[Omnia tempus habent--on the significance of time for pathoanatomic thinking].
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Biomedical subjects
Publications and source records attributed to U Bleyl.
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Sepsis and non-septic shock in pregnancy show characteristic modifications which are caused a) by physiologic changes in hemostasis primarily in the third trimester of pregnancy, b) by etiologic distinctions of shock regarded as pregnancy-specific, c) by hemodynamic changes in the circulation during pregnancy, d) by the ability of the healthy, young organism to compensate adequately. In the dead fetus syndrome and in non-septic shock, i.e., in amnionic fluid embolism and in abruptio placentae, the clinical picture is often governed by marked secundary fibrinolysis. Retroplacental hematoma, the characteristic feature of premature placental separation, remains controversial as either the cause or sequela of the hemostatic disorder. Etiologic, pathogenetic, and morphologic similarities exist between septic abortion, chorioamnionitis, and puerperal sepsis, but the varying response of the maternal organism during the course of pregnancy leads to different clinical and morphologic pictures. Due to a decrease in fibrinolytic activity as a consequence of pregnancy, the hypercoagulability state in a septic endotoxic shock predisposes the kidneys to bilateral renal cortical necrosis, principally in the amnion infection syndrome.
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Germ-free and conventional rats were fed cholesterol or normal pellets and part of both groups were immunized repeatedly with horseradish peroxidase (HRP). Four days after the last injections all the rats were killed, aortas removed and prepared for immunocytology and chemical analysis. Free peroxidase was not detected in the arterial wall and in all immunized rats only faint staining of free anti-HRP antibodies occurred in the intima. In contrast there was a consistent deposition of HRP-anti-HRP antibody complexes in the inner two thirds of the arterial wall in all HRP-immunized animals. Immunization and cholesterol feeding increased the cholesterol content of the aorta and produced early lesions, whereas cholesterol feeding or immunization alone was less effective.
In states of plasmic hypercoagulability and consumption coagulopathy ethanol favours the non-enzymatic polymerization of circulating soluble fibrinogen fibrin monomer complexes (FFMC) in vitro. The ethanol-gelation test of Godal and Abildgaard makes use of this phenomenon, called paracoagulation. The present studies show that it is also possible to visualize soluble FFMC by means of ethanol-gelation. In the electron microscope, FFMC, polymerized non-enzymatically by ethanol in the spleen, are characterized by plump or slender mycelioid fibrillar precipitates that show a uniform rhythmic transverse striation, a period-coincidental filamentary arrangement and an average periodicity of 23 nm. The ultrastructure demonstrates these ethanol-induced filaments to be in vitro-polymerized fibrin monomer derivatives. Paracoagulation with ethanol allows the identification of soluble FFMC in the tissue prior to the formation of highly polymerized fibrin-rich microthrombi, the established equivalents of the DIC-syndrome. The electron microscope studies also show the existence of a second type of fibrillary structure in the tissue polymerized by ethanol. This second type lacks the characteristic periodicity of fibrin and the period-coincidental arrangement of the filamentary structures, but is characterized by closely packed or chain-like aligned, irregularly sized spherical bodies. There is some evidence that these spherical bodies in vitro represent non-enzymatically polymerized complexes of fibrin monomers and fibrin degradation products (FDP), the equivalent of a limited local or generalized fibrinolysis in vivo.
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Twenty mongrel dogs are subjected to a standardized traumatic hemorrhagic shock. After reinfusion of the dogs' own blood the animals are continuously observed for the 72 hr. Deterioration of general hemodynamics and activation of intravascular coagulation is more pronounced in the nonsurviving animals. Correspondingly, histologic alterations particularly of the liver and intestine are more marked in the nonsurvivors. Increase of partial thromboplastin time and long-lasting increase of the prothrombin time (Quick) appear to be early signs of a fatal prognosis.
In a group of 70 premature and newborn infants, treated with artificial ventilation, 24.3% developed bronchopulmonary dysplasia (BPD). Only in a very few cases did the typical radiological stages, as described by Northway, succeed each other in a chronological order. It is impossible to differentiate BPD stage I or II from RDS stage III and IV without a knowledge of the clinical course and of the duration of artificial ventilation. The lower the gestational age, the more severe and earlier do the radiological and histological changes occur. The radiological differential diagnosis of BPD includes Wilson-Mikity-syndrome, congenital pulmonary lymphangiectasia, neonatal tuberculosis, cystic fibrosis and Hamman-Rich-syndrome.
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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.
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.
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.
Twenty-six anesthesized mongrel dogs were subjected to a standardized traumatic hemorrhagic shock. Compared with the control group prophylactic treatment with high doses of methylprednisolone reduced functional and histologic alterations of the lung. Methylprednisolone in combination with heparin pretreatment prevents microthrombi but produces more alveolar bleeding.
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.