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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 415 records · Page 23Linked to original sources
PubMed1986

Platelet half-life, plasma thromboxane B2 and circulating endothelial-cells in peripheral vascular disease.

We studied platelet half-life (T/2), plasma thromboxane B2-levels (TXB2) and circulating endothelial cells in 107 patients with a mean age of 63 +/- 6.8 years and angiographically proven peripheral vascular disease (PVD). Patients were divided into 4 groups according to Fontaine but also according to additional clinical manifestations of atherosclerosis like coronary heart disease (CHD) and cerebrovascular disease (CVD). Furthermore, the influence of sex and smoking was investigated. Compared to patients without atherosclerotic manifestations we could detect an enhanced platelet consumption measured as shortened platelet half-life time (79.2 +/- 9.1 vs 100.9 +/- 5.6 hours, p less than 0.001 and an increased platelet activity measured as increased TXB2-plasma levels (51.6 +/- 20.9 vs 23.2 +/- 11.2 ng/ml, p less than 0.001). Correspondingly, the amount of circulating endothelial cells was increased 45.2 +/- 25.7 vs 20.3 +/- 23.4, p less than 0.001). Patients with PVD who smoked had the shortest actual platelet half-life, the highest TXB2 plasma levels and the greatest amount of circulating endothelial cells compared to non-smoking patients and controls. Patients with clinical stage IV according to Fontaine had the shortest platelet half-life, the highest TXB2 plasma levels and the greatest amount of circulating endothelial cells compared to the other clinical stages. Analyzing the influence of additional clinical manifestations of atherosclerosis we could detect only in patients with PVD and CHD significant differences compared to the other groups.

Adult↗
PubMed1986

Platelet sensitivity to prostacyclin in smokers and non-smokers.

Platelet activating effect of cigarette smoking appears to be important in the development of atherosclerosis. We previously demonstrated a reduced sensitivity of platelets to exogenous prostacyclin (PGI2) in vitro from patients with proven atherosclerotic disease, indicating a possible role of altered platelet function in the development of atherosclerosis. We now hypothesize that cigarette smoking might be an important cause of altered platelet sensitivity to PGI2 observed in patients with atherosclerosis. To test this hypothesis, the response of platelets to exogenous PGI2 was tested in chronic smokers and non-smokers, prior to and after smoking two cigarettes (active smoking) and prior to and after exposure to a tobacco smoke-contaminated atmosphere (passive smoking). This study indicates that platelets of chronic smokers are less sensitive to exogenous PGI2 than platelets of non-smokers. In addition, active as well as passive smoking decreases platelet sensitivity to PGI2 in non-smokers, whereas chronic smokers exhibit no further decline. We conclude that decreased platelet sensitivity to PGI2 might be an important contributing factor to the altered platelet function observed in patients with atherosclerosis.

Adult↗
PubMed1986

Limited value of 111-indium platelet scintigraphy in renal transplant patients receiving cyclosporine.

Since the differential diagnosis between cyclosporine (CyA) nephrotoxicity and acute graft rejection is still a problem in clinical routine, we studied retrospectively the value of 111-indium (In) platelet scintigraphy in 53 patients immunosuppressed with CyA and prednisolone. Autologous platelets were labeled once per week. After daily gamma camera imaging, the platelet deposition in the graft was expressed as platelet-uptake ratio (PUR). The patients were monitored during the first 4-6 weeks after surgery. PUR values measured during an episode of graft dysfunction were compared to the histological diagnosis. The PUR of well-functioning and stable grafts measured 1.07 +/- 0.11 (mean +/- SD). The 111-In platelet scintigraphy failed to register acute interstitial rejection. The PUR values in episodes of chronic vascular rejection, of acute tubular necrosis due to prolonged ischemia times, of tubular CyA nephrotoxicity and of cytomegalovirus (CMV) infection did not differ from the PUR of well-functioning and stable grafts as well. The PUR was significantly increased to 1.48 +/- 0.26 because of a marked platelet deposition in the graft in episodes of acute vascular rejection. In 4 cases of microvascular CyA nephrotoxicity the same phenomenon of significantly increased PUR (1.33 +/- 0.18), could be encountered, too. Two of these 4 cases resembled the hemolytic uremic syndrome (HUS). The value of PUR measurement for diagnosis of acute vascular rejection and microvascular CyA nephrotoxicity together, was: sensitivity 0.62, specificity 0.95, predictive value of positive result 0.64, predictive value of negative result 0.94.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Hemodynamic effects of nitroglycerin following acute inhibition of prostaglandin synthesis].

The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Effect of leukotrienes C4 and D4 on prostaglandin I2-liberation from human lymphatics.

Whereas prostaglandin I2 (PGI2), a major metabolite of human lymphatics, does not itself affect lymphatic contractility significantly, it is able to counterbalance the contractile response to thromboxane and leukotrienes. We now demonstrate that leukotrienes C4 and D4 evoke a dose-dependent increased production of PGI2 from human lymphatics. It is likely that leukotrienes either exert a contractile rhythmic effect on human lymphatics or, alternatively, evoke increased PGI2-formation which relaxes human lymphatics. These mechanisms may be of local importance in regulating lymphatic "tone" at sites of inflammation as leukotrienes are liberated from activated white blood cells.

Adolescent↗
PubMed1986

[Prostacyclin- and thromboxane synthesis in the vascular wall after gammatron irradiation].

One year aged rabbits were exposed to a single dose of 100, 500 or 1000 rd (1.0, 5.0 or 10 Gy) to the abdominal aorta. The non-irradiated thoracic aortic segment served as control. The animals were killed between one and 336 hours after the irradiation. Four animals were examined in each group. The prostacyclin formation was assessed by means of a radioimmunoassay against its stable breakdown 6-oxo-PGF1 alpha, the thromboxane A2-formation using a radioimmunoassay for thromboxane B2. Local irradiation causes a temporary increase of both the compounds. In contrast to thromboxane B2, the 6-oxo-PGF1 alpha exhibits a long-lasting depression. The higher the radiation dose, the more intensive the increase and the long-lasting depression of 6-oxo-PGF1 alpha. The liberation of eicosanoids and subsequent hemostatic dysregulation at different intervals after irradiation might contribute to an important extent to the radiation induced vasculopathy.

Animals↗
PubMed1986

Enhanced prostaglandin I2-formation of human lymphatics during pulsatile perfusion.

Previous studies demonstrate that prostacyclin (prostaglandin I2, PGI2) is the main arachidonic acid product in human lymph vessels. Pulsatile perfusion increases and prolongs PGI2-formation as do leukotrienes (LT) such as LTC4. Thus, physical activity besides local mechanical and biochemical influences on lymph pressure and flow also stimulates local lymphatic PGI2 synthesis, a prime counterbalancing factor in lymphatic constriction induced by other eicosanoids.

Adolescent↗
PubMed1986

Platelet plasma membrane changes in human type IIa hypercholesterolemia.

We have examined platelets collected from hypercholesterolemic (HC) young patients (n = 12) and from normocholesterolemic young volunteers (n = 9) by means of freeze fracture. The mean value of the surface density per square micrometer of the openings of the surface-connected canalicular system was significantly higher (p less than 0.03) in the HC patients (2.4 +/- 0.6) compared with the controls (1.8 +/- 0.5). It was also positively correlated with the low-density lipoprotein cholesterolemia/total cholesterol ratio (p less than 0.005) and inversely correlated with the high-density lipoprotein cholesterolemia/total cholesterol ratio (p less than 0.01). These data indicate that the circulating platelets of HC type IIa patients appear changed at ultrastructural level and that their modification may be somehow related to the atherogenetic processes.

Adolescent↗
PubMed1986

Shortened platelet half-life in multiple myeloma.

Various defects in platelet function have been reported as being associated with multiple myeloma. In 30 myeloma patients and 15 healthy controls, we investigated platelet survival using in vitro labeling of autologous platelets with 111indium-oxine and measuring the in vivo kinetics of the radioisotope. Significantly shortened platelet half-life in patients averaged 73 hours, while platelet half-life in the healthy controls averaged 107 hours. In myeloma patients, serum levels of thromboxane B2, beta-thromboglobulin, and platelet factor 4 were significantly elevated; aggregation indices were within the pathological range; platelet counts and spleen-liver indices, however, were comparable to those of the healthy control group. No statistical correlation was found between platelet half-life and paraprotein concentrations. Our findings suggest an initial--so far unexplained--intravascular process of platelet activation and consumption that finally manifests in shortened platelet half-life. It seems that overt thrombocytopenia develops only when the compensatory capacity of the bone marrow finally becomes exhausted. Further studies should be able to elucidate the pathophysiologic processes involved.

Blood Platelets↗
PubMed1985

[Is the tonisation of varicose veins due to elevated prostacyclin synthesis caused by dihydroergotamine?].

Prostacyclin is the most potent inhibitor of platelet aggregation and a very strong vasodilator. A few reports on a moderate vasoconstrictory response in certain vascular segments in various species have received less attention. We demonstrated recently that PGI2 dilates the arterial wall and has a constrictory effect on the venous wall. Normal and varicose human veins show a dose-dependent constrictory response to PGI2. Pretreatment of patients with 2.5 mg dihydroergotamine t.i.d. for 10 days increases venous PGI2 synthesis significantly. In vitro contractility response is identical in normal and varicose veins. Furthermore, no difference in contractility was registered in veins derived from treated and untreated patients. The significantly enhanced formation of PGI2 evoked by dihydroergotamine might be responsible for the tonisation of normal, healthy veins, as well as varicose veins.

Adult↗
PubMed1985

[Defects in the prostaglandin system. IV. Inborn, nonfamilial plasma factor deficiency].

On routine screening of 143 newborn infants, complete plasma factor deficiency was discovered in 4 cases. All the relatives, however, exhibited normal plasma factor activity. Up to now all 4 babies are healthy. Long-term follow up should clarify whether an inborn plasma factor deficiency might predispose to diseases accompanied by haemostatic imbalance.

Biological Assay↗
PubMed1985

[Defects in the prostaglandin system. V. Inherited (?) disorder of prostacyclin degradation in the plasma (Wien-Döbling defect)].

The case report is presented of a woman of child-bearing age who developed myocardial infarction. An extremely shortened in vitro half-life of PGI2 in plasma was detected in this patient. This new familial defect "Wien-Döbling", in the prostaglandin system might affect an essential coregulator of haemostatic balance in man. It is not known whether this short half-life of PGI2 in vitro is due to accelerated degradation or a failure in stabilization of this biologically active compound.

Adult↗
PubMed1985

[Platelet function after the single administration of buflomedil].

Earlier investigations have demonstrated that buflomedil, a substance which is successful in the clinical treatment of peripheral vascular disease, exerts an inhibitory effect on ADP-induced aggregation ex vivo and in vitro. In the presented study the effect of buflomedil on platelets is investigated. Clinically widely used platelet function tests were performed after a single oral dose of buflomedil (300 mg) to healthy volunteers. Again, an ex vivo inhibition of ADP-induced aggregation was confirmed. None of the other parameters examined was influenced by the administered drug, such as plasma thromboxane B2, the platelet proteins, the platelet sensitivity to antiaggregatory prostaglandins and the prostacyclin synthesis stimulating plasma factor.

Adult↗