-82% for detecting carotid atherosclerotic lesions. There was, however, no significant correlation between scintigraphy and ultrasonography. CONCLUSION: However, the data provide evidence that the two imaging techniques are visualizing different aspects of atherogenesis. On the one hand a functional one reflecting the activity of the disease (111In-HIG) and on the other hand the morphological one resembling the extent of the disease (ultrasonography).

Aged↗
PubMed1997

[Isoprostanes, a new substance group in angiology--of future significance?].

F2-isoprostanes are prostaglandin F2-like compounds being formed by non-enzymatic peroxidation of arachidonic acid in vivo. They have a variety of biological actions. The most important compound of this group is 8-epi-PGF(2 alpha) being capable to induce vasconstriction in particular of lung- and renal vascular tissue. Isoprostanes are present in esterified form; in free form they become available after hydrolysis by phospholipase A. An increase in isoprostanes is an important indicator of oxidative stress in-vivo due to a variety of different noxi such as metal- or non-metal ions for cigarette smoke. Isoprostanes show an activation of platelets; as a consequence of the interaction of 8-epi-PGF(2 alpha) with specific receptors platelet aggregation may be induced or may be enhanced together with other agonists. Due to these preliminary results isoprostanes could become an interesting substance in angiology in the future for diagnosis of oxidative stress as well as in the understanding of the pathogenesis of atherosclerosis.

Animals↗
PubMed1997

Isoprostane 8-epi-prostaglandin F2 alpha is a potent contractor of human peripheral lymphatics.

Isoprostanes are products of free radical-catalyzed peroxidation and 8-epi-prostaglandin (PG) F2 alpha is the most important vasomodulator of this group of compounds. In human lower leg lymphatics isolated from 5 different patients without a smoking history or hyperlipidemia, 8-epi-PGF2 alpha stimulated in vitro contraction more strongly than the thromboxane receptor agonist U46619. Other isoprostanes (8-epi-PGE1, 8-epi-PGE2) had only limited lymphatic contractile potency. These data suggest a potentially relevant role for epi-8-PGF2 alpha in facilitating lymph transport especially in conditions of inflammation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

[Multi-drug management after myocardial infarct].

Since the results of studies done with angiotensin-converting-enzyme(ACE)-inhibitors, systemic thrombolysis and primary percutaneous transluminal angioplasty (PTCA) have been published, post-myocardial infarction therapy has changed dramatically. In most european countries systemic thrombolysis as early as possible is the standard therapy. Cardiologists prefer more and more immediate revascularisation if the technical standard of the hospital is allowing an acute intervention. Pharmacological therapy is done initially with beta-blockers and platelet aggregation inhibitors, if necessary intravenously, since the results of the e.g. GUSTO- and the AIRE-study are known. If left ventricular dysfunction exists or develops, ACE-inhibitors are given after the third day post myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1997

[Acetylsalicylic acid after myocardial infarct].

There is no doubt about the positive influence of acetylsalicylic acid on vascular disease. The antithrombotic therapy with acetylsalicylic acid is a fundamental of secondary prevention of vascular events, especially in nonfatal myocardial infarction, instable angina pectoris, stroke and in patients with amaurosis fugax. Clinical studies done since 1990 about the effect of a low-dose therapy confirmed the experimental results, which showed that 25-50 mg acetylsalicylic acid per day are enough, to suppress platelet function as far as necessary, without influencing the protective function of prostacyclin synthesis. Side-effects can be reduced to a minimum with a reduced dosage. The wide-spread use of a low-dose acetylsalicylic acid therapy in primary prevention especially in patients at high risk has to be reevaluated in further studies.

Aspirin↗
PubMed1996

The prostacyclin stimulating plasma factor activity improves thromboresistance only if vascular PGI2-production is intact.

PGI2 is important in regulating platelet vessel wall interaction (1). In perfusion chamber experiments the amount of PGI2 formed was inversely related to the amount of platelets deposited (2). In 1978 a plasma factor was described which stimulates vascular PGI2-production (3). In later years, this activity has been monitored in different patient groups (for review see 4). Interestingly, it has been found that diseases associated with an increased bleeding tendency such as uraemia (5) or hepatic failure (6) were associated with an increased PF-activity while others with an enhanced thrombophilia sometimes show an absence of PF-activity (7). Recently, the PGI2 stimulating plasma factor has been purified and cloned (8). It was the aim of these experiments to assess whether PF-activity plays a role in local hemostasis regulation under in-vivo flow conditions and whether this is dependent on the presence of an intact PGI2-formation.

Adult↗
PubMed1996

Decreased susceptibility of low-density lipoproteins to in-vitro oxidation after dextran-sulfate LDL-apheresis treatment.

Low-density lipoproteins (LDL)-apheresis is a well established treatment of severe hypercholesterolemia resulting in fast clinical improvement and angiographically proven regression after 6 months of therapy. The underlying mechanisms, beside lipoprotein removal, are still under debate. Recently, oxidized LDL were shown to be of key importance in foam cell formation and atherosclerotic lesion development. We examined the influence of dextran-sulfate LDL-apheresis on the susceptibility of LDL to oxidation in 6 patients (5 males, 1 female, age: 41-60 years) suffering from severe heterozygous hypercholesterolemia or combined hyperlipidemia. LDL-apheresis influenced the oxidizability of LDL by a significant (P < 0.01) prolongation of the median of lag time (min) for LDL samples (before treatment 75, range: 31-176 versus after treatment 129.5, range 45-286). A significant (P < 0.01) difference could be also observed in the amount of conjugated dienes as expressed by the maximum rate in absorbance (before treatment 15.39, range: 5.29-21.22 versus after treatment 20.20, range 12.88-72.33). Thiobarbituric acid reactive substances (TBARS) formation was significantly decreased in LDL obtained after apheresis treatment as compared to pretreatment LDL. Electrophoretic mobility (EM) of LDL obtained before and after LDL-apheresis revealed a significant increase (P < 0.05) from a mean of 8.8 +/- 0.5 to a mean of 10.5 +/- 0.5 mm. The titers of plasma autoantibodies against oxLDL (oLAb) which varied considerably interindividually, were not influenced by LDL-apheresis treatment. Levels of F2-isoprostanes, as measured by plasma levels of 8-iso-prostaglandin-F2 alpha (8-iso-PGF2 alpha), reflecting oxidative stress, did not change, either. In summary, our findings provide evidence that even one single dextran sulfate LDL-apheresis treatment decreases LDL-oxidizability, which is an additional beneficial effect to that of lipid lowering.

Adult↗
PubMed1996

A case of myocardial infarction complicating pregnancy--a role for prostacyclin synthesis stimulating plasma factor and lipoprotein (a)?

Coronary heart disease and myocardial infarction (MI) is rarely seen in women below the age of 40 years and even more rarely during pregnancy. The first case of MI during pregnancy was described by Katz in 1992 (1). Current literature reviewed by Samara et al. 1989 (2) listed only 62 cases of proven MI during pregnancy or in the puerperium, the maternal mortality rate being as high as 24%. In this paper we are going to report on a 26-year old pregnant woman suffering from MI, probably as a result of a haemostatic imbalance caused by a lack of prostacyclin synthesis stimulating plasma factor (PF) and elevated lipoprotein (a) (Lp (a)). The potentially deleterious thromboembolic complications in patients with PF-deficiency, especially in combination with elevated Lp (a), should be carefully considered.

Adult↗
PubMed1996

Ex-vivo and in-vivo platelet function in patients with severe hypercholesterolemia undergoing LDL-apheresis.

Patients with severe familial hypercholesterolemia (HC) show abnormal platelet function and shortened platelet survival. Atherosclerosis is associated with platelet hyperactivity. Low-density lipoporotein (LDL)-apheresis eliminates the most atherogenic lipid fraction and inhibits the progression of atherosclerosis inducing even regression. In order to assess the influence of LDL-apheresis on platelet function ex-vivo and in-vivo, 6 patients with severe heterozygous HC, all of them being pharmacologically treated with HMG-CoA reductase inhibitors and anion exchange resins were investigated. Ex-vivo platelet function was assessed by the aggregation response to ADP before starting apheresis treatment, as well as after 2 and 24 weeks, respectively. In-vivo platelet function was determined by measuring platelet survival after radiolabeling with 111In-oxine before starting LDL-apheresis and after 24 weeks of twice monthly treatment. LDL-apheresis therapy induced a significant (p < 0.01) drop in cholesterol by 64%, LDL-cholesterol by 77% and in triglycerides by 46% over a period of 24 weeks. ADP-induced platelet aggregation revealed a decreased aggregability of platelets with a decline in the maximal amplitude and the slope of the response curve. Changes in platelet sensitivity to prostaglandins (PG) were significantly for PGI2, but did not reach statistical significance for PGE1. The results revealed a significant (p < 0.001) increase in platelet survival of 111In-oxine-radiolabeled autologous platelets from a mean of 106.50 hours before to 137.50 hours (p < 0.01) after treatment, being accompanied by an increase in labeling efficiency (p < 0.001) and recovery (p < 0.001). These data provide evidence for improved hemostatic regulation in vivo as a result of maintainance of lipid-lowering achieved with LDL-apheresis.

Adult↗
PubMed1996

Passive smoking and platelet thromboxane.

While active smoking is known to enhance platelet thromboxane production, no data on passive smoking is available yet. The influence of single and repeated exposure to passive smoke for 60 minutes in a 18 m3 room was assessed in non-smokers as compared to sex and age matched smokers. All the evaluated measures (malondialdehyde, plasma thromboxane B2, 11-dehydro-thromboxane B2, serum thromboxane B2, conversion of exogenous arachidonic acid to thromboxane B2 and to hydroxy-5, 8,10-heptadecatrienoic acid) were higher in smokers than non-smokers at baseline, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of non-smokers rendered their platelets more activated becoming close to the behaviour of smokers. These results indicate that passive smoking may activate thromboxane A2 release from the platelets, contributing to the development of hemostatic imbalance.

Adult↗
PubMed1996

Apolipoprotein A and biological half-life of prostaglandin I2 in HIV-1 infection.

Disturbances in lipid and lipoprotein metabolism being reported for HIV-1 infection are a common sign of severe infections. Apolipoprotein A being the main constituent protein of HDL has been described to function as the prostaglandinI2 (PGI2)-stabilising factor. PGI2 is not only one of the most potent biological antiaggregatory substances but seems to exert cell-protective properties in the central nervous system, too. PGI2 half-life as well as lipid [total-cholesterol (total-c), triglycerides] and (apo)lipoprotein [LDL-c, HDL-c and apolipoprotein (apo) AI] levels were investigated in 14 HIV-1 positive patients (13 males, 1 female, aged from 29 to 57 yrs). Patients exhibited decreased levels of total-c, LDL-c, HDL-c and apo AI, respectively, while elevated triglyceride levels were observed. PGI2 half-life was shortened (median 53, range: 15-161 seconds) in the patients' plasma as compared with normal controls ranging from 9-12 minutes. In patients with neurological manifestation (n = 8) the decrease of PGI2 half-life (median: 34 seconds, range: 15-67 seconds) was significantly more pronounced (p < 0.05) than in patients (n = 6) with the absence of any central nervous manifestation (median: 83.5, range: 29-161 seconds). The dramatic changes in both HDL-c and apolipoprotein AI as seen during HIV-1 infection are likely to impair PGI2-stabilisation thus being associated with the presence of peripheral neuropathy, dementia and haemostatic imbalance.

AIDS Dementia Complex↗
PubMed1996

Prostaglandin E1 increases binding of 123I-low-density lipoprotein to the human liver in vivo.

Previous in vitro radioligand binding data have shown that prostaglandin E1 (PGE1) increases the number and the binding affinity of low-density lipoprotein (LDL) receptors of the human liver. Experimental data in normo- and hypercholesterolaemic rabbits have confirmed these findings, showing a significant increase in LDL-binding to the liver in vivo after prolonged PGE1 therapy. METHODS. This study aimed to confirm the experimental and animal data in human in vivo. 123I-LDL binding to the liver was quantified in vivo in patients suffering from peripheral vascular disease, seven of them with heterozygous familial hypercholesterolaemia (HC) and five with normal total plasma cholesterol, after PGE1 administration (5 ng.kg-1.min-1; 6 h daily for 5 days/week for 5 weeks). LDL uptake by the liver was quantified by single photon emission computer tomography (SPECT). RESULTS. The amount of LDL trapped by the liver in normocholesterolaemics (45.6%) was significantly higher than in hypercholesterolaemics (22.0%). PGE1 induced an increase in liver LDL binding, which was more pronounced in HC (+38.2%) than in normocholesterolaemic patients (+8.11%).

Aged↗
PubMed1996

Prostaglandin E1 decreases circulating endothelial cells.

Prostaglandin E1 (PGE1) has been claimed to have cytoprotective effects and also to decrease thrombogenicity. The effect of intraarterial (i.a.) and intravenous (i.v.) administration of PGE1 on the number of circulating endothelial cells (CEC) was investigated in patients with peripheral vascular disease (PVD). Patients with hyperlipoproteinemia and also smokers exhibited higher numbers of CEC. PGE1 significantly (p < 0.01) decreased CEC. In parallel, plate let survival was prolonged (r = 0.82). This effect lasted for more than a month after stopping PGE1-therapy. The observed decrease in CEC reflects the decreased thrombogenicity and improved haemostasis achieved after PGE1.

Alprostadil↗