ACE-inhibitor influence on rat glomerular prostaglandin-synthesis.
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6-Ketoprostaglandin F1 alpha↗
Biomedical subjects
H Sinzinger
Publications and source records attributed to H Sinzinger.
Platelet aggregation and platelet sensitivity-behaviour during normal and abnormal glucose tolerance testing.
Platelet aggregation response to ADP and platelet sensitivity to the antiaggregatory prostaglandin I2 (PGI2) were measured in 15 patients and 8 healthy volunteers undergoing intravenous glucose tolerance testing (GTT). Eight patients (5 female, 3 male, 44-57a) showed pathological GTT, in 7 patients (6 female, 1 male, 39-55a) and the healthy volunteers (6 female, 2 male, 24-39a) a normal response was monitored. After GTT in patients with pathological GTT the slope of the ADP-induced aggregation curve was diminished showing high variations, whereas the height of the aggregation curve remained unaltered. The platelet sensitivity to PGI2 was significantly (p less than 0.05) decreased during the performance of GTT and returned to prevalues until the end of GTT. In the patients as well as in the healthy volunteers with normal GTT no change could be monitored during the test. However, healthy volunteers showed significant (p less than 0.05) lower prevalues. The findings indicate, that an abnormal glucose tolerance is associated with a decreased platelet sensitivity to PGI2.
Adult↗
Pathomechanisms of atherosclerosis beneficially affected by prostaglandin E1 (PGE1)--an update.
The antiplatelet action of PGE1 was the basic concept for introducing this substance into clinical therapy of atherosclerosis. However, in the meanwhile a variety of other mechanisms have been discovered, which might be of importance, especially concerning the long-term benefit seen after treatment with PGE1, such as stabilization of endothelial lining, reflected by a decreased number of circulating endothelial cells and a decreased thrombogenicity (potentiated by endogenous EDRF-release), an inhibitory action on smooth muscle cells of the vessel wall such as decrease in mitotic and proliferative activity associated with a diminished extracellular matrix formation, an increase in fibrinolytic capacity, beneficial effects on white and red blood cells and some beneficial effects on the lipid metabolism by decreasing the arterial wall cholesterol content and upregulation of LDL-receptors as well as a moderate drop in serum cholesterol, seen in severe hypercholesterolemics only. It is assumed, that especially the vascular effects together with the hypolipidemic actions of PGE1 might be of major importance underlying the long-term benefit.
Alprostadil↗
[Defects in the prostaglandin system. VI. Acquired plasma factor defect].
A 44 year-old male was admitted to hospital in October 1984 presenting with enzymatic and electrocardiographic signs of posterior wall myocardial infarction. At this time 2 separate examinations revealed normal plasma factor activity. At the 1 year follow-up (November 1985) plasma factor activity was still present. However, in February 1987 for the first time, the patient's plasma failed to enhance PGI2 synthesis from vascular tissue in vitro. 3 further follow-up examinations within the next 6 weeks again revealed an acquired absence of plasma factor activity of unknown cause. No deterioration in clinical condition occurred. All relatives tested showed normal plasma factor activity.
Adult↗
[Defects in the prostaglandin system. VII. (Generalized, inherited [?]) cyclooxygenase defect].
Investigation of platelet function in a 55 year-old male suffering from peripheral vascular disease revealed platelet cyclooxygenase deficiency. Examination of femoral artery tissue at a later date likewise showed the presence of a cyclooxygenase defect. Investigated relatives were not affected. A 39 year-old male smoker admitted with an acute myocardial infarct without prodromal symptoms exhibited similar laboratory findings. In contrast to the cases reported in the literature so far, both our patients suffered from severe atherosclerosis, a relatively high platelet activity and an additional cyclooxygenase defect of cells other than the platelets. The patient with peripheral vascular disease died from sudden cardiac arrest.
Adult↗
[Defects in the prostaglandin system. VIII. A pathologic thrombocyte population in myeloproliferative syndrome, which forms no thromboxane from exogenous arachidonic acid].
In 2 out of 29 patients suffering from the myeloproliferative syndrome a lack of thromboxane conversion by platelets from exogenous arachidonic acid was discovered. In one patient PGE2 (30.9%) and 12-HETE (12-Hydroxyeicosatetraenoic acid) (42.8%) were formed instead, whilst in the other patient 12-HETE (72.9%) was the main metabolic product. In both the patients, serum and plasma TXB2, as well as malondialdehyde, were quite low. It is claimed that this phenomenon is due to the expression of a pathological population of platelets related to the disease.
Aged↗
[Collection, preparation and storage of human plasma for radioimmunologic determination of thromboxane B2].
There are at present several methods available for the quantitative determination of thromboxane B2. However, they give results differing in precision and biological information. If it were possible to exclude sampling and storage artefacts, radioimmunological plasma thromboxane B2 measurement would be the method of choice for routine clinical determinations. The optimum conditions for processing the plasma for such purposes were assessed in 10 healthy volunteers (6m, 4f, 24-37a). They include a 30-minute resting period before blood sampling, constant needle diameter, blood withdrawal without venous occlusion, proper anticoagulation and cyclooxygenase inhibition. Storage at -70 degrees C for less than 2 weeks and the avoidance of repeated freezing and thawing are further prerequisites. In contrast to widely-held opinion, the plasma levels of thromboxane B2 obtained using these precautions are of practical value, roughly comparable to those employing the platelet proteins beta-thromboglobulin and platelet factor 4. However, practically speaking determinations are limited to a small number of carefully handled samples. Hence, the method cannot be unreservedly applied to daily routine clinical use.
Blood Platelets↗
[Effect of PGE1 on the left ventricular ejection fraction].
12 patients with impaired left ventricular function were submitted to left ventricular ejection fraction measurements before and after increasing doses of PGE1 administered by i.v. or i.a. infusion. 6 responders out of the 12 patients showed a significant (p less than 0.01) improvement in LVEF, whereas the LVEF remained unchanged in the remaining 6 patients. 4 of the responders had received intravenous and 2 had received intraarterial PGE 1. Afterload reduction, venous tonisation, increased myocardial contractility and metabolic effects may be causative factors. These results suggest that PGE 1 therapy may be of therapeutic benefit in some patients with impaired LVEF.
Adult↗
[Prevalence of plasma factor deficiency in the Vienna population. Results of a screening study of 1,300 adults].
A screening investigation for the presence of risk factors for the development of atherosclerosis demonstrates a plasma factor deficiency in 0.8% in the Viennese population. These findings are in agreement with the data of a newborn screening performed earlier. All the persons were clinically healthy. In 4 of them at least 1 family member suffered from the same defect. The pathogenetic relevance of the plasma factor defect for thrombophilia at young age is discussed.
Adolescent↗
[Prostaglandin E1 between pathomechanism and therapy].
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Alprostadil↗
[Fibrinolytic activity, thrombocyte function and pharmacokinetics during intra-arterial or intravenous prostaglandin E1 infusion in patients with chronic arterial occlusive disease].
Monitoring various parameters of fibrinolytic activity in 6 patients with arterial occlusive disease during intra-arterial (i.a.) or intravenous (i.v.) prostaglandin (PG) E1 infusions indicated activation of the endogenous fibrinolytic system. However, due to the small number of patients not all test parameters revealed significant changes. None of the PGE1 infusion regimens used (1.25 or 2.5 ng/kg/min i.a. or 5 or 10 ng/kg/min i.v. for 120 min in each case) led to any significant change in various parameters checked for ex-vivo platelet function. In agreement with these data the radioimmunological determination of PGE1 in venous plasma did not reveal any significant rise. On the other hand, the circulating metabolite of PGE1, 15-keto-13, 14-dihydro-PGE1, reached plasma levels which correlated well with expected theoretical values taking the infusion rate into consideration. A potential mechanism by which even low plasma concentrations of PGE1 might affect platelet function in vivo is discussed.
Alprostadil↗
[Liver function parameters and fibrinogen in intra-arterial and intravenous PGE1 infusion].
It has been claimed that PGE 1 pathologically alters liver function, the effect being less pronounced after intra-arterial administration. A retrospective data analysis of 4 different studies does not support this view. There was no effect on serum transaminases, fibrinogen or blood sedimentation rate. Furthermore, there was no difference between the i.a. and i.v. route of PGE 1 therapy under the investigated conditions. Thus, the claim that impaired liver function is less pronounced after i.a. PGE 1 administration is no longer valid.
Aged↗
Comparable effect of prostaglandin E1 in decreasing in vivo platelet deposition on human lesion sites after intravenous and intraarterial application.
It had been claimed that prostaglandin E1 is degraded during first lung passage to a major extent. Clinical results, however, as well as various platelet function tests and coagulation parameters revealed no apparent difference after i.v. and i.a. infusion. Thus, we examined the question what the quantitative difference between i.v. and i.a. PGE1-application would be upon in-vivo platelet function assessed by platelet uptake over active lesion sites as well as platelet half-life monitoring after autologous 111-In-oxine platelet labelling. In patients suffering from peripheral vascular disease stage II according to Fontaine PGE1 was able to decrease platelet uptake after i.v. and i.a. therapy to a comparable extent; similarily, a significant prolongation in platelet half-life was noted, again revealing no difference. As the decrease in platelet uptake is assumed to be predominantly a vascular effect, it is hypothetized that more stable derivatives of PGE1 are active, counterbalancing a lower biological activity with a longer half-life.
Alprostadil↗
[Technic and clinical use of radioactive labelling of autologous granulocytes].
Gamma-camera imaging after injection of radiolabelled autologous leucocytes can be very helpful in the diagnosis, localization and further clinical treatment of inflammatory diseases. We present a technique allowing sterile separation of white blood cells and labelling with 99mTc-phytate or -oxine and with 111In-oxine, -oxine sulphate or -tropolone. The method is non-invasive and the radiation dose amounts to less than 80 mrad using 100 microCi 111Indium. The use of radiolabelled granulocytes is of particular diagnostic value in patients with septicaemia of unknown origin. Whole body scanning allows not only visualization of enhanced splenic uptake in septicaemia, but also localization of an inflammatory process. Preferential indications for a diagnostic approach using radiolabelled granulocytes are inflammatory abdominal processes which cannot easily be documented by means of other non-invasive techniques, such as inflammatory bowel disease (Crohn's diseases and ulcerative colitis), arthritic processes and abscesses of the liver and spleen, as well as subphrenic and retroperitoneal abscesses. Untreated osteomyelitis can be located with the help of labelled granulocytes, but in patients treated with antibiotics a false negative result is obtained in approximately 50% of cases for as yet unknown reasons, even in the presence of a still active osteomyelitic process.
Abscess↗
Insufficient binding of monoclonal antibody Mabgc to granulocytes in vivo and in vitro.
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Antibodies, Monoclonal↗
Platelet viability (aggregation, migration, recovery) after radiolabelling from hypercholesterolemics using various tracers (oxine, oxine-sulphate, tropolone, MPO).
Earlier results indicated a diminished labelling efficiency and recovery negatively linked to actual cholesterol and lipoprotein values in hyperlipoproteinemics. This study was designed to examine whether other alternative tracers exhibit similar results and to study the influence on platelet viability in the presence or absence of PGI2. We demonstrate that no substantial difference occurs between the four tracers concerning labelling efficiency and recovery in normo- and hypercholesterolemics. Cholesterol severely affects the labelling parameters for all the tracers to a comparable extent. The absolute platelet function varies considerably, however, the percent changes in normo- and hypercholesterolemics seen before and after the labelling procedure do not differ significantly. PGI2 improves recovery in general, however, without affecting labelling efficiency or in vitro viability testing. As prolonged incubation further increases labelling efficiency, the presence and extent of hyperlipoproteinemia should be known in order to avoid poor labeling and viability and subsequently poor clinical results.
Adult↗
Reduced biological half-life of plasma prostacyclin in pre-eclampsia.
The biological half-life of prostacyclin was short (5.02 +/- 2.10 min) in 5 out of 7 patients with pre-eclampsia; in the remaining two patients the half-life was normal at 9.78 and 10.27 min, respectively. Four weeks after delivery, the half-life was 5.83 min in one patient but had returned to normal 10.16 +/- 1.77 min) in the other four. In normal pregnancy and healthy non-pregnant females the values were within the normal range. The shortened half-life of PGI2 may account for a decreased local availability of biologically active PGI2 with the consequent decrease in placental perfusion, growth retardation and thrombosis which are often seen in pre-eclampsia.
Adult↗
Evaluation of prostaglandin-receptors in human and rat liver: interspecies differences at the prostaglandin receptor-level.
The properties of PGE1-, PGE2- and iloprost (stable PGI2-analogue)-binding sites on normal human and rat liver surface cell membranes were investigated. The specific binding of [3H]PGE1 to human (rat) liver surface cell membranes could be displaced most effectively by unlabeled PGE1 (IC-50:2.5 +/- 1.7, (6.1 +/- 2.1) microM) and the specific binding of [3H]PGE2 by unlabeled PGE2 (IC-50: 1.9 +/- 0.9 (2.0 +/- 0.8) microM. The Scatchard analysis on [3H]PGE1- as well as on [3H]iloprost-binding was curvilinear whereas it was clearly linear on [3H]PGE2-binding in both the species. The high-affinity [3H]PGE1-sites showed a Bmax of 36.3 +/- 5.2 (21.3 +/- 4.3) fmol/mg protein and a Kd of 2.1 +/- 1.8 (1.9 +/- 0.7) nM, the low-affinity [3H]PGE1-sites a Bmax of 93.4 +/- 18.2 (86.1 +/- 13.2) fmol/mg protein and a Kd of 10.5 +/- 2.9 (15.1 +/- 3.2) nM. The high-affinity [3H]iloprost-sites exhibited a Bmax of 71.4 +/- 13.9 (35.9 +/- 8.2) fmol/mg protein and a Kd of 4.1 +/- 1.2 (1.7 +/- 1.8) nM, the low-affinity [3H]iloprost-sites a Bmax of 217.3 +/- 42.1 (142.9 +/- 17.8) fmol/mg protein and a Kd of 16.3 +/- 4.9 (9.2 +/- 7.2) nM. The [3H]PGE2-sites showed a Bmax of 135.4 +/- 51.9 (38.8 +/- 7.4) fmol/mg protein and a Kd of 16.2 +/- 3.2 (2.5 +/- 1.2) nM. It is assumed that prostaglandins of the E-series are promising substances in the regulation of human and rat liver function since liver cells are able to bind reasonable amounts of these substances in a high affinity manner. However, interspecies differences in the affinity of the prostaglandins to their receptor-sites make it strange to assume that the same biological findings claimed several times for the rat liver are relevant for human too.
Animals↗