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F R Matthias

Publications and source records attributed to F R Matthias.

At least 37 records · Page 2Linked to original sources
PubMed1986

[Changes in the coagulation system in shock].

Disorders of the coagulation system in shock are caused by injuries of the endothelium, influx of thromboplastic material into the blood and stasis. In this way, the intrinsic and the extrinsic system is activated. Fibrin is generated in the blood stream and forms high molecular complexes together with fibrinogen (hypercoagulability). With progress of the shock fibrin can deposit in the small vessels with the consequence of impaired circulation. Finally clotting factors and inhibitors (e.g. antithrombin III) are consumed by disseminated intravascular coagulation. This results in a bleeding tendency (consumption coagulopathy). In this survey particular shock formes (endotoxin induced, cardiogenic, traumatic, hemorrhagic) are discussed with regard to the reflections of the blood coagulation. The therapy of shock-induced disorders of blood coagulation are focused on treatment of primary disease, prevention or elimination of microthrombi, substitution of blood respective plasma components.

Blood Coagulation↗
PubMed1984

Comparison of sympathomimetic amines with collagen, calcium ionophor and adenosine diphosphate in their effects on thromboxane formation of human platelet rich plasma.

Platelet rich plasma (PRP) was stimulated by addition of epinephrine, norepinephrine, dopamine, dobutamine, ADP, collagen or A 23187 in various concentrations. Before, during and after aggregation the levels of thromboxane B2 (TxB2) were measured by radioimmunoassay. After addition of collagen or A 23187 a strong stimulation of thromboxane synthesis was observed, beginning with the early aggregation phase. TxB2 values after complete aggregation amounted to 110-220 ng/ml and up to 500 ng/ml, respectively. After ADP, epinephrine and norepinephrine the thromboxane formation took place mainly in the late aggregation phase and reached levels of 37-51 ng TxB2/ml PRP. Dopamine and dobutamine in concentrations up to 50 microM failed to stimulate platelet's thromboxane synthesis and induced only small changes of optical density of PRP.

Adenosine Diphosphate↗
PubMed1983

Effects of prostacyclin during cardiopulmonary bypass in men on plasma levels of beta-thromboglobulin, platelet factor 4, thromboxane B2, 6-keto-prostaglandin F1 alpha and heparin.

A randomized double-blind study was carried out on 40 male patients requiring aorto-coronary bypass surgery. 20 patients received a constant dose of 8 ng kg-1 min-1 of prostacyclin (PGI2), beginning two minutes before extracorporeal circulation (ECC) and ending together with ECC. Compared to the placebo-treated patient group (n = 20), PGI2-treatment significantly reduced the ECC-induced release of platelet alpha-granule proteins, beta-thromboglobulin (1178 ng/ml vs. 1926 ng/ml) and platelet factor 4 (837 ng/ml vs. 1245 ng/ml) into plasma (mean of max. values). Furthermore the decrease of platelet counts during ECC was less pronounced in PGI2-treated patients. Application of PGI2 had no effect on the increase in thromboxane B2 (TxB2) plasma levels, which amounted to 0.6 ng/ml at the end of ECC. PGI2-treatment resulted in significantly elevated plasma concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (2.1 ng/ml) throughout the infusion off prostacyclin. 6-keto-PGF1 alpha plasma levels increased up to 1.2 ng/ml in the control group patients, indicating a stimulation of endogenous PGI2 formation during ECC.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

[Disseminated intravascular coagulation and circulatory shock].

The authors describe the pathophysiology of disseminated intravascular coagulation and the coagulopathy of utilization. The clinical and laboratory data on different types of shock are described. The efficacy of different antithrombotic agents in shock with disseminated intravascular coagulation is shown.

Blood Coagulation Disorders↗
PubMed1981

[Pathophysiology of hemodynamic and metabolic disturbances following circulatory shock (author's transl)].

Circulatory shock is defined as a syndrome of hemodynamic and metabolic disturbances. Impairment of macro- and microcirculation initiated by different causes is followed by a reversible and later on by an irreversible disturbance of cell metabolism. Breakdown of organ function may be the consequence. The shock specific discomposure of the hemostatic system is characterized by an inactivation of blood coagulation. This leads first to hypercoagulability accompanied by a tendency to thrombosis; later on the impairment of the hemostatic balance is followed by the consumption of coagulation factors and by hypocoagulability with a more or less pronounced bleeding tendency. Treatment of shock is the main prerequisite to avoid and overcome shock induced coagulation disorder. Heparin administration, fresh blood and fresh plasma are adjuvant measures. Substitution of concentrates of clotting factors are indicated only in states of total consumption of the coagulation system.

Blood Coagulation Tests↗
PubMed1979

Separation of fibrinogen degradation products (FDP) by means of adsorption to insolubilized fibrinmonomer (FM-ag).

The phenomenon of complex formation between fibrinmonomer and fibrinogen degradation products was investigated by means of adsorption of FDP to insolubilized thrombin-modified fibrinogen (FM-ag). Since it could be demonstrated that there are different adsorption characteristics for early FDP and late FDP, the possibility of separation of FDP by means of affinity chromatography on FM-ag columns was evaluated using plasmic digests of 3H-Ac-labelled fibrinogen. The identification of FDP was performed by disc-electrophoresis. The results indicate that the adsorption of early FDP is comparable to the behaviour of fibrinogen, whereas late FDP show essential difference in the affinity towards FM-ag, evident by the result that fragment E adsorbs only to a minimal extents. Fragments D and E derived from fibrinogen as well as from non-crosslinked fibrin, revealed identical adsorption characteristics. Under specified conditions the procedure is suitable as a preparative method for the separation of fragments D and E.

Adsorption↗
PubMed1979

Adsorption of fibrinogen and fragment D of fibrinogen onto the insolubilized alpha-chain of fibrin.

After thrombin treatment insolubilized fibrinmonomer, which is obtained from insolubilized fibrinogen covalently bound to agarose, adsorbs soluble fibrin and its derivatives from solutions. The immobilized proteins are attached to the agarose by the 'A' alpha-chain. After reduction of the disulfide bridges the beta- and gamma-chains can be removed from the agarose. After thrombin treatment the immobilized alpha-chain adsorbs fibrinogen and fragment D. To some extent the beta- and gamma-chain do not seem necessary for the adsorption. The amount adsorbed increases, when thrombin treatment of the insolubilized protein follows the reduction process. This may indicate that the fibrinopeptides 'A' of the insolubilized alpha-chain are better accessible after the removal of the beta- and gamma-chains.

Adsorption↗
PubMed1978

Soluble plasma fibrin and platelet prostaglandin endoperoxides following myocardial infarction.

Following myocardial infarction, soluble fibrin in plasma is often elevated as a sign of an activated plasmatic coagulation system. Soluble fibrin in plasma is most pronounced in shock patients under catecholamine administration. With the improvement of the clinical situation the fibrin concentration declines to normal. Following incubation with N-ethylmaleimide an increased production of prostaglandin endoperoxides is observed in the platelets of patients after myocardial infarction compared to normal platelets. Plasma of patients exhibits an endoperoxide-producing effect on normal platelets. The stimulating effect of patient plasma diminishes together with the fall of soluble plasma fibrin. These phenomena may be considered as signs of a relation between the plasmatic and thrombocytic coagulation system.

Blood Coagulation↗
PubMed1977

[Dysfibrinogenemia. A new case: dysfibrinogenemia Giessen III (author's transl)].

A new case of dysfibrinogenemia is reported which shows no signs of a haermorrhagic diathesis (dysfibrinogenemia Giessen III). The abnormal fibrinogen was detected by only slight but characteristic alterations of some parameter of the coagulation analysis (prolonged clotting times after addition of thrombin, Reptilase and thrombin coagulase; low fibrinogen concentration determined by methods based on clot formation in comparison to the immunological fibrinogen determination; delayed fibrin polymerization). In addition, clinical features and diagnosis of dysfibrinogenemia are described in general.

Batroxobin↗