fibrin and Embolism

Atrial fibrillation, an increasingly common arrhythmia whose prevalence will reach epidemic proportions over the next two decades, is characterized by atrial/atrial appendage inflammation, fibrosis, remodeling, and endocardial thrombosis. Biomarkers measured within the peripheral circulation reflect these pathobiologic events with evidence of heightened thrombin generation and activity, platelet activity, fibrin formation, endocardial injury, inflammatory mediator release, and reduced fibrinolytic potential Unfortunately, the correlation between traditional biomarkers and clinical events is weak at best, as is their ability to predict successful treatment (prevention of cardioembolism) with antithrombotic agents. Future efforts devoted to the investigation of cellular biomarkers will likely provide greater practical yield and insights concerning the development, diagnosis, prognosis, and management of atrial fibrillation.

Topics: Atrial Fibrillation; Biomarkers; Blood Platelets; Comorbidity; Electric Countershock; Embolism; Fibrin; Humans; Myocardium; Platelet Activation; Stroke; Thrombin

The fibrinolytic system comprises a proenzyme, plasminogen, which can be activated to the active enzyme plasmin, that will degrade fibrin by different types of plasminogen activators. Inhibition of fibrinolysis may occur at the level of plasmin or at the level of the activators. Fibrinolysis in human blood seems to be regulated by specific molecular interactions between these components. In plasma, normally no systemic plasminogen activation occurs. When fibrin is formed, small amounts of plasminogen activator and plasminogen adsorb to the fibrin, and plasmin is generated in situ. The formed plasmin, which remains transiently complexed to fibrin, is only slowly inactivated by alpha 2-antiplasmin, while plasmin, which is released from digested fibrin, is rapidly and irreversibly neutralized. The fibrinolytic process, thus, seems to be triggered by and confined to fibrin. Thrombus formation may occur as the result of insufficient activation of the fibrinolytic system and (or) the presence of excess inhibitors, while excessive activation and/or deficiency of inhibitors might cause excessive plasmin formation and a bleeding tendency. Evidence obtained in animal models suggests that tissue-type plasminogen activator, obtained by recombinant DNA technology, may constitute a specific clot-selective thrombolytic agent with higher specific activity and fewer side effects than those currently in use.

Topics: alpha-2-Antiplasmin; alpha-Macroglobulins; Animals; Behcet Syndrome; Binding Sites; Disseminated Intravascular Coagulation; Embolism; Female; Fibrin; Fibrinolysin; Fibrinolysis; Fibrinolytic Agents; Humans; In Vitro Techniques; Kidney Diseases; Kinetics; Liver Diseases; Lysine; Plasminogen; Plasminogen Activators; Plasminogen Inactivators; Pregnancy; Streptokinase; Thrombosis; Tissue Plasminogen Activator; Urokinase-Type Plasminogen Activator

Topics: Animals; Aorta; Autoradiography; Basement Membrane; Blood Vessels; Embolism; Endothelium; Fibrin; Fibrinolysis; HeLa Cells; Humans; Microscopy, Electron; Mitosis; Neoplasm Metastasis; Neoplasms; Neoplasms, Experimental; Neoplastic Cells, Circulating; Plasminogen; Platelet Adhesiveness; Saphenous Vein; Thromboplastin; Thymidine; Tritium

Topics: Alloys; Animals; Anticoagulants; Aorta; Blood Vessel Prosthesis; Cattle; Collagen; Embolism; Fibrin; Granulation Tissue; Heart Valve Prosthesis; Heart Valves; Hemolysis; Humans; Plastics; Prosthesis Design; Silicone Elastomers; Thrombosis; Time Factors

Central venous catheters, which provide a unique convenience in the management of critical patients, have many advantages, as well as early and late complications. Early complications include pneumothorax, vascular perforation, hematoma formation, air embolism, or catheter malposition that may occur during or shortly after catheter insertion. Late complications include infection, venous stenosis, catheter thrombosis, and catheter tip migration. In the literature, embolization of a calcified fibrin sheath due to a central venous catheter to the pulmonary artery has been reported only in one case.. The purpose of this report is to present bilateral pulmonary artery embolism in a patient who presented with cough and chest pain caused by calcified fibrin sheath of the port catheter removed before that was used for regular chemotherapeutic infusions due to liposarcoma, as the second case in the literature with imaging findings. The patient underwent medical treatment, and as a result of the treatment, symptoms regressed.. Central venous catheters have many complications, and although it is rare, pulmonary embolism is one of them. The embolism of a calcified sheath is even rare, but it is still possible. However, an embolism can cause significant morbidity and even mortality for a patient if it occurs. As physicians, we should be aware of this entity to diagnose.

Topics: Catheterization, Central Venous; Embolism; Fibrin; Humans; Pulmonary Artery

In cases of acute ischemic stroke (AIS), mechanical thrombectomy (MT) can be used to directly remove lodged thromboemboli. Despite improvements in patient outcomes, one of the key factors affecting MT success is the mechanical properties of the occlusive thrombus. Therefore, the goal of this study was to investigate the viscoelastic properties of embolus analogs (EAs) and determine the influence of EA hematocrit and loading frequency. Bovine blood EAs were created over a range of physiological hematocrits (0-60%) and cyclic uniaxial compression testing was performed at three loading frequencies to mimic in vivo loading conditions, followed by stress-relaxation testing. It was found that EAs exhibited behaviors typical of hyper-viscoelastic materials and that EA hematocrit played a large role in both EA stiffness and relaxation, with both parameters decreasing as hematocrit increased from 0 to 60%. The viscoelastic behavior of the EAs was also affected by the frequency at which they were loaded, with significant increases in peak stresses between the 0.5 and 2 Hz loaded EAs. Lower hematocrit EAs had very dense fibrin networks while the higher hematocrit EAs consisted of closely packed RBCs with little fibrin present. These results suggest that fibrin contributes to EA stiffness and relaxation behaviors while RBCs play a role in decreasing the overall viscous response and strain-rate dependency. An Ogden hyperelastic model was found to best reproduce the EA loading data while a 3-term Prony series was fit to the stress relaxation data. A hyper-viscoelastic modeling framework was then implemented combining the loading and stress-relaxation fits and the results could match the full cyclic loading data for EAs of varying hematocrit and loading frequency. The results of the experimental mechanical characterization and hyper-viscoelastic curve fitting can be incorporated in future modeling efforts to optimize mechanical thrombectomy for AIS patients.

Topics: Animals; Cattle; Elasticity; Embolism; Fibrin; Humans; Ischemic Stroke; Stress, Mechanical; Thromboembolism; Viscosity

Recombinant tissue-type plasminogen activator (rtPA, or Alteplase) is the first approved thrombolytic drug for acute ischemic stroke, but suffers from a short half-life and poor resistance to plasminogen activator inhibitor (PAI-1), limiting its clinical use. The development of novel thrombolytic agents with improved benefit/risk balance has always been of great significance. In this study, we identified a mutant of serine protease domain of tPA (named ΔtPA

Topics: Animals; Embolism; Fibrin; Fibrinolytic Agents; Ischemic Stroke; Mice; Plasminogen Activator Inhibitor 1; Stroke; Thrombolytic Therapy; Tissue Plasminogen Activator

Previous reports have suggested that direct oral anticoagulants exert a prothrombolytic effect against intracardiac thrombi. We hypothesized that these anticoagulants may also help recanalize occluded intracranial arteries via prothrombolytic effects. In this study, we evaluated the effects of rivaroxaban, a direct oral anticoagulant, on fibrin emboli within the cerebrocortical microvessels in a mouse model of embolic stroke. Fibrin emboli prepared ex vivo were injected into the common carotid artery of male C57BL/6 mice, and embolization in the microvessels on the brain surface was observed through a cranial window. Oral administration of rivaroxaban was initiated a week before injection of the emboli. The number and sizes of the emboli were measured at two time points: immediately after and 3 h after the embolus injection in the rivaroxaban-treated mice (n =6) and untreated mice (n =7). The rates of recanalization and change in the embolus size were analyzed between the two groups. Complete recanalization was observed only in the rivaroxaban group (three mice in the rivaroxaban group compared with none in the control group). A significantly higher rate of reduction of the embolus size was observed in the rivaroxaban group than in the control group (P=0.0216). No significant differences between the two groups were observed in the serum levels of the following coagulation markers: thrombin-antithrombin III complexes, D-dimers, or plasmin-α2-plasmin inhibitor complex. Our findings indicate that rivaroxaban may promote reduction in the size of stagnated fibrin emboli in cerebrocortical microvessels in cases of embolic stroke.

Topics: Administration, Oral; alpha-2-Antiplasmin; Animals; Anticoagulants; Antithrombin III; Biomarkers; Blood Coagulation; Carotid Arteries; Cerebral Cortex; Cerebrovascular Circulation; Disease Models, Animal; Embolism; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Male; Mice; Mice, Inbred C57BL; Microvessels; Peptide Hydrolases; Rivaroxaban; Stroke

Occlusion of the microvasculature by blood clots, atheromatous fragments, or circulating debris is a frequent phenomenon in most human organs. Emboli are cleared from the microvasculature by hemodynamic pressure and the fibrinolytic system. An alternative mechanism of clearance is angiophagy, in which emboli are engulfed by the endothelium and translocate through the microvascular wall. We report that endothelial lamellipodia surround emboli within hours of occlusion, markedly reducing hemodynamic washout and tissue plasminogen activator-mediated fibrinolysis in mice. Over the next few days, emboli are completely engulfed by the endothelium and extravasated into the perivascular space, leading to vessel recanalization and blood flow reestablishment. We find that this mechanism is not limited to the brain, as previously thought, but also occurs in the heart, retina, kidney, and lung. In the lung, emboli cross into the alveolar space where they are degraded by macrophages, whereas in the kidney, they enter the renal tubules, constituting potential routes for permanent removal of circulating debris. Retina photography and angiography in patients with embolic occlusions provide indirect evidence suggesting that angiophagy may also occur in humans. Thus, angiophagy appears to be a ubiquitous mechanism that could be a therapeutic target with broad implications in vascular occlusive disorders. Given its biphasic nature-initially causing embolus retention, and subsequently driving embolus extravasation-it is likely that different therapeutic strategies will be required during these distinct post-occlusion time windows.

Topics: Animals; Brain; Cerebrovascular Circulation; Coronary Circulation; Embolism; Fibrin; Fibrinolysis; Fundus Oculi; Green Fluorescent Proteins; Hemodynamics; Humans; Kidney Tubules; Lung; Macrophages; Mice; Mice, Transgenic; Microcirculation; Microglia; Microscopy, Electron, Transmission; Microvessels; Monocytes; Phagocytosis; Retina; Retinal Vessels; Thrombosis

Topics: Anticoagulants; Embolism; Fibrin; Humans; Molecular Targeted Therapy; Platelet Aggregation Inhibitors

At sites of vascular injury, thrombin is an important mediator in thrombus growth and stability. Using microfluidic flow devices as well as patterned surfaces of collagen and tissue factor (TF), we sought to determine the role that fibrin plays in clot stability without interfering with the production of thrombin.. We deployed an 8-channel microfluidic device to study coagulation during corn trypsin inhibitor-treated (XIIa-inhibited) whole blood perfusion over lipidated TF linked to a fibrillar collagen type 1 surface. Clot growth and embolization were measured at initial inlet venous (200 s(-1)) or arterial (1000 s(-1)) wall shear rates under constant flow rate or pressure relief mode in the presence or absence of Gly-Pro-Arg-Pro (GPRP) to block fibrin polymerization. Numerical calculations for each mode defined hemodynamic forces on the growing thrombi. In either mode at inlet venous flow, increasing amounts of TF on the surface led to a modest dose-dependent increase (up to 2-fold) in platelet deposition, but resulted in massive fibrin accumulation (>50-fold) only when exceeding a critical TF threshold. At a venous inlet flow, GPRP led to a slight 20% increase in platelet accumulation (P<0.01) in pressure relief mode with thrombi resisting ≈1500 s(-1) before full channel occlusion. GPRP-treated thrombi were unstable under constant flow rate, where shear forces caused embolization at a maximum shear rate of ≈2300 s(-1) (69 dynes/cm2). In constant flow rate mode, the nonocclusive platelet-fibrin deposits (no GPRP) withstood maximum shear rates of ≈29 000 s(-1) (870 dyne/cm2) at ≈95% of full channel occlusion. For arterial inlet shear rate, embolization was marked for either mode with GPRP present when shear forces reached 87 dynes/cm2 (≈2900 s(-1)). Under constant flow rate, platelet-fibrin deposits (no GPRP) withstood maximums of 2400 dynes/cm2 (80,000 s(-1)) at ≈90% of full channel occlusion prior to embolization.. Fibrin increased clot strength by 12- to 28-fold. Under pressure relief mode, ≈2-fold more fibrin was produced under venous flow (P<0.001). These studies define embolization criteria for clots formed with surface TF-triggered thrombin production (±fibrin) under venous and arterial flows.

Topics: Adult; Anticoagulants; Blood Coagulation; Blood Platelets; Collagen Type I; Computer Simulation; Embolism; Factor XIIa; Fibrin; Humans; Liposomes; Male; Microfluidic Analytical Techniques; Microscopy, Confocal; Models, Biological; Numerical Analysis, Computer-Assisted; Oligopeptides; Plant Proteins; Platelet Adhesiveness; Platelet Aggregation; Regional Blood Flow; Stress, Mechanical; Thrombin; Thromboplastin; Thrombosis; Time Factors; Young Adult

Cerebral microvascular occlusion is a common phenomenon throughout life that might require greater recognition as a mechanism of brain pathology. Failure to recanalize microvessels promptly may lead to the disruption of brain circuits and significant functional deficits. Haemodynamic forces and the fibrinolytic system are considered to be the principal mechanisms responsible for recanalization of occluded cerebral capillaries and terminal arterioles. Here we identify a previously unrecognized cellular mechanism that may also be critical for this recanalization. By using high-resolution fixed-tissue microscopy and two-photon imaging in living mice we observed that a large fraction of microemboli infused through the internal carotid artery failed to be lysed or washed out within 48 h. Instead, emboli were found to translocate outside the vessel lumen within 2-7 days, leading to complete re-establishment of blood flow and sparing of the vessel. Recanalization occurred by a previously unknown mechanism of microvascular plasticity involving the rapid envelopment of emboli by endothelial membrane projections that subsequently form a new vessel wall. This was followed by the formation of an endothelial opening through which emboli translocated into the perivascular parenchyma. The rate of embolus extravasation was significantly decreased by pharmacological inhibition of matrix metalloproteinase 2/9 activity. In aged mice, extravasation was markedly delayed, resulting in persistent tissue hypoxia, synaptic damage and cell death. Alterations in the efficiency of the protective mechanism that we have identified may have important implications in microvascular pathology, stroke recovery and age-related cognitive decline.

Topics: Aging; Animals; Blood Coagulation; Brain; Carotid Arteries; Cell Death; Cell Hypoxia; Cell Line; Cell Membrane Structures; Cerebrovascular Circulation; Cholesterol; Dendrites; Embolism; Endothelial Cells; Endothelium, Vascular; Fibrin; Fibrinogen; Humans; Mice; Microspheres; Microvessels; Synapses; Thrombin

To evaluate the occurrence, size and composition of embolized debris captured during routine directional atherectomy using the SilverHawk device.. 15 consecutive eligible patients with a nonocclusive superficial femoral artery (SFA) were enrolled. Patients were included if they were > 18 years of age and had > or = 70% stenosis in the SFA. All lesions underwent plaque excision with the SilverHawk atherectomy device. A FilterWire EZ was used for distal protection and retrieval of embolized material. Specimens were collected separately from the filter basket and the SilverHawk atherectomy device's nosecone and were studied by a pathologist for number, size and composition.. Visible debris captured in the filter was found in the majority of patients 14/15 (93%). Clinically-significant debris was found in 7/15 (47%) patients. The proportion of captured debris ranged from 0.1-0.4 cm. Microscopy revealed that the shaved particles consisted predominantly of collagen, fibrin, lipid-laden macrophages, cholesterol and calcium. Analysis of the embolized material revealed a different composition, mostly consisting of collagen with fibrosis, cholesterol and macrophages.. In this single-center comparative study we have shown that during SilverHawk atherectomy of SFA lesions, distal embolization is universal. The debris captured in the filter is different in overall composition from the captured material in the nosecone of the SilverHawk device. Debris large enough to cause clinically-significant embolization, no-reflow and ischemia following SFA interventions occurred in nearly 50% of cases.

Topics: Aged; Atherectomy; Calcium; Cholesterol; Collagen; Debridement; Embolism; Female; Femoral Artery; Fibrin; Humans; Macrophages; Male; Middle Aged; Peripheral Vascular Diseases; Retrospective Studies; Risk Factors

Topics: Atherectomy; Calcium; Cholesterol; Collagen; Debridement; Embolism; Femoral Artery; Fibrin; Humans; Macrophages

Topics: Catheterization, Central Venous; Device Removal; Embolism; Female; Fibrin; Humans; Male; Middle Aged; Prospective Studies

Percutaneous transluminal renal angioplasty and stent placement with use of a coronary protection device was performed in a total of four patients with hypertension (n = 4) and/or renal insufficiency (n = 3) referred for revascularization of five renal arteries. Renal revascularization was successful in all five renal arteries (100%), but renal revascularization under protection by the FilterWire EX was achieved in only three of five renal arteries (60%). In one of these three, only a suboptimal seal was achieved between the vessel wall and the filter basket. Nevertheless, use of the device was safe and fibrin and/or cholesterol fragments were retrieved from three renal arteries. The FilterWire EX needs to be modified for the renal circulation to achieve the full theoretical advantages of these systems in this vascular bed.

Topics: Aged; Aged, 80 and over; Alloys; Angioplasty, Balloon; Cholesterol; Embolism; Female; Fibrin; Filtration; Humans; Hypertension; Male; Middle Aged; Polyurethanes; Renal Artery Obstruction; Renal Insufficiency; Retrospective Studies; Stents; Treatment Outcome

Two mathematical models of clot growth in the fluid flows have been considered. The first one is the model of embolus growth in a wall-adjacent flow. The effect of hydrodynamic flows on proceeding chemical reactions and the backward effect of the growing clot on the flow are taken into account. The growing thrombus is assumed to be porous and having low permeability, that is in good agreement with experimental data. The exact solutions determining the distribution of a fluid velocity close to the embolus have been used. Numerical analysis of these solutions have demonstrated that hydrodynamic flows can essentially affect the processes of blood coagulation, and consequently on the clot structure. Their presence might lead to the destruction of chemical fronts having a cylindrical symmetry and formation of the so-called chemical spots. The second model describes the initial stage of thrombus growing in the hemorrhage into a natural internal space. It permits accounting for vessel geometry and provides studying the effects of geometric parameters on fluid flows and coagulation processes. The process of thrombus growth is shown to depend on the ratio of typical values of blood velocity in the vessel and rate of chemical reactions.

Topics: Blood Coagulation; Blood Flow Velocity; Computer Simulation; Embolism; Fibrin; Models, Theoretical; Thrombosis

Topics: Blindness; Blood Platelets; Embolism; Female; Fibrin; Humans; Middle Aged; Ophthalmoscopy; Radiography; Retinal Artery Occlusion; Vision, Monocular

Explant analysis of left ventricular assist systems (LVAS) should permit a better evaluation of long-term evolution of materials and tissue healing in patients supported by mechanical devices and a precise understanding of embolic phenomena, observed clinically.. Five Novacor LVAS and their conduits have been explanted after 156 days (range 61-226 days) of mechanical support. The pseudo-intima (PI) developed in the inflow and outflow conduits was characterized microscopically, using monoclonal antibodies.. The morphological aspects of PI were quite different in the inflow and outflow conduits. Blood coagulation between the basal surface of the PI and the Dacron tube, irregular collagen type I matrix with plasma infiltration, macrophages, and neutrophil granulocyte elastase characterized the nonadherent, loose, and potentially thrombogenic PI growth in the inflow conduit. The PI from collagen types I and IV with circumferentially oriented alpha-smooth muscle cell actin-positive cells was anchored to the outflow conduits.. The observations, which have to be confirmed by a more extensive study on a larger number of specimens, suggest the role of the biomaterial itself, as well as the configuration, physical characteristics, and rheology in the conduit. They also suggest that thromboembolic complications of LVAS may eventually be related to this host tissue response.

Topics: Adolescent; Adult; Blood Coagulation; Blood Vessel Prosthesis; Cell Count; Collagen; Embolism; Female; Fibrin; Heart-Assist Devices; Humans; Immunoenzyme Techniques; Male; Materials Testing; Middle Aged; Polyethylene Terephthalates; Prosthesis Design; Rheology; Shock, Cardiogenic; Tunica Intima; Wound Healing

We developed a new model of embolic cerebral ischemia in the rat which provides a reproducible and predictable infarct volume within the territory supplied by the middle cerebral artery (MCA). The MCA was occluded by an embolus in Wistar rats (n = 71). An additional three non-embolized rats were used as a control. Cerebral blood flow (CBF) was measured by means of laser Doppler flowmetry (LDF) and perfusion weighted imaging (PWI) before and after embolization. The evolution of the lesion was monitored by diffusion weighted imaging (DWI). Cerebral vascular perfusion patterns were examined using laser scanning confocal microscopy. Infarct volumes were measured on hematoxylin and eosin (H&E) stained coronal sections. The lodgment of the clot at the origin of the MCA and the ischemic cell damage were examined using light microscopy. Regional CBF in the ipsilateral parietal cortex decreased to 43 +/- 4.1% (P < 0.05) of preischemic levels (n = 10). Confocal microscopic examination revealed a reduction of cerebral plasma perfusion in the ipsilateral MCA territory (n = 6). MRI measurements showed a reduction in CBF and a hyperintensity DWI encompassing the territory supplied by the MCA (n = 4). An embolus was found in all rats at 24 h after embolization. The infarct volume as a percentage of the contralateral hemisphere was 32.5 +/- 3.31% at 24 h (n = 20), 33.0 +/- 3.6% at 48 h (n = 13), and 34.5 +/- 4.74% at 168 h (n = 12) after embolization. This model of embolic focal cerebral ischemia results in ischemic cell damage and provides a reproducible and predictable infarct volume. This model is relevant to thromboembolic stroke in humans and may be useful in documenting the safety and efficacy of fibrinolytic intervention and in investigating therapies complementary to antithrombotic therapy.

Topics: Animals; Arterial Occlusive Diseases; Blood Gas Analysis; Blood Pressure; Brain Ischemia; Cerebral Infarction; Cerebrovascular Circulation; Disease Models, Animal; Embolism; Fibrin; Magnetic Resonance Imaging; Male; Microscopy, Confocal; Rats; Rats, Wistar

Topics: Aged; Cholecystitis; Cholestasis; Chronic Disease; Embolism; Fibrin; Hepatic Duct, Common; Humans; Male; Postoperative Complications

Eighty-five patients with retinal emboli, visible ophthalmoscopically, were studied retrospectively. All the patients had presented with transient or permanent visual loss. Follow up from the time of presentation was one year to 12 years with a mean of 4.5 years. Life expectancy in the 58 medically treated patients who presented with cholesterol emboli was significantly reduced (p = 0.028). Stroke was the commonest cause of death and was significantly more frequent than in the general population (p less than 0.001); there was also an increased total incidence of cerebrovascular disease (fatal and non-fatal) compared with the Oxfordshire Stroke Project (p less than 0.001). The mortality from ischaemic heart disease was not significantly increased. We report a series of 85 patients with retinal emboli, 69 of whom had cholesterol emboli (70 fundi), 15 calcific emboli and one platelet-fibrin embolus. The natural history of medically treated patients with cholesterol emboli is compared both with an age and sex matched population and with patients with amaurosis fugax but no visible retinal emboli.

Topics: Adult; Aged; Aged, 80 and over; Blindness; Calcinosis; Cholesterol; Embolism; Female; Fibrin; Humans; Male; Middle Aged; Platelet Aggregation; Prognosis; Retinal Artery; Retinal Diseases; Risk Factors

A male rhesus macaque was found to have what appeared to be numerous platelet-fibrin emboli in retinal vessels in the perimacular area. Indocyanine green (ICG) dye fluorescence and fluorescein angiograms of the fundus demonstrated leakage of fluorescein, but not ICG, from the involved arterioles. Histopathologic changes in the eyes included occlusion of retinal and choroidal vessels with platelet-fibrin emboli, inner retinal ischemia, ischemic injury to the parafoveal capillary bed distally to occlusion of precapillary arterioles, and retinal exudate limited to the regions of capillary damage. Differential leakage of fluorescein may be explained by the difference in binding affinities of the 2 dyes to blood protein: 20% to 40% of the circulating fluorescein is unbound, and 98% of ICG is bound to serum albumin. Simultaneously or serially performed angiograms with fluorescent probes of different sizes might be used to obtain a qualitative measure of vascular integrity in persons with embolism, diabetic retinopathy, sickle cell retinopathy, vasculitis, and other disorders known to produce focal retinal and choroidal vascular occlusion.

Topics: Animals; Blood Platelets; Embolism; Fibrin; Fluorescein; Fluorescein Angiography; Fluoresceins; Indocyanine Green; Male; Monkey Diseases; Retina; Retinal Diseases; Retinal Vessels

Report on a case of amaurosis fugax during which the wandering of a fibrin platelet embolus through the vessels of the central arteria was photographed.

Topics: Blindness; Carotid Artery Thrombosis; Embolism; Fibrin; Fluorescein Angiography; Humans; Male; Middle Aged; Platelet Aggregation; Retinal Vessels

The fungicidal effect of amphotericin B and 5-fluorocytosine (5-FC) on fungi incorporated into blood and fibrin clots was investigated. Amphotericin B was ineffective against fungi incorporated into blood clots, but effective in the eradication of fungi in fibrin clots. 5-FC was ineffective both against fungi incorporated in blood clots as well as in fibrin clots. The combination of 5-FC and amphotericin B was likewise ineffective against fungi incorporated into blood clots. The failure of these drugs to penetrate blood clots may explain the treatment failure in fungal endocarditis.

Topics: Amphotericin B; Blood; Blood Platelets; Candida; Cytosine; Embolism; Endocarditis, Bacterial; Fibrin; Flucytosine; Humans; Models, Biological

Topics: Animals; Embolism; Fibrin; Humans; Platelet Aggregation; Rheology; Thrombin; Thrombosis

Topics: Animals; Blood Proteins; Chromatography, Affinity; Dogs; Electrophoresis, Polyacrylamide Gel; Embolism; Fibrin; Fibrinogen; Humans; Iodine Radioisotopes; Plasminogen; Serum Albumin, Radio-Iodinated; Sodium Dodecyl Sulfate; Thrombosis

Topics: Animals; Dogs; Embolism; False Positive Reactions; Fibrin; Fibrinogen; Fibrinolysis; Iodine Radioisotopes; Models, Biological; Phlebography; Radionuclide Imaging; Thrombin; Thrombophlebitis

Topics: Animals; Blood Platelets; Carotid Arteries; Dogs; Embolism; Endothelium; Femoral Artery; Fibrin; Leg; Microscopy, Electron, Scanning; Thrombophlebitis; Thrombosis; Time Factors; Vasa Vasorum

Topics: Angiocardiography; Blood Platelets; Cardiac Catheterization; Coronary Disease; Coronary Vessels; Embolism; Fibrin; Humans; Male; Methods; Middle Aged

After the intravenous injection of Walker 256 tumour cells into rats the platelet count decreased rapidly and remained low during the following period of observation. The platelet decrease was closely related to the number of cells injected. Intra-arterial tumour cell injections required a considerably higher tumour cell count to produce a comparable thrombocytopenia. Non-viable tumour cells and tumour cell fragments induced a similar decrease of circulating platelets. Neither viable tumour cells nor tumour cell fragments aggregated rat platelets in vitro. The presence of fibrin monomers in tumour cell injected animals suggested intravascular fibrin deposition; the plasma fibrinogen level, however, did not decrease significantly. Isotope studies using (51)Cr labelled platelets revealed a rapid disappearance of the platelets from the circulation and their trapping in the lung-the primary site of tumour cell lodgement. Dipyridamole and ancrod pretreatment did not influence the decrease of platelets and their accumulation in the lung after tumour cell injection. In contrast, heparin completely prevented the thrombocytopenia and the platelet trapping in the lung. From the present experiments it is concluded that embolic tumour cells lead to early endothelial damage, resulting in local thrombin formation with subsequent irreversible platelet aggregation.

Topics: Animals; Blood Cell Count; Blood Platelets; Carcinoma 256, Walker; Chromium; Chromium Isotopes; Dipyridamole; Embolism; Endothelium; Fibrin; Fibrinogen; Heparin; Injections, Intra-Arterial; Injections, Intravenous; Kidney; Liver; Lung; Neoplasm Metastasis; Platelet Adhesiveness; Rats; Spleen; Thrombin; Thrombocytopenia; Time Factors

Topics: Animals; Arteriosclerosis; Blood Platelets; Cholesterol; Embolism; Fibrin; Humans; Leukocytes; Macrophages; Male; Microscopy, Electron; Protein Binding; Rabbits; Renal Artery; Renal Artery Obstruction; Time Factors

Topics: Blood; Blood Platelets; Blood Pressure Determination; Embolism; Extracorporeal Circulation; Fibrin; Filtration; Heart-Lung Machine; Humans; Leukocyte Count; Polymers

Topics: Adult; Aged; Arteriosclerosis; Autopsy; Blood Platelets; Calcinosis; Cholesterol; Coronary Disease; Coronary Vessels; Embolism; Erythrocytes; Female; Fibrin; Heart Ventricles; Hemorrhage; Humans; Leukocytes; Male; Middle Aged; Myocardial Infarction; Myocardium; Thrombosis; Time Factors

Topics: Adhesiveness; Animals; Blood Platelets; Blood Vessels; Carcinoma 256, Walker; Embolism; Epithelium; Fibrin; Lymphoma; Microscopy, Electron; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms, Experimental; Neoplastic Cells, Circulating; Rats; Surface Properties

Topics: Aged; Anticoagulants; Autopsy; Capillaries; Dextrans; Embolism; Female; Fibrin; Hemorrhage; Humans; Infusions, Parenteral; Kidney Glomerulus; Male; Postoperative Complications; Transfusion Reaction

Topics: Arteriosclerosis; Arteriosclerosis Obliterans; Blood Vessels; Collagen; Connective Tissue; Diabetic Angiopathies; Elastic Tissue; Embolism; Endarteritis; Fibrin; Humans; Hyalin; Ischemia; Necrosis; Vasa Vasorum

Topics: Animals; Biopsy; Blood Cell Count; Blood Coagulation; Blood Coagulation Disorders; Blood Platelets; Bone Marrow Examination; Dogs; Embolism; Endotoxins; Escherichia coli; Fibrin; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Fluorescent Antibody Technique; Liver; Microscopy, Electron; Mononuclear Phagocyte System; Neutrophils; Phagocytosis; Platelet Adhesiveness; Precipitin Tests; Protein Denaturation; Spleen; Streptokinase; Thrombin; Thrombosis; Zymosan

Topics: Adenosine Diphosphate; Animals; Blood Coagulation; Cheek; Cricetinae; Ear, External; Embolism; Female; Fibrin; Fibrinogen; Injections, Intraperitoneal; Injections, Intravenous; Leukocytes; Male; Microcirculation; Microscopy, Phase-Contrast; Platelet Adhesiveness; Rabbits; Sulfonic Acids; Thromboplastin

Topics: Animals; Capillaries; Cricetinae; Eclampsia; Embolism; Female; Fetus; Fibrin; Humans; Infant, Newborn; Kidney; Lung; Maternal-Fetal Exchange; Microcirculation; Placenta; Pregnancy; Regional Blood Flow; Respiratory Distress Syndrome, Newborn; Transillumination; Umbilical Veins; Uterus; Veins

Topics: Adult; Animals; Blood Coagulation; Blood Platelets; Child; Dogs; Embolism; Extracorporeal Circulation; Fibrin; Filtration; Heart-Lung Machine; Humans; Pressure; Veins

Topics: Blood Platelets; Embolism; Fibrin; Fibrinolytic Agents; Humans; Thrombosis

Topics: Aortic Diseases; Brain; Cholesterol; Embolism; Female; Fibrin; Heart Atria; Heart Neoplasms; Humans; Kidney; Male; Middle Aged; Myxoma; Paresis; Spinal Cord; Spinal Cord Diseases; Vertebral Artery

Topics: Afibrinogenemia; Blood Coagulation Tests; Blood Platelets; Embolism; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Hemorrhage; Humans; Immunoelectrophoresis; Pregnancy; Pregnancy Complications, Hematologic; Thrombelastography

Topics: Amniotic Fluid; Animals; Embolism; Endocardium; Female; Fibrin; Lung; Pregnancy; Rabbits; Shock

Topics: Aneurysm; Blood Platelets; Cervical Rib; Embolism; Fibrin; Humans; Pathology; Subclavian Artery; Thoracic Outlet Syndrome; Thrombosis; Vascular Surgical Procedures

Topics: Blindness; Blood Platelets; Carotid Artery Thrombosis; Carotid Artery, Internal; Cerebral Infarction; Embolism; Endarteritis; Fibrin; Hemiplegia; Humans; Intracranial Embolism; Intracranial Embolism and Thrombosis; Ischemic Attack, Transient; Leukocytes; Retinal Vessels; Thrombosis

Topics: Aminocaproates; Aminocaproic Acid; Amniotic Fluid; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Transfusion; Embolism; Embolism, Amniotic Fluid; Female; Fibrin; Fibrinolysin; Fibrinolysis; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Male; Physiology; Plasminogen; Pregnancy; Prostatic Neoplasms

Topics: Embolism; Fibrin; Forensic Medicine; Fractures, Bone; Humans; Pulmonary Embolism; Wounds and Injuries

Topics: Embolism; Embolism, Fat; Female; Fibrin; Hemorrhage; Hemorrhagic Disorders; Humans; Postpartum Hemorrhage; Postpartum Period; Pulmonary Embolism

Topics: Amnion; Amniotic Fluid; Capillaries; Embolism; Fibrin; Humans; Pulmonary Embolism; Thrombosis

Topics: Afibrinogenemia; Amniotic Fluid; Embolism; Embolism, Amniotic Fluid; Female; Fibrin; Fibrinogen; Humans; Pregnancy; Pregnancy Complications; Thrombosis

Topics: Embolism; Embolism, Air; Fibrin; Pneumothorax; Pneumothorax, Artificial; Tissue Adhesions

Topics: Embolism; Fibrin; Fibrinogen; Fibrinolytic Agents; Humans; Thrombosis; Trypsin

Topics: Amniotic Fluid; Embolism; Embolism, Amniotic Fluid; Female; Fibrin; Hemorrhage; Humans; Labor, Obstetric; Obstetrics; Pregnancy

Topics: Blood Coagulation; Blood Coagulation Disorders; Embolism; Female; Fibrin; Hemorrhagic Disorders; Heparin; Humans; Infant, Newborn; Meconium; Placenta; Pregnancy; Shock

Topics: Embolism; Fibrin; Humans; Lung; Pulmonary Embolism; Thrombosis

Topics: Embolism; Embolism, Fat; Fibrin; Food; Humans; Intracranial Embolism; Intracranial Embolism and Thrombosis; Thrombosis

Topics: Disseminated Intravascular Coagulation; Embolism; Female; Fibrin; Humans; Placenta; Pregnancy

Topics: Disseminated Intravascular Coagulation; Eclampsia; Embolism; Female; Fibrin; Humans; Placenta; Pregnancy

Topics: Animals; Embolism; Embolism, Air; Fibrin; Heart; Rabbits