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Biomedical subjects

G Ostermann

Publications and source records attributed to G Ostermann.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Megakaryocytic myelosis--clinical aspects, morphology and platelet function].

The study reviews 22 patients, aged between 19 to 73 years, with megakaryocytic myelosis. In the course of the disease 11 patients presented haemorrhagic manifestations, 12 patients thrombotic complications, and 6 patients the association of haemorrhage and thrombosis. The maximum platelet counts ranged from 524 to 2700 x 10(9)/l. The bone marrow showed a conspicuous megakaryocytic proliferation with polyploidy of the nuclei, giant forms and clusters. Marked alterations of erythro- and granulopoiesis were excluded. There was no evidence for a reactive thrombocytosis in any case. Patients with thrombocythaemia due to megakaryocytic myelosis (n = 14), with secondary thrombocytosis of various origin (n = 16), and a control group of healthy donors (n = 20) were investigated with respect to the aggregation behaviour and the total calcium content of blood platelets. In 9 of 14 patients with megakaryocytic myelosis platelet rich plasma did not respond to epinephrine (15 mumol/l), a concentration which induced at least weak aggregation in 14 of 16 patients with secondary thrombocytosis and also in healthy subjects. In patients with megakaryocytic myelosis the mean extent of aggregation induced by epinephrine, collagen or adenosine diphosphate was significant lower as compared to controls whereas in patients with secondary thrombocytosis in most cases this parameter did not differ significantly from that of controls. The total calcium content of platelets was significantly lower in both groups of patients as compared to controls. In 14 patients with megakaryocytic myelosis the concentration of the glycoprotein (GP) IIb-IIIa complex was estimated by crossed- and rocket-immunoelectrophoresis and found to be decreased in 8 of them.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Blood platelet behaviour in patients with a type I diabetes mellitus.

Platelets appear to be involved in the development of vascular diseases in diabetic patients. In a number of studies, platelet adhesion and aggregation has been found to be enhanced in diabetic patients indicating a platelet hyperreactivity. However, contradictory results on hyperreactivity of diabetic platelets towards agonists published in the literature leading to the problem of reliability of agonist-induced aggregation as a parameter which is able to reflect an altered platelet reactivity. Therefore, we introduced the quantification of actin filaments of platelets as an early indicator of platelet hyperreactivity. In 20 patients with type I diabetes mellitus agonist-induced aggregation, spontaneous aggregation, malondialdehyde (MDA)-formation, plasma lipid status and the ability of plasma to degrade platelet activating factor (PAF) as well as the G- to F-actin equilibrium of platelets were assayed. Compared to an age- and sex-matched control group F-actin values, spontaneous aggregation and PAF-hydrolase were significantly increased in diabetic patients.

Actin Cytoskeleton↗
PubMed1989

The contribution of individual lipoproteins to the degradation of platelet-activating factor in human serum.

Platelet-activating factor (PAF) is rapidly degraded in vivo by the action of a specific acetylhydrolase. Measuring the PAF-acetylhydrolase activity in serum from 12 healthy volunteers a maximum velocity of 67.2 +/- 11.8 nmol/min X ml and a Km value of 15.8 +/- 2.9 mumol/l were ascertained. More than 90% of the activity was found to be associated with lipoproteins. It was detected in isolated VLDL, LDL, Lp(a) as well as HDL2 but not in HDL3. The PAF-acetylhydrolase activities associated with the various lipoproteins were shown to behave like a unique enzyme with distinct kinetic properties. Because VLDL and LDL were found to take up about 5 and 2.5 times more PAF with respect to their mass than HDL, it is concluded that lipoproteins affect the PAF-acetylhydrolase activity at the level of substrate presentation. As a consequence of the distinct kinetic properties, the lipoprotein-associated PAF-acetylhydrolase activities do not contribute proportionately to the degradation of PAF in serum. The latter is shown to depend primarily on the amount of PAF-acetylhydrolase bound to the apoprotein B-containing lipoproteins.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1989

Enhanced degradation of platelet-activating factor in serum from diabetic patients.

The degradation of platelet-activating factor (PAF) and lipid concentrations were measured in sera from 20 patients with insulin-dependent diabetes mellitus and from 20 age- and sex-matched healthy volunteers. The PAF-degrading capacity as well as triglycerides and total and very low density and low-density lipoprotein cholesterol were found to be significantly increased in the patients group, whereas the difference observed in high-density lipoprotein cholesterol was statistically nonsignificant. There were also a series of close relationships between the degradation of PAF and some lipid variables in the control group. These results confirm the parallel changes of lipoproteins and PAF-degrading capacity described previously in serum from atherosclerotic patients and extend it to patients suffering from diabetes mellitus.

Adult↗
PubMed1989

Apolipoproteins as risk indicators of ischemic heart disease.

About 50% of the individuals with a coronary risk show lipid levels within the normal range. Therefore, apolipoprotein profiles could be better risk indicators than TC or TG. Apolipoproteins generally discussed in this context are apo A1, apo B, and apo E. Their diagnostic validity, however, is ambigously evaluated. The individual iso-protein pattern of apo E is important for the differential diagnosis of the type III hyperlipidemia with its strong predisposition for premature atherosclerosis. Moreover, the extent of the apo E sialylation seems to be important because the modification of apo E by sialic acid alters its metabolism. Our date provide evidence that in IDDM and NIDDM the degree of apo E sialylation is increased. Concerning apo A1 and B we tried to find out parameters suitable for the prediction of the coronary risk both in the hyperlipidemic and the normolipidemic state. 64 male survivors of a myocardial infarc"ion and 60 matched controls were included in the study (group I). From group I a supopulation showing non-pathological values for TC and TG was selected (group II with 31 survivors and 44 controls). The diagnostic validity of the parameters apo A1, apo B, TC, HDL-C, apo A1/apo B, TC/apo B, HDL-C/apo B, TG, TG/apo A1, TG/HDL-C, TC-HDL-C/apo B determined by calculation of their sensitivities, specificities, efficiencies, and predictive values. Only the parameters TC/apo B, HDL-C/apo B, and apo B were suitable in the order given for detection of the coronary risk. Using the TC/apo B ratio 71-76% of the controls and 79% of the survivors could be exactly reclassified independent of the group they belonged to.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMed1989

[Assay of fructosamine. Value and limits in diabetology].

Fructosamine test using a Nitroblue Tetrazolium (NBT) method offers many advantages: quickness, reproducibility, easy automation and unexpansiveness, but a standardization of the different methods is needed. The results can be expressed in absolute value of equivalent DMF per liter, except in pregnancy where mumol per g of protein is used. The interpretation of the results can be difficult in case of quantitative and/or qualitative proteins abnormalities: icterus and severe chronic renal insufficiency. Fructosamine is significantly higher in diabetic patients. It gives a good correlation with glycated haemoglobin but the provided information is different, concerning a shorter period of 2 to 3 weeks and perhaps more sensitive to recent glycaemic variations. Fructosamine test does not seem to be a good screening test for diabetes and impaired glucose tolerance. The test indications of the assay could be: situations where the dosage of glycated haemoglobin is not interpretable, diabetic pregnancy follow-up and short term evaluation of a therapeutic change on glycaemic control. However, the individual significance of fructosamine concentration remains to be assessed and seems to be less accurate than glycated albumin.

Biological Assay↗
PubMed1988

The degradation of platelet-activating factor in serum and its discriminative value in atherosclerotic patients.

Platelet-activating factor (PAF) is transformed in vivo rapidly into the biologically inactive lyso-PAF. This reaction as well as lipid parameters were quantified in serum from 40 survivors of myocardial infarction and 36 healthy controls matched for age and body weight. The PAF-degrading capacity was 23% (p less than 0.001) higher in patients compared with the control group. Using the degradation of PAF as an univariate discriminator more than 70% of subjects were classified correctly. This is comparable with the discriminatory value of the best lipid variables, apolipoprotein B and HDL-cholesterol. Statistically significant differences in the degradation of PAF were found also by comparing subgroups which were matched for plasma levels of total cholesterol, VLDL/LDL-cholesterol or apolipoprotein B. The ratio by 48% (p less than 0.0001) in the case group was identified as an additional good discriminator between both groups. In contrast, platelet aggregation tests which were performed in acetylsalicyclic acid treated platelet-rich plasma discriminated poorly between patients and controls.

Apolipoproteins↗
PubMed1988

Efficacy and acceptability of rilmenidine for mild to moderate systemic hypertension.

A double-blind multicenter trial compared rilmenidine with placebo in the treatment of 126 patients with mild to moderate hypertension after a 4-week placebo run-in period. Patients with mild hypertension (study 1) with mean supine diastolic blood pressure (BP) between 95 and 104 mm Hg received either rilmenidine 1 mg/day (n = 31) or placebo (n = 35) for 4 weeks. In study 2, patients with moderate hypertension (mean supine diastolic BP between 105 and 115 mm Hg) received either rilmenidine 1 mg twice a day (n = 30) or placebo twice a day (n = 30) for 4 weeks. All 61 patients taking rilmenidine completed the study; 8 of the 65 patients taking placebo were withdrawn because of an increase in BP. Rilmenidine significantly reduced mean systolic and diastolic BP compared with placebo in both studies. BP was normalized (systolic less than 160 mm Hg and diastolic less than or equal to 90 mm Hg in 61% of the patients taking rilmenidine as opposed to 23% of those taking placebo (p less than 0.001). There was no significant difference in the incidence of either dry mouth or daytime drowsiness between rilmenidine, 1 mg/day, and placebo. Dry mouth was significantly more frequent with rilmenidine, 2 mg/day, than with placebo, but this difference was transient and no longer significant at the end of the study. No unexpected adverse effects occurred. Rilmenidine as single therapy appears to be effective and well accepted in the management of mild to moderate hypertension, in particular at the 1-mg/day dose, which normalized 84% of mild hypertensive patients and did not induce any significant adverse effects compared with placebo.

Adrenergic beta-Agonists↗
PubMed1988

Proaggregatory and inhibitory effects of 2-O-ethyl analogues of platelet-activating factor (PAF) on human and rabbit platelets.

A series of 8 analogues of platelet-activating factor (PAF) in which both the acetyl group and the polar head are changed, were tested for biological activities on human and rabbit platelets in plasma. Two of these compounds, 1-O-hexadecyl-2-O-ethyl-rac-glycero-3-phosphoric acid-5'-trimethylammoniumpentyl ester and 1-O-hexadecyl-2-O-ethyl-rac-glycero-3-phosphoric acid-6'-trimethylammoniumhexyl ester inhibit selectively the PAF-induced aggregation response without showing any agonistic activity. Schild analysis revealed a competitive antagonism and KB values of 4.4 and 10.5 mumol/l, respectively. These results point to a crucial role of the distance between the phosphoryl group and the polar head for expression of PAF-antagonistic properties. Moreover, the substituent at the 2-position was found to influence predominantly the agonistic behaviour.

Animals↗
PubMed1988

Blood platelet calcium content and aggregation behaviour in myeloproliferative disorders and secondary thrombocytosis.

In 19 patients affected by various kinds of myeloproliferative disorders (MPD) and in 15 patients with secondary thrombocytosis (ST) due to a variety of aetiologies some tests of platelet function and chemistry were performed. The MPD patients showed slightly to excessively elevated platelet counts at the time of investigation and a great deal of them had a history of thrombotic and/or haemorrhagic events. The total calcium content of platelets was significantly lower (2P less than 0.001) in both groups of patients as compared to controls. In 14 of 19 patients with MPD platelet rich plasma did not respond to epinephrine (15 mumol/l), a concentration which induced at least weak aggregation in all patients with ST but one and also in healthy subjects. In patients with MPD the mean extent of all kinds of induced aggregation was significantly lower (2P less than 0.002) as compared to controls whereas in patients with ST in most cases this parameter did not differ significantly from that of controls. The results as a whole confirm the concept of an acquired storage pool deficiency in patients with MPD.

Adult↗
PubMed1988

Hereditary dysfibrinogenaemia: structural and functional studies on three fibrinogen variants.

Dysfunctional fibrinogens occurring in three unrelated families were studied. Fibrinogen Erfurt I consists of B beta chains with a slightly lower molecular mass than normal. The same structural abnormality was also detected in fibrin beta chains. The variant is present in platelets too. Fibrinogen Erfurt II is characterized by the absent thrombin-induced release of FPA. With fibrinogen Berlin cleavage of the B beta chains by thrombin is slow but complete. All carriers of the three abnormal fibrinogens seem to be heterozygous for the underlying mutant gene.

Adult↗
PubMed1988

Effects of synthetic analogues of platelet-activating factor (PAF) on fibrinolytic activity in the rat.

PAF and structural analogues were investigated for their in vivo effects on fibrinolytic activity (FA) in the rat. The i.v. administration of 1 and 4 micrograms/kg PAF caused a dose-dependent increase in FA which was shown to be attributable to the release of tissue-type plasminogen activator (t-PA). 1-O-hexadecyl-2-O-ethyl-glycero-3-phosphoric acid-2'-N-propargyl-N,N'- dimethylammoniumethyl ester (I) and 1-O-hexadecyl-2-(n-propyl)-propanediol-3-phosphocholine (II) increased FA according to their proaggregatory activity. In contrast, 1-O-hexadecyl-2-O-ethyl-rac-glycero-3-phosphoric acid-5'-trimethylammoniumpentyl ester (III), a competitive antagonist of PAF, reduced the PAF induced increase of FA by 30%. Under identical conditions BN 52021 given at 1 and 10 micrograms/kg amounts diminished the effect of PAF by 47 and 77%, respectively. These results indicate that the PAF induced PA release in vivo is receptor mediated.

Animals↗
PubMed1988

Effect of specific antagonists on PAF-induced platelet aggregation and release of plasminogen activator.

We investigated the inhibitory effects of two synthetic phospholipids KO-286,001 and KO-286,006 on the platelet-activating factor (PAF) induced release of plasminogen activator (PA) in the isolated pig ear preparation as well as aggregation of pig platelets. The action was compared with that of the natural PAF antagonist BN 52021. The activator release induced by 5 x 10(-9) mol/l PAF was inhibited by 10(-6) mol/l KO-286,006, whereas BN 52021 and KO-286,001 had no effect. All three PAF antagonists tested inhibited the aggregation in a dose-dependent manner. Comparison of the IC50 values confirmed the considerably lower inhibitory action of BN 52021 and KO-286,001. Our results suggested that similar receptor sites are involved in both PAF activities tested and furthermore, that are species differences in the inhibition of PAF effects.

Animals↗