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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 433 records · Page 24Linked to original sources
PubMed1985

[Accelerated degradation of prostacyclin in diabetic plasma--a further factor in the impairment of hemostatic balance?].

Prostacyclin is degraded in human plasma in vitro with an average half-life of 10 minutes. The degradation in plasma of patients suffering from type II diabetes mellitus is significantly enhanced. However, the inactivation of prostacyclin in plasma in patients with clinical manifestations of atherosclerosis, such as peripheral vascular disease, is unchanged. Methodological studies reveal that storage of plasma at various temperatures up to investigation, repeated freezing and thawing, as well as the addition of thromboxane-synthetase inhibitors do not exert any effect on plasmatic degradation of PGI2. In addition, no differences are found in plasmatic degradation in diabetics in accordance with the mode of treatment. The presence of a factor in human plasma in diabetics capable of increasing PGI2 degradation or the loss of a possible stabilizer could be one further important parameter, amongst others responsible for the development of either macro- or microangiopathy in diabetes mellitus.

Aged↗
PubMed1985

[Treatment of venous thrombosis of the retina with prostacyclin].

Prostacyclin (PGI2) was used in the treatment of 10 patients with retinal venous thrombosis. All changes in 6 eyes with the non-ischaemic type of venous obstruction resolved completely, with marked visual improvement. The course of 3 ischaemic venous thromboses was unaffected by the treatment. In one eye ischaemic retinal areas were first noted months after therapy. All ischaemic fundi were subjected to adequate laser coagulation. In spite of the small number of patients it can be concluded that PGI2 does not seem to alter the course of the ischaemic type of retinal venous thrombosis.

Epoprostenol↗
PubMed1985

[Resorption of prostaglandin E2 following various methods of local administration for ripening of the cervix and end the induction of labor].

PGEM concentration was determined radioimmunologically in a non-pregnant woman in whom PGE2 was infused intravenously at increasing dosage and in women in whom labour was induced by various methods for local application of PGE2. There was excellent correlation between the amount of PGE2 infused intravenously and the levels of PGEM determined in the peripheral plasma. The following methods of local application of PGE2 were included in the study: 0.4 mg PGE2 gel placed retroamnially by means of a balloon catheter; 0.4 and 0.5 mg PGE2 gel applied endocervically; 1.5 mg PGE2 given pericervically through a portio adapter and 3 mg PGE2 placed intravaginally in form of a single vaginal tablet; also included was a control group where only vaginal examination was performed. Blood was withdrawn before, and then 30 minutes, 1, 2 and 3 hours after PGE2 administration. Mean levels of PGEM in the maternal peripheral plasma showed no change within or between the various groups, with the exception of one patient in the portio adapter group where hyperstimulation occurred. After removal of the adapter PGEM levels dropped to baseline values. It is concluded from the present study that local application of doses currently used to soften the cervix and/or induce labour at term does not give rise to PGEM concentrations in the maternal blood of the same magnitude as achieved by intravenous PGE2 administration.

Abortion, Induced↗
PubMed1985

[Defects in the prostaglandin system. II. Familial platelet-prostacyclin receptor defect (Wien-Hietzing defect)--pathogenetic significance for (early) development of atherosclerosis?].

A case is reported of a 10 year-old girl admitted to hospital because of severe intermittent claudication. Occlusion of the left popliteal artery was diagnosed. Since successful surgical intervention the patient has been symptom-free. No causative factor was detected for this premature occlusion. During intensive laboratory check-up an extreme diminution in sensitivity of the platelets to prostacyclin and a receptor defect were discovered. This defect seems to be genetically determined. The extent to which this as yet unreported platelet defect might have contributed to the development of atherosclerosis at such an early age is discussed.

Arteriosclerosis↗
PubMed1985

[Protein binding of thromboxane--one of the sources of error in thromboxane determination].

The determination of thromboxane A2 (TxA2), the main metabolite of arachidonic acid (AA) in platelets, is very difficult due to extreme instability of this compound. Only stable end products such as TxB2, the hydrolysis product of TxA2, and malondialdehyde (MDA) can be analysed by means of routine techniques. Since the presence of proteins interferes with the photometric determination of MDA, these have to be eliminated by acidification. The TxB2 concentration was measured in the supernatant in parallel with MDA determinations before and after protein precipitation. A significant difference was found between these two TxB2 concentrations. The TxB2 values after precipitation were significantly lower than before precipitation, indicating that a high percentage (about 70%) of TxB2 is bound to proteins. Protein precipitation in a biological sample might, thus, cause misinterpretation of the measured value.

Blood Platelets↗
PubMed1985

[Prostaglandins in the cardiovascular system--of importance clinically?].

Prostaglandins are biologically extremely active substances and an important role has been attributed to them in particular with respect to pathophysiology of the cardiovascular system. In contrast to the extremely potent biological effects in vitro the therapeutic results have been varied so far. On the basis of these reports it has been prematurely concluded that prostaglandins are not of clinical importance. The fact that primary defects, as well as defects associated with the presence of other diseases, occur in conjunction with a disturbance in haemostatic regulation is gaining increasing attention. In contrast to the findings with coagulation disturbances, defects in the prostaglandin system seem predominantly to affect the arterial system. With increasing specificity of detection methods and broadening of the methodological spectrum the number of defects detected in the prostaglandin system is increasing. The place of prostaglandins in the development of vascular diseases and their importance with respect to clinical treatment cannot be assessed definitely as yet in view of the insufficiency of information in all areas at present.

Cardiovascular System↗
PubMed1985

Platelet sensitivity to antiaggregatory prostaglandins (PGE1,D2,I2) in patients with peripheral vascular disease.

Platelet sensitivity to antiaggregatory prostaglandins (PGI2, PGE1, PGD2) was studied in 143 patients (122 male) with angiographically proven peripheral vascular disease and compared with age-matched clinically normal controls. Patients had a significantly lower platelet sensitivity to PGI2, PGE1, and PGD2 than controls. Clinical stages had no significant influence on the platelet sensitivity to PGI2 and PGE1. Patients with stage IIa had a lower sensitivity to PGD2 than patients with stage IV, the difference not being significant. Analyzing the influence of risk factors like diabetes, hyperlipoproteinemia, or smoking, there seemed to be an inverse relation between risk factors and platelet sensitivity to PGI2 and PGE1. Smokers especially, together with smokers exhibiting an additional risk factor, exhibited the highest prostaglandin consumption (PGI2, PGE1) and therefore the lowest platelet sensitivity. However, it has to be emphasized that the differences were not significant. There was a significant correlation between platelet sensitivity to PGI2 and PGE1, whereas this was not the case between the respective sensitivities to PGI2 and PGD2. This supports the hypothesis that both these prostaglandins (PGI2, PGE1) share the same receptor on the platelet surface, whereas PGD2 has its own receptor.

Adenosine Diphosphate↗
PubMed1985

Double blind study of the influence of co-dergocrine on platelet parameters in healthy volunteers.

In 20 healthy volunteers double-blind randomized study was done to examine the effect of co-dergocrine (Hydergine) on platelet function. All the volunteers were pretreated with 3 X 1 placebo for 1 week, followed by the randomized study in which 10 volunteers each received drug or placebo for 6 weeks. Various platelet function parameters, such as the peripheral platelet count, plasma thromboxane B2, platelet sensitivity to the antiaggregatory prostaglandins PGI2, PGE1 and PGD2, ADP-induced aggregation, collagen-induced aggregation, the WU-test, the platelet proteins platelet factor 4 and beta-thromboglobulin, malondialdehyde, circulating endothelial cells and the intracellular c-AMP level in platelets were examined. Treatment with co-dergocrine decreased platelet activity to a significant extent, as shown by a number of platelet function parameters, such as thromboxane B2, WU-test, beta-thromboglobulin, platelet factor 4, malondialdehyde and ADP-induced aggregation. The findings suggest that co-dergocrine might be able to decrease platelet activity and improve interaction with the walls of to a blood-vessel significant degree.

Adult↗
PubMed1985

Organisation of experimental thrombosis by blood cells. Evidence of the transformation of mononuclear cells into myofibroblasts and endothelial cells.

To clarify whether thrombus organisation was carried out by local cell activity or by elements of the circulating blood we developed an artificial prosthesis, made of an impermeable polyurethane material with an athrombogenic surface but with a central part consisting of a DACRON velour ring which was thrombogenic. We implanted these devices into the aorta of 10 sheep. In these animals, organisation of the central thrombus by local aortic cells could be excluded. After varying periods of time (2-84 days), the device was removed and the organized thrombus investigated by light and electron microscopy. From our investigations the organisation process with the development of mesenchymal cellular elements proceeded in 3 steps: The activation of the mononuclear macrophage system, the appearance of myofibroblastic cells and endothelial formation. The activation of the mononuclear macrophage system is probably induced by chemospecific products of metabolism arising from aging thrombotic material. Apart from mononuclear elements such as monocytes, macrophages, and giant cells we observed fibroblast-like and myofibroblast-like cells. The matrix contained collagen. Endothelium developed on the surface of the organizing thrombus. The final stage was characterized by the formation of a pseudovessel wall, which followed the pattern of the vascular model. Our findings support the hypothesis that a thrombus may be organized by cells derived from the circulating blood.

Animals↗
PubMed1985

The prostacyclin synthesis stimulating plasma factor is unchanged during acute angina pectoris.

Earlier studies have demonstrated that the levels of prostacyclin synthesis stimulating plasma factor are changed during various clinical situations thus leading to disturbances in hemostatic balance. Therefore, we studied the plasma factor in 20 patients undergoing acute anginal attacks in order to see whether there is any influence or a timedependent change after the event. The patients were subdivided into males or females as well as into those with or without maturity onset diabetes and who were smokers or no-smokers. As in-vitro test systems the rat abdominal aorta, human coronary artery and cultured endothelial and smooth muscle cells obtained from minipigs were used. Our findings demonstrate that incubating the different tissue samples in plasma leads to a significant increase of prostacyclin formation or of its stable breakdown 6-oxo-PGF1 respectively, in comparison to buffer control incubation. However, in none of the groups was a change observed during an anginal attack or in rate 60 and 120 minutes thereafter. These findings suggest that the prostacyclin synthesis stimulating plasma factor is not involved in hemostatic dysregulation, which has been observed to occur during and immediately after a coronary anginal attack.

Adult↗
PubMed1985

Prostaglandin synthesis in dental cysts.

The synthesis of prostaglandins by dental squamous cell cysts was studied. Radiothinlayer-chromatography (RTLC) showed C14-labelled arachidonic acid to be converted into the prostaglandins PGE2, 6-oxo-PGF1 alpha, PGF2 alpha and PDG2. In addition, hydroxyfatty acid synthesis in excess of total prostaglandin production was observed. The substances mentioned are thought to be causally involved in the osteolytic activity of dental cysts.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Evidence that PGI2-generation in human dental cysts is stimulated by leucotrienes C4 and D4.

Various prostaglandins, particularly PGE2 and PGI2, appear to play a major role in osteolytic processes. The bone-destructive action of dental squamous cell cysts is thought to be caused or at least mediated by prostaglandins. Both leucotrienes and prostaglandins are synthesized from a common precursor substance, i.e. arachidonic acid, in a series of reactions. There is a special relation between leucotrienes and PGI2 in that PGI2 synthesis in endothelial cells can be enhanced by LTC4 and LTD4. R-TLC showed conversion of the arachidonic acid added into PGI2 in 8 out of 12 cases, as reflected by the stable degradation product 6-oxo-PGF1 alpha. In 8 cases bioassay showed PGI2 synthesis without addition of LTC4 and LTD4. Incremental LTC4 and LTD4 additions were found to cause a highly significant increase of PGI2 synthesis rates. In summary, LTC4 and LTD4 stimulate PGI2 synthesis in chronic inflammatory processes in vivo and may thus elicit or accelerate osteolysis.

Arachidonic Acids↗
PubMed1985

Treatment with recombinant interferon-alpha-2C: multiple myeloma and thrombocythaemia in myeloproliferative diseases.

Forty-two patients with multiple myeloma were allocated to two groups to receive either polychemotherapy with vincristine, melphalan, cyclophosphamide and prednisolone, or recombinant interferon-alpha 2C monotherapy. The response rate of 43% in the interferon group was significantly lower than that in the chemotherapy group (89%). Patients with stage I disease showed better response rates than those with stage II or stage III disease. Eleven patients with thrombocythaemia due to polycythaemia vera, chronic myeloid leukaemia or essential thrombocythaemia were treated with recombinant interferon-alpha 2C and complete remissions were achieved in 7 of the 8 evaluable patients. Side-effects were common on interferon therapy, but could be reduced by dose reduction and were reversed by cessation of treatment.

Adult↗