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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 343 records · Page 19Linked to original sources
PubMed1988

Indium 111-A-bleomycin--a new tracer for imaging orofacial neoplasms.

Forty-six patients with maxillofacial squamous cell cancer of variable keratinization underwent radioisotope diagnosis using Indium 111-A-bleomycin. This new technique was applied to expand the battery of diagnostic tools available for detecting maxillofacial neoplasms. Its high specificity (100%) and sensitivity (96%) make it well suited for detection of both local and distant recurrences as well as tumor regrowth. Preliminary whole body retention measurements also indicate that this technique looks promising for potential therapeutic use.

Aged↗
PubMed1988

Diminished platelet residence time on active human atherosclerotic lesions in-vivo--evidence for an optimal dose of aspirin?

Although aspirin is an old drug, its optimal dose for the treatment of human atherosclerosis has not been finally proven. Various in-vitro and ex-vivo platelet function tests revealed a dose range from 1 to 3000 mg as being optimal. It was thus the goal to examine its in-vivo efficacy in human suffering from peripheral vascular disease in 7 different doses ranging from 1 mg to 1000 mg a day. All these patients have been treated for 3 months. Platelet half-life and platelet uptake ratio show an in part significant improvement being most pronounced at the daily doses of 20 and 1000 mg respectively. No change occurs in the placebo treated controls. These findings indicate, that 20 or 1000 mg aspirin taken daily per os, are superior to the other doses examined concerning the in-vivo platelet function (as measured by platelet half-life) and rendering the arterial surface less thrombogenic (as reflected by platelet uptake ratio-measurements).

Administration, Oral↗
PubMed1988

Epoprostenol in patients with Raynaud's disease.

Prostaglandin metabolism and the clinical effect of epoprostenol (prostacyclin, PGI2) infusions were studied in thirteen patients with Raynaud's disease. Epoprostenol was infused at 5 ng/kg/min for six hours daily for two consecutive five day periods, separated by a two day interval. No beneficial effects either during or after infusion could be detected in terms of frequency of severity of attacks or on skin temperature measurement. Raynaud's patients had significantly lower serum thromboxane B2 levels than normal controls though plasma levels of thromboxane B2, 6-oxo-PGF1 and the bicyclic metabolite of PGE2 did not differ between the two groups. Platelets from Raynaud's patients had a significantly lower conversion rate of arachidonic acid into thromboxane B2 and HHT and a significantly higher rate of HETE production than platelets from controls.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Stimulation of prostacyclin formation by the platelet-derived growth factor--an important pathomechanism for atherogenesis?

The capacity of vascular tissue in generating PGI2 has been accepted to be a key property in hemostatic balancing at a local level. Earlier it has been shown that PDGF is able to enhance SMC-proliferation. As this process is associated with c-AMP changes which again are influenced by PGI2, the question arose, whether PDGF itself exerts an effect on PGI2-synthesis. Using normal and atherosclerotic human arterial tissue, animal arteries and cultured cells with and without addition of various PDGF-concentrations this question was answered by means of bioassay and RIA-determination in a static and a pulsatile perfusion chamber system as well. In general, between 10 and 50 ng PDGF/ml, a significant increase either in PGI2-formation or 6-oxo-PGF1 alpha can be seen. A similar dose dependent stimulation of PGI2-synthesis can be monitored for vascular tissue and cultured cells as well. Static incubation and perfusion chamber experiments reveal comparable findings of PDGF stimulatory capacity on PGI2-formation. In contrast, no such effect can be seen using human umbilical artery. The half-life of PGI2-formation in the perfusion chamber model is comparable in presence and absence of PDGF as well. The stimulatory effect of PDGF on atherosclerotic vascular tissue is significantly less pronounced than onto normal one. Concluding from our findings we speculate that PGI2 prevents PDGF-release from platelets, thus decreasing smooth muscle cell proliferation and improving cellular lipid metabolism; an insufficient response of vascular tissue onto PDGF to generate PGI2 might be a key event in the pathogenesis of early atherosclerosis favouring a negative vicious cycle.

Animals↗
PubMed1988

High-performance-liquid-chromatographic analysis of radiolabelled prostaglandins and fatty acids with the radial compression column.

The method described is a rapid and reproducible separation of different prostanoids. With the use of a reversed phase 5 micron-radial compression column instead of a steel column-HPLC analysis is improved within a shorter time. In order to separate also the non-polar substances like arachidonic acid (AA) and hydroxy fatty acids in an appropriate time, a gradient-elution is used. The radioactivity is counted immediately after the column within a radioactivity monitor. With this system it is possible to examine the AA-metabolites enzymatically formed in cells or tissue from exogenous AA.

Aged↗
PubMed1988

PGE1 reduces collagen and glycosaminoglycan synthesis in rabbit aorta.

In 18 male rabbits the influence of PGE1 on collagen and glycosaminoglycan synthesis assessed by means of the incorporation of radiolabelled precursors has been examined. It is demonstrated that PGE1 induces a 20-30% drop both in 14C-proline and 35S incorporation into the vessel wall. These findings are in line with earlier data on the inhibition of proliferation of smooth muscle cells and a decrease in mitotic activity. The results present one piece of evidence more that PGE1 is acting as an anti-atherosclerotic agent in vivo at the vascular level. This pathomechanism, as well as the fact that this vascular effect is achieved--in an animal experiment at least--via an intravenous PGE1-application, offers new basics for the treatment of atherosclerosis in man.

Alprostadil↗
PubMed1988

Local prostaglandin E2 in patients with oral malignancies undergoing chemo- and radiotherapy.

Patients undergoing chemo- and/or radiotherapy for malignancies were often found to develop annoying inflammation of the oral mucosa. As prostaglandins are known to be cytoprotective. Prostaglandin E2 was given to 10 patients who received combined radio- and chemotherapy for oral neoplasms. Patients receiving PGE2 reported substantially less intense pain then those in the control group. Our statistically significant results indicate that topical treatment of side effects produced by combined radio- and chemotherapy of oral neoplasms with PGE2 holds promise and is clearly superior to conventional treatment modalities.

Adult↗
PubMed1988

Decrease of prostaglandin I2 binding sites in thyroid cancer.

The properties of specific prostaglandin I2 (prostacyclin, PGI2) binding sites in normal thyroid tissue have been characterised. Tissue samples obtained intraoperatively from patients with 'cold' solitary thyroid nodules (as preoperatively selected by thyroid gland scintigraphy, thyroid gland ultrasonography and Papanicolaou cytology following fine needle aspiration of the nodule area) have been used for thyroid membrane preparation. Employing [3H]iloprost, a chemically stable PGI2-analogue as a radioligand, saturation experiments for comparative binding studies have been attempted. Scatchard analysis of the binding data obtained for normal thyroid parenchyma distant to the nodule area revealed heterogeneity of the [3H]iloprost sites exhibiting a high-affinity binding capacity (Bmax) of 613.2 +/- 130.4 fmol mg-1 membrane protein and a low-affinity binding capacity of 5.1 +/- 1.6 pmol mg-1 membrane protein. The equilibrium dissociation constant (Kd) amounted to 18.9 +/- 8.9 nM and to 131.5 +/- 39.2 nM, respectively. Scatchard analysis of the binding data obtained for benign thyroid adenoma indicated significant lower binding capacities exhibiting a Bmax of 325.8 +/- 110.0 fmol mg-1 membrane protein (Kd: 31.0 +/- 7.5 nM) for the high-affinity sites and of 3.9 +/- 2.5 pmol mg-1 membrane protein (Kd: 364.9 +/- 183.6) for the low affinity sites. In cancer tissue a selective loss of the low affinity sites and a significant diminution of the high-affinity sites was observed: in well differentiated cancer the high-affinity sites showed a Bmax of 299.7 +/- 46.0 fmol mg-1 membrane protein (Kd: 38.9 +/- 7.3 nM), in anaplastic cancer, less differentiated papillar and follicular cancers of 180.6 +/- 25.1 fmol mg-1 membrane protein (Kd: 54.6 +/- 16.7 nM). Well differentiated papillar and follicular cancers did not differ from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1988

The effect of various antibiotics on the labelling efficiency of human white blood cells with 111In-oxine.

Earlier clinical studies revealed that in patients suffering from chronic osteomyelitis (n = 10) undergoing antibiotic therapy the white blood cell scanning missed the right diagnosis in 40% of cases, whereas all the acute untreated cases (n = 6) were imaged correctly. Thus, it was suspected that an impaired labelling efficiency and white blood cell function might have been causative. Retrospective analysis of labelling efficiency exhibited no difference between patients on antibiotics (n = 12) and those not on antibiotics (n = 29). Prospective cellular viability testing in 81 patients, 71 of whom were on various antibiotics, using latex particles (phagocytosis) and the Trypan blue exclusion test, did not reveal any different function behaviour either. Examining the labelling efficiency (after 111In-oxine and 111In-oxine-sulphate labelling), recovery, half-life and viability of white blood cells of 107 patients undergoing therapy with various antibodies as compared to controls, it becomes evident that the antibiotic therapy is not causative of the clinical difference observed.

Adult↗
PubMed1988

Imaging and kinetics studies with radiolabelled autologous low-density lipoproteins (LDL) in human atherosclerosis.

Experimental data in rabbits show a significantly (P less than 0.01) increased vascular uptake of autologous 125I-radiolabelled low-density lipoproteins (LDL) at various time intervals after experimental lesioning. In some vascular areas in patients, a positive gamma-camera image can be obtained as early as 30 min after reinjection of autologous 123I-labelled LDL only. Monitoring of kinetics provides reliable information on localized increased LDL entry in certain vascular areas. Although a number of methodological improvements are needed, the technique described may be of clinical value in the future.

Adult↗
PubMed1988

Effects of exercise on parameters of blood coagulation, platelet function and the prostaglandin system.

Acute exercise causes a temporary short lasting activation of blood coagulation, platelet function and the prostaglandin system, the extent of these alterations being significantly less pronounced in well trained athletes than in untrained persons. The reversal is also much faster in athletes, thus providing an underestimated indicator of the individual training status. Changes in platelet function and some plasma parameters of coagulation exhibit a significant correlation to base excess, pH and lactate. Immediately after acute exercise there is, therefore, an increased risk for acute thrombosis if an additional risk such as doping and/or smoking and/or contraceptive pill use is present. This risk is again higher in untrained than in well exercised persons. Patients with clinically manifest atherosclerosis (predominantly with risk factors) performing only occasionally anaerobic exercise are more likely to be at special risk. The overall response of the coagulation system, platelet function and prostaglandin system is significantly impaired. In contrast, regular exercise causes decreased activity of platelets and the coagulation system resulting in an improvement in haemostatic balance. As well as the psychological factors beneficially influencing the subjective feeling, it seems rather likely that the above mentioned mechanisms may be one factor underlying the decreased death rate from cardiovascular disease in persons performing regular physical activity.

Blood Coagulation↗
PubMed1988

The platelet rebound phenomenon during PGI2-infusion occurs at the receptor level.

In 6 patients treated with continuous prostaglandin I2 (PGI2)-infusion using a portable pump at a rate of 5 ng/kg/min for 7 days drug receptor interaction of [3H]Iloprost, a stable PGI2 analogue, with a particulate platelet membrane fraction was investigated. Saturation binding experiments of the high affinity platelet prostacyclin receptor performed before and at the end of PGI2 infusion revealed a significant increase of dissociation constant (Kd) and increase in maximal number of binding sites (Bmax). These findings suggest that continuous long-term PGI2 infusion results in a functional desensitization of the membrane-bound PGI2 platelet receptor with a decrease in receptor affinity and an increase in number of binding sites as suggested earlier based upon platelet sensitivity behaviour.

Aged↗
PubMed1988

In vivo modulation of platelet deposition on human atherosclerotic lesions by various antiaggregatory prostaglandins.

The influence of intravenous infusions of various prostaglandins on in vivo platelet function was studied after labelling of autologous platelets with 100 mu ci 111 indium-oxinesulfate in patients with peripheral vascular disease stage II according to FONTAINE. PGI2 (5 ng/kg/min) provoked a significant decrease of platelet deposition and a prolongation in platelet half-life time (74 +/- 6 vs 68 +/- 5 hours). PGE1 (25 ng/kg/min) failed to influence platelet deposition, but prolonged significantly platelet half-life time (82 +/- 6 vs 76 +/- 8 hours). CG 4203 (25 ng/kg/min) decreased significantly platelet deposition and prolonged significantly platelet half-life time (73 +/- 10 vs 67 +/- 11 hours). Iloprost (1 and 2 ng/kg/min) reduced significantly platelet deposition without dose relation. Half-life time was increased significantly after therapy compared to placebo (1 ng: 76 +/- 7 vs 69 +/- 7; 2 ng: 73 +/- 9 vs 67 +/- 9 hours).

Aged↗