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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 559 records · Page 31Linked to original sources
PubMed1980

Enhanced 6-oxo-PGF1 alpha levels in plasma during hemodialysis.

The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Prostacyclin (PGI2)-generation by different types of human atherosclerotic lesions.

Unaltered human arterial tissue as well as different types of macroscopically and microscopically characterized atherosclerotic lesions were microdissected under a preparation microscope. The prostacyclin formation was examined using its potent platelet aggregation inhibition in vitro according to Moncada's bioassay. In contrast to different PGI2-formation in various experimental animal models the generation in the different lesion types in terms of wet weight was statistically significantly (p less than 0.001) diminished in comparison to normal control tissue. However, the PGI2- formation in different lesion types is comparable. Accepting the hypothesis delivered earlier by us, that the arterial wall is able to react upon exogenous noxes with a temporarily enhanced PGI2-formation, followed (after ceasing) by a decrease of PGI2-synthesis (exhaustion phenomenon) it can be concluded, that the critical stage is prior to the fatty streak formation, which is a preatherosclerotic lesion. Therefore, PGI2-generation-exhaustion might be mainly responsible for initiation and progression of atherosclerosis, probably before any detectable morphological alterations.

Aged↗
PubMed1980

Quantitative investigation of sudanophilic lesions around the aortic ostia of human fetuses, newborn and children.

The sudanophilic lesions around the aortic ostia of 10 fetus, 10 newborns and 10 children aged up to 1 year were studied using a polar coordinate mapping method. The periorificial sudanophilic lesions develop initially distal to the orifices and show a continuous increase with age in percentage and extent. In children the lesions nearly completely surround all the ostia with a significant distal peak. There was no sex difference; the involvement of the right and left side was comparable. The comparison of the morphological data from the parents and children with anamnestics showed no relationship.

Adipose Tissue↗
PubMed1980

[Age dependence of vascular prostacyclin formation in man (author's transl)].

The synthesis of prostacyclin (PGI2), the most potent known inhibitor of platelet aggregation, varies with age. After 30 years the production decreases, but increases again in the 6th and 7th decade. Contrary to these physiological variations patients suffering from juvenile onset diabetes or peripheral angiopathy show a markedly decreased prostacyclin synthesis. Since the prostacyclin system in thought to be an important blood vessel protector, the pathological low level of PGI2-synthesis could be a key position in development or progression of vascular complications.

Adult↗
PubMed1980

Platelet proteins (beta-TG and PF4) in atherosclerosis and related diseases.

The mean plasma concentrations of beta-TG and PF4 were significantly elevated in patients with diabetes mellitus, peripheral vascular disease and coronary artery disease reflecting enhanced in vivo platelet activity in some of these patients. No correlations could be observed between state of metabolic control and concentrations of platelet specific proteins in diabetic subjects. High mean beta-TG levels were noticed in diabetic patients with increasing severity of retinopathy. Raised beta-TG values decreased significantly after two weeks of treatment with dipyridamole in 10 type-I diabetics. In patients with peripheral vascular disease the WU-test, but not the ADP- or collagen induced platelet aggregation was significantly different between patients and controls, but there were no correlations between the mentioned platelet function tests.

Arteriosclerosis↗
PubMed1980

Effect of experimentally induced diabetes on swine vascular prostacyclin (PGI2) synthesis.

Repeated administration of streptozotocin to Göttingen miniature swine led to the development of a mild form of diabetes. The amount of PGI2 generated by the vessels (abdominal aorta, thoracic aorta, pulmonary artery), as estimated by reference to inhibition of ADP-induced platelet aggregation, was lower in the treated animals than in the controls. The decrease in the synthesis of PGI2 may contribute to the prethrombotic state in diabetes mellitus.

Animals↗
PubMed1980

Influence of proteoglycans (PG) and glycosaminoglycans (GAG) on ADP-, collagen- and thrombin-induced platelet aggregation.

PGs and GAGs have been isolated from fresh bovine aortas according to the method of Hascall and chemically characterized. These PGs and GAGs had only little effects on ADP- and collagen-induced platelet aggregation, but had very potent inhibitory action on thrombin-induced platelet aggregation and prolonged thrombin-clotting-time. Of the standard GAGs investigated hyaluronic acid, chondroitin-4-sulfate and chondroitin-6-sulfate had only little inhibitory action on thrombin-induced platelet aggregation, whereas heparin was very potent in this respect. The unsaturated disaccharides originating after degradation of GAGs with chondroitinases had no effect on platelet aggregation. No differences between PGs and GAGs in inhibiting thrombin-induced platelet aggregation could be detected.

Adenosine Diphosphate↗
PubMed1980

Prostacyclin synthesis in human lymphatics.

The ability of human lymphatics to generate prostacyclin in important amounts (4.5 +/- 2.1 pg/mg/min) is described. The prostacyclin produced, exhibits the same properties as reported for arterial and venous tissue. No age and sex difference could be observed. The role of prostacyclin in physiology of lymphatics, however, is unknown.

Adolescent↗
PubMed1980

The effect of ballooning on minipig aortic prostacyclin formation - a time course.

The effect of a single endothelial injury with an arterial embolectomy catheter on minipig abdominal aorta prostacyclin formation was studied in 17 male animals as a function of time. The normal non deendothelialized abdominal aorta generated 4,41 pg PGI2/mg/min. One hour after endothelial injury PGI2-synthesis was decreased to the half; after two hours no PGI2-production could be detected. After 4 hours the PGI2-generation reached about the half of the strating values being thereafter nearly constant up to 24 hours. This experiment is presented as a model for studying early changes in PGI2-synthesis as it could occur during atherogenesis. The in vitro abrasion of endothelium demonstrated, that about 15% of the total PGI2 are formed by the endothelial sheet. Punching out the tissue samples revealed a strong correlation expressing PGI2-formation in terms of wet weight or surface area respectively.

Animals↗
PubMed1980

Effect of proteoglycans (Pg) and glycosaminoglycans (GAG) on prostacyclin (PGI2) and PGI2-formation of rat arteries.

Heparin had no effect on PGI2-activity if heparin and PGI2 have been incubated-together in an ice bath for 3 minutes. But heparin was able - unlike the other Pg or GAG - to abolish PGI2-activity if it had been incubated with PGI2 in an ice bath for 15 minutes. Pg and GAG, which had been isolated from bovine aortas according to the method of Hascall, and commerically available GAG (hyaluronic acid, chondroitin-40-sulfate, chondroitin-6-sulfate and heparin) had no effect on PGI2-formation of rat aortas in short time incubation (3 min). After long time incubation (15 min) or rat aortas in heparin less PGI2 was detectable compared to a buffer incubation. These data suggest that Pg and GAG do not influence PGI2-formation of arteries. The diminished PGI2-activity after long time incubation should be due to the PGI2-degrading effect of heparin.

Animals↗
PubMed1980

Evidence that thrombus organizing blood derived cells produce prostaglandin I2-.

An artificial vessel replacement, which is athrombogenic and impermeable for a migration from the adjacent tissue, was implanted end to end into the thoracic aorta of 10 sheep. The center of this tube has a Dacron surface, which is known to trap blood elements. We examined the tissue samples built up by blood derived cells between 2 and 84 days morphologically by means of light microscopy as well as by SEM and TEM. We checked the thrombus fragments of 7 cases for their PGI2-generation using MONCADA's bioassay. In our specimens we found an average activity of 4, 7 pg PGI2 mg/min. The morphological examination revealed different stages of thrombosis and organization consisting of a large number of cells. Macrophages, fibroblast like cells, myofibroblasts as well as endothelial cells and foreign body giant cells around the Dacron fibers could be found. Our experimental design excludes the ingrowth of mesenchymal elements, which suggests that blood derived cells are able to produce PGI2.

Aging↗