Search PubMed⌕ Search

Biomedical subjects

U Bleyl

Publications and source records attributed to U Bleyl.

At least 55 records · Page 3Linked to original sources
PubMed1976

Globular hyaline microthrombi--their nature and morphogenesis.

The ultrastructure of globular hyaline microthrombi (GHM) is characterized by a spherical space lattice of frequently interconnected bundles of fibres of different width, with a periodic transverse striation and the fibrin-characteristic axial periodicity of 23 nm. These are surrounded by plump or slender bundles of fibres spreading radially over the surface which are only ocassionally interlinked. These filamentary formations of the so-called corona are also characterized by the fibrin-characteristic periodicity. Part of the GHM, however, lacks this axial periodicity, and periodic striation is then only visible in the radially extending fibrils of the corona. The spherical sace lattices with their plump or slender fibrillary fibrin bundles are also replaced by mosaic-like or nearly amorphous fine-grained precipitates. All intermediate stages between these main types of GHM can be found. The disappearance of the axial periodicity and of the fibrillary structure of the spherical space lattices is considered to be the morphological equivalent of seocndary fibrinolysis, here called endolysis, in the centre of the GHM. The morphogenesis of the GHM in states of shock of different aetiologies is discussed.

Blood↗
PubMed1976

On the metabolism of lipoprotein-X (LP-X).

The characteristic low-density lipoprotein of cholestasis (LP-X) earlier described for humans is found with identical properties in dogs and rats after experimental cholestasis. After ligation of the common bile duct, LP-X may be detected in the plasma within the first 20 hours. A period of marked increase in concentration is followed by decreasing plasma concentrations and LP-X becomes undetectable 7-10 days after ligation of the bile duct in rats. High plasma bile salt concentration may alter the structural integrity of LP-X and may in part be responsible for its disappearance after long-lasting and severe biliary obstruction. Plasma decay curves for isolated LP-X injected intravenously into healthy animals revealed a rapid early fall in concentration followed by a gradual decline. The calculated fractional catabolic rate of LP-X was found to be 0.450 +/- 0.069 for dogs and 1.553 +/- 0.096 for rats corresponding to a mean biological half life of 37.7 +/- 6.4 h or 10.7 +/- 0.6 h, respectively. In vitro LP-X degradation occurs in post-heparin plasma, however, it seems to be too early to speculate on the enzyme activity and on the mode of action responsible for this disappearance.

Animals↗
PubMed1976

Topography of human urokinase activity in renal tissue.

Frozen sections of human kidneys were studied with a modified technique after TODD [22] )fibrinogen slides). Urokinase activity could be demonstrated in the juxtamedullary region (venae arcuatae, venae interlobulares, vasa recta) and in the epithelium of the calyces. Urokinase activity was specifically blocked by highly purified urokinase antibodies.

Animals↗
PubMed1976

[Pulmonary hemodynamics, coagulation and morphological changes in the lung after thrombocyte aggregation inhibition and intravasal coagulation in experimental trauma and hemorrhagic shock].

26 mongrel dogs are subjected to a standardized bone trauma followed by a hypotonic hemorrhagic shock. Compared with a control and heparin group prophylactic treatment with Dipyridamol and Acetylsalicylic Acid decreases pulmonary vascular resistance significantly. After an initial period of hyperocagulability secondary fibrinolysis develops. The decrease of the fibrinogen level and the fall of total platelet count after trauma and hemorrhage can partly be prevented by the application of heparin, likewise the development of pulmonary microthrombosis. Histological examination shows a markedly diminished pulmonary microthrombosis.

Airway Resistance↗
PubMed1976

Experimental galactosamine-induced hepatitis. Effect of anticoagulant and antifibrinolytic agents on microclot formation.

An experimental hepatitis was induced in rabbits by intravenous infusion of 1 g galactosamine per kilogram of body weight. Galactosamine administration caused microclot formation in kidneys, liver, lungs, and spleen in a low percentage. If, however, animals were infused with the fibrinolysis inhibitor epsilon-aminocaproic acid in addition to galactosamine, microclots were generated in a high percentage. The microclots exhibited typical staining characteristics like those observed in the generalized Shwartzman reaction. Some animals developed bilateral renal cortical necrosis. Heparin treatment prevented the occurrence of microclot fromation after galactosamine administration, but it neither prolonged the survival time of the animals nor prevented or reduced liver cell damage. Increases in serum GPT and bilirubin levels were similar in heparin-treated and untreated rabbits. The experiments indicate that disseminated intravascular coagulation is involved in galactosamine-induced hepatitis but does not contribute to the severity of the liver injury.

Alanine Transaminase↗
PubMed1975

Changes of coagulation and fat-metabolism following pulmonary microembolism after trauma and hemorrhage.

In 16 of 24 anesthetized mongrel dogs a standardized bone trauma was performed to both hind legs by open osteootmy. During the following 6 hours the most important hemodynamic parameters, total platelet count (GTZ) and its separate fractions (NKF, KF) were continously monitored. Five hours after the trauma 50% of the total blood volume (taken to be 80 ml/kg body weight) was withdrawn from two of the four groups of animals. The trauma caused no direct effect on the pulmonary hemodynamics. In the following hours there was a slight decrease of cardiac output (HZV) in the traumatised animals. Besides a moderate increase in mean pulmonary pressure (MPP), pulmonary vascular resistance (PVR) increased by 72% of the pretraumatic values. The application of intravascular catheters diminished the total platelet count markedly in the injured, as in the uninjured animals. The increase in PVR was caused less by a mechanical obstruction of the pulmonary capillary bed than by vasoactive substances released by the platelets. The following hemorrhage led to a more marked hemodynamic reaction in the injured animals. All these animals died before the end of the calculated hemorrhage. All animals without trauma survived. Irreversible aggregation of platelets developed in the pulmonary capillary bed caused by the marked pulmonary hypocirculation. Histological examination showed a marked disseminated pulmonary microthrombosis in all animals with trauma and hemorrhage. The initial phase of experimental pulmonary microembolism caused by trauma was characterized by pulmonary hypocirculation and an activated coagulation with simultaneously diminished total platelet count.

Animals↗
PubMed1975

Light and electron microscopic examinations of experimentally produced heart muscle necroses following normobaric hyperoxia.

Heart muscle necroses following normobaric hyperoxia as examined under a light microscope occur after 40 hours exposure in the rabbit and increase in intensity with prolongation of the exposition time. Simultaneous arterial blood gas analysis excludes a hypoxemis as the cause, In addition electron microscopic examination of the necroses demonstrate the primary changes in the myofibrils but not in the mitochondria. The ultramorphological picture is however, quite similar to the myocardial necroses after epinephrine application in the rabbit. A pathogenetic relationship between heart muscle necroses after normobaric hyperoxia and after epinephrine should be considered.

Cardiomyopathies↗
PubMed1975

[Significance of intravascular coagulation and acidosis on increase of pulmonary vascular resistance following trauma and hemorrhagic shock].

24 anesthetized mongrel dogs are subjected to a standardized trauma followed by a hypotonic hemorrhagic shock. Compared with the control group (n equals 8) prophylactic treatment with heparin in the second group (n equals 8) reduces the rise of pulmonary vascular resistance only insignificantly. The correction of the metabolic acidosis with Tris does not prevent a rise of PVR in third group (n equals 8).

Acidosis↗