fibrin and Hypertension

Fibrinogen conversion into insoluble fibrin and the formation of a stable clot is the final step of the coagulation cascade. Fibrin clot porosity and its susceptibility to plasmin-mediated lysis are the key fibrin measures, describing the properties of clots prepared ex vivo from citrated plasma. Cardiovascular disease (CVD), referring to coronary heart disease, heart failure, stroke, and hypertension, has been shown to be associated with the formation of dense fibrin networks that are relatively resistant to lysis. Denser fibrin mesh characterized acute patients at the onset of myocardial infarction or ischaemic stroke, while hypofibrinolysis has been identified as a persistent fibrin feature in patients following thrombotic events or in those with stable coronary artery disease. Traditional cardiovascular risk factors, such as smoking, diabetes mellitus, hyperlipidaemia, obesity, and hypertension, have also been linked with unfavourably altered fibrin clot properties, while some lifestyle modifications and pharmacological treatment, in particular statins and anticoagulants, may improve fibrin structure and function. Prospective studies have suggested that prothrombotic fibrin clot phenotype can predict cardiovascular events in short- and long-term follow-ups. Mutations and splice variants of the fibrinogen molecule that have been proved to be associated with thrombophilia or increased cardiovascular risk, along with fibrinogen post-translational modifications, prothrombotic state, inflammation, platelet activation, and neutrophil extracellular traps formation, contribute also to prothrombotic fibrin clot phenotype. Moreover, about 500 clot-bound proteins have been identified within plasma fibrin clots, including fibronectin, α2-antiplasmin, factor XIII, complement component C3, and histidine-rich glycoprotein. This review summarizes the current knowledge on the mechanisms underlying unfavourable fibrin clot properties and their implications in CVD and its thrombo-embolic manifestations.

Topics: Brain Ischemia; Cardiovascular Diseases; Fibrin; Fibrinogen; Humans; Hypertension; Prospective Studies; Stroke; Thrombosis

Topics: Blood Gas Monitoring, Transcutaneous; Edema; Evidence-Based Medicine; Fibrin; Fibrinolysis; Humans; Hypertension; Models, Cardiovascular; Oxygen; Oxygen Consumption; Pulmonary Diffusing Capacity; Risk Factors; Varicose Ulcer

The etiology of venous ulceration is far more complex than Homans' theory of stagnation and hypo-oxygenation. Indeed, studies have shown that flow in lipodermatosclerotic limbs is actually faster than normal. We suggest, therefore, that the terms "stasis dermatitis" and "stasis ulcer" be dropped from medical parlance. The term "lipodermatosclerosis with ulceration" as used by the British, or simply "venous ulcer," would seem more appropriate. Venous hypertension, produced by incompetence of deep and communicating vein valves and thrombosis of segments of the deep system, is closely correlated with the development of venous ulcers. Precisely how this venous hypertension translates into ulceration is unclear. Burnand et al showed that fibrin cuffs are deposited around the capillaries in lipodermatosclerotic limbs. These cuffs may serve as barriers to the diffusion of oxygen, leading to local ischemia and epidermal necrosis. Others suggest that trapped leukocytes in the microcirculation alter capillary permeability by releasing various inflammatory mediators that hasten the flow of fibrinogen across the capillary membrane and promote the formation of fibrin cuffs. Proof of this hypothesis is still lacking, but may eventually come from using radioactive WBC tagging procedures. A synthesis of these two theories may in fact explain the etiology of venous ulceration.

Topics: Capillary Permeability; Cell Hypoxia; Chronic Disease; Fibrin; Fibrinogen; Humans; Hypertension; Leg Ulcer; Leukocytes; Microcirculation; Necrosis; Terminology as Topic; Thrombosis; Venous Insufficiency; Venous Pressure

Topics: Arteries; Arteriosclerosis; Cytoskeleton; Fibrin; Golgi Apparatus; Humans; Hypertension; Microtubule-Associated Proteins; Muscle, Smooth, Vascular

Topics: Animals; Clinical Enzyme Tests; Coronary Disease; Diagnosis, Differential; Dogs; Fibrin; Fibrin Fibrinogen Degradation Products; Heparin; Humans; Hypertension; Lung Diseases; Myocardial Infarction; Pulmonary Embolism; Solubility; Thrombophlebitis

1. The lack of a general agreement on the definition of PE makes the interpretation of laboratory findings in different series of these patients difficult. 2. Thrombocytopenia is the most common hemostatic abnormality in patients with PE and is caused by platelet consumption. 3. There is little concrete evidence that thrombin mediates the thrombocytopenia in most of these patients. 4. Immune mechanisms or severe vasospasm with resultant endothelial damage may contribute to the thrombocytopenia in some patients.

Topics: Anemia, Hemolytic; Disseminated Intravascular Coagulation; Eclampsia; Epoprostenol; Factor VIII; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Humans; Hypertension; Platelet Count; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Hematologic; Thrombin; Thrombocytopenia; Thromboxane A2

Topics: Adenosine Diphosphate; Blood Platelets; Coronary Vessels; Dyspnea; Fibrin; Histamine; Humans; Hypertension; Hypoxia; Platelet Factor 4; Prostaglandins; Pulmonary Embolism; Serotonin

Topics: Animals; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Eclampsia; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hemostasis; Heparin; Humans; Hypertension; Placental Insufficiency; Pre-Eclampsia; Pregnancy

Topics: Adrenal Glands; Aldosterone; Anemia; Biopsy, Needle; Cholinesterases; Erythropoietin; Fibrin; Graft Rejection; Humans; Hyperparathyroidism; Hypertension; Juxtaglomerular Apparatus; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Polycythemia; Proteinuria; Radioisotope Renography; Renin; Transplantation, Homologous; Ultrasonography

Background In addition to its role on blood pressure, aldosterone (ALDO) also affects the hemostatic system leading to increased experimental thrombosis. Striatin is an intermediate in the rapid, nongenomic actions of ALDO. Striatin heterozygote knockout (

Topics: Aldosterone; Animals; Calmodulin-Binding Proteins; Fibrin; Hypertension; Membrane Proteins; Mice; Nerve Tissue Proteins; Sodium Chloride, Dietary; Thrombosis; Transcription Factors

Hypertension links to a prothrombotic state driven by endothelial dysfunction, reduced fibrinolytic potential and platelet hyperactivity. We hypothesized that ramipril treatment would favourably modify the haemostatic response to a submaximal aerobic exercise session in hypertensives.. Twenty-four hypertensive patients underwent a submaximal exercise test before and after 13±2 months of treatment with ramipril ± hydrochlorothiazide. Hypercoagulability (prothrombin fragments [PF1+2], thrombin- antithrombin complex [TAT] and D-dimers [Dd]), fibrinolytic activity (plasmin-a2-antiplasmin complex [PAP]), endothelial function (von Willebrand factor [vWf] and soluble thrombomodulin [sTM]), and platelet function (soluble P-selectin [sPsel]) were measured before, at peak and one hour after exercise.. Antihypertensive treatment resulted in an increase of PAP, vWf and sTM. During the first exercise, PF1+2 were mildly increased at peak exercise (p<0.05), while D-dimers, PAP and vWf varied significantly throughout the exercise (p<0.001). During the second exercise session, PF1+2 were decreased post-exercise (p<0.05), PAP was increased at peak and post-exercise (p<0.001) and vWf was increased at peak (p<0.05) and post-exercise (p<0.001).. The haemostatic response to exercise in hypertensives after approximately one year of ramipril treatment is characterized by the attenuated activation of coagulation, enhanced fibrinolysis and endothelial activation.

Topics: Blood Platelets; Blood Pressure; Demography; Endothelium, Vascular; Exercise; Fibrin; Fibrinolysis; Hemostasis; Humans; Hypertension; Male; Middle Aged; Ramipril; Thrombin; Time Factors

We sought to determine plasma fibrin clot properties in hypertensive subjects and to evaluate potential effects of antihypertensive therapy on these parameters.. Sixty-one patients (30 men, 31 women) with essential arterial hypertension stage 1 or 2 (aged 46.6 ± 14.4 years), free of clinically evident vascular disease, were randomly allocated for monotherapy with one of the 5 antihypertensive agents, i.e. quinapril, losartan, amlodipine, hydrochlorothiazide, or bisoprolol. Plasma fibrin clot permeability, turbidimetry and efficiency of fibrinolysis were investigated at baseline and after 6 months of therapy.. Baseline systolic blood pressure in a 24-hour ambulatory monitoring was correlated with clot permeability (r=-0.37, p<0.05), lysis time (r=0.42, p<0.05) and maximal D-dimer concentration released from clots (r=0.45, p<0.05). Antihypertensive treatment resulted in reduction of systolic/diastolic blood pressure in office measurements and 24-hour monitoring (all p<0.001), accompanied by an increase in clot permeability, reduction in clot lysis time and lower maximal D-dimer concentration released from fibrin clots (all p<0.05). No changes were observed in turbidimetric variables. Posttreatment changes in plasma fibrin clot properties were related to reductions in systolic blood pressure, complement component C3 and total cholesterol.. Reduction in systolic blood pressure during antihypertensive treatment leads to increased plasma fibrin clot permeation and susceptibility to lysis, which might be a novel antithrombotic mechanism of blood pressure lowering therapy.

Topics: Adult; Amlodipine; Antihypertensive Agents; Bisoprolol; Blood Coagulation; Female; Fibrin; Humans; Hydrochlorothiazide; Hypertension; Losartan; Male; Middle Aged; Quinapril; Tetrahydroisoquinolines

Topics: Acrylates; Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Cholesterol; Endothelium, Vascular; Fibrin; Humans; Hypertension; Imidazoles; Male; Receptors, Angiotensin; Thiophenes

The aim of the study was to investigate a new possible background of increased risk of cardiovascular events in two forms of endocrine hypertension: in primary aldosteronism (PA) and pheochromocytoma/paraganglioma (PPGL) in comparison to essential hypertension (EHT).. Prothrombotic properties of the fibrin clot structure, impaired fibrinolysis and enhanced thrombin generation have been reported to be associated with increased cardiovascular risk.. Patients with PA and PPGL were evaluated at baseline and re-evaluated 3 months after causative treatment. At baseline PA and PPGL patients were compared to matched EHT patients and to healthy controls.. The study included 35 patients with PA, 16 patients with PPGL and two reference groups of patients with EHT (32 and 22 patients) and healthy controls (35 and 23 subjects).. All subjects underwent evaluation according to the study protocol that included plasma fibrin clot permeability (Ks), clot lysis time, endogenous thrombin potential.. There were no differences in clot structure and fibrinolytic activity in PA and PPGL patients as compared to matched patients with EHT, whereas all hypertensive groups were characterized by more compact fibrin clot structure, faster clot formation and enhanced thrombin generation in comparison to healthy controls. Both in PA and PPGL patients, fibrin clot properties and fibrinolytic parameters remained stable after the causative treatment.. Patients with PA and PPGL are at a prothrombic state comparable to patients with EHT. The results suggest the higher risk of cardiovascular events observed in hypertensive PA and PPGL as compared to EHT is not mediated through investigated prothrombic mechanisms.

Topics: Adrenal Gland Neoplasms; Aldosterone; Catecholamines; Fibrin; Fibrin Clot Lysis Time; Fibrinolysis; Humans; Hypertension

Forensic investigations generally contain extensive morphological examinations to accurately diagnose the cause of death. Thus, the appearance of a new disease often creates emerging challenges in morphological examinations due to the lack of available data from autopsy- or biopsy-based research. Since late December 2019, an outbreak of a novel seventh coronavirus disease has been reported in China caused by "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2). On March 11, 2020, the new clinical condition COVID-19 (Corona-Virus-Disease-19) was declared a pandemic by the World Health Organization (WHO). Patients with COVID-19 mainly have a mild disease course, but severe disease onset might result in death due to proceeded lung injury with massive alveolar damage and progressive respiratory failure. However, the detailed mechanisms that cause organ injury still remain unclear. We investigated the morphological findings of a COVID-19 patient who died during self-isolation. Pathologic examination revealed massive bilateral alveolar damage, indicating early-phase "acute respiratory distress syndrome" (ARDS). This case emphasizes the possibility of a rapid severe disease onset in previously mild clinical condition and highlights the necessity of a complete autopsy to gain a better understanding of the pathophysiological changes in SARS-CoV-2 infections.

Topics: Alveolar Epithelial Cells; Autopsy; Betacoronavirus; Coronavirus Infections; Cough; COVID-19; Diabetes Mellitus, Type 2; Fever; Fibrin; Fibrosis; Humans; Hyperplasia; Hypertension; Lung; Lymphocytes; Macrophages; Male; Megakaryocytes; Metaplasia; Middle Aged; Neutrophils; Pandemics; Pneumonia, Viral; Quarantine; SARS-CoV-2; Tachycardia; Thrombosis

Traumatic brain injury (TBI) induces blood-brain barrier (BBB) disruption, which contributes to secondary injury of brain tissue and development of chronic cognitive decline. However, single mild (m)TBI, the most frequent form of brain trauma disrupts the BBB only transiently. We hypothesized, that co-morbid conditions exacerbate persistent BBB disruption after mTBI leading to long term cognitive dysfunction. Since hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive Wistar and spontaneously hypertensive rats (SHR) and we assessed BBB permeability, extravasation of blood-borne substances, neuroinflammation and cognitive function two weeks after trauma. We found that mTBI induced a significant BBB disruption two weeks after trauma in SHRs but not in normotensive Wistar rats, which was associated with a significant accumulation of fibrin and increased neuronal expression of inflammatory cytokines TNFα, IL-1β and IL-6 in the cortex and hippocampus. SHRs showed impaired learning and memory two weeks after mild TBI, whereas cognitive function of normotensive Wistar rats remained intact. Future studies should establish the mechanisms through which hypertension and mild TBI interact to promote persistent BBB disruption, neuroinflammation and cognitive decline to provide neuroprotection and improve cognitive function in patients with mTBI.

Topics: Animals; Blood-Brain Barrier; Brain Injuries, Traumatic; Capillary Permeability; Cerebral Cortex; Cognition; Fibrin; Hippocampus; Hypertension; Interleukins; Male; Rats; Rats, Inbred SHR; Tumor Necrosis Factor-alpha

Cardiovascular diseases are the major cause of mortality and morbidity, causing over 17.9 million deaths a year worldwide. Currently used therapy is often having side effects and expensive, dietary interventions and alternative medicines are required. Clerodendrum colebrookianum has been used to treat cardiac hypertension but anticoagulant potency was not evaluated.. To characterize an active anticoagulant fraction (AAFCC) and a 30 kDa fibrin(ogen)olytic serine protease (clerofibrase) isolated from aqueous leave extract of C. colebrookianum.. AAFCC/clerofibrase was subjected to extensive biochemical and pharmacological characterization including LC-MS/MS, amino acid compositional and GC-MS analyses. Interaction between clerofibrase with fibrinogen was studied by spectrofluorometric analysis. In vitro thrombolytic, antiplatelet and cytotoxicity assay were performed. In vivo toxicity, anticoagulant, defibrinogen and antithrombotic activities were determined on Swiss albino mice.. The in vitro anticoagulant activity of AAFCC was found to be superior to heparin and clerofibrase and comparable to Nattokinase and warfarin. The proteomics and amino acid composition analyses suggest that clerofibrase is a previously uncharacterized novel plant protease capable of degrading the -αβ chains of fibrinogen/fibrin. AAFCC/clerofibrase exerts their anticoagulant action via fibrinogenolytic activity and partially by antiplatelet activity albeit they have no effect on thrombin and FXa inhibition. The spectrofluorometric analysis revealed the binding of clerofibrase to fibrinogen but not to thrombin and FXa. The phytochemical constituents and bioactive components of AAFCC were characterized by biochemical, and GC-MS analyses. The AAFCC and clerofibrase inhibited collagen/ADP-induced mammalian platelet aggregation, showed in vitro thrombolytic activity, and non-cytotoxic to mammalian cells. The AAFCC showed and dose-dependent in vivo plasma defibrinogenating and anticoagulant activities and inhibited k-carrageen-induced thrombus formation in the tails of mice.. The potent in vivo anticoagulant and antithrombotic effects of AAFCC suggests its pharmacological significance as herbal anticoagulant drug for the prevention and/or treatment of hyperfibrinogenemia- and thrombosis associated cardiovascular disorders.

Topics: Animals; Anticoagulants; Clerodendrum; Cytochrome P-450 Enzyme System; Factor Xa; Female; Fibrin; Fibrinogen; Fibrinolytic Agents; HEK293 Cells; Humans; Hypertension; Male; Medicine, Traditional; Mice; Plant Extracts; Plant Leaves; Plants, Medicinal; Serine Endopeptidases; Thrombin; Thrombosis

Topics: Cardiovascular Diseases; Fibrin; Humans; Hypertension; Risk Factors; Sleep Apnea, Obstructive; Thrombosis

We investigated plasma fibrin clot properties in high-risk hypertensive patients with obstructive sleep apnoea (OSA) and assessed the impact of continuous positive airway pressure (CPAP) treatment on clot phenotype.. We studied 50 hypertensive patients with clinically significant OSA (age 50.0 ± 8.8 years, 39 M, 11 F). In total, 38 hypertensive patients without OSA balanced for age, sex, blood pressure, cardiovascular risk factors, and metabolic status served as controls. Plasma fibrin clot properties, including clot permeability coefficient, clot lysis time (CLT), and turbidimetric parameters of clot formation were determined. Patients underwent transthoracic echocardiography, carotid ultrasonography, evaluation of endothelial function and calcium score index of coronary arteries, and Doppler imaging of renal arteries.. Compared with controls, OSA patients were characterized by more compact fibrin structure (lower median clot permeability coefficient, 6.00 vs. 7.25 10 cm; P < 0.001), impaired fibrinolysis (longer median CLT, 108.00 vs. 92.50 min; P < 0.001), and by faster clot formation (shorter median lag phase, 40.50 vs. 42.50 s; P = 0.041), and higher median maximum clot absorbency indicating denser fibrin networks (0.87 vs. 0.81; P = 0.028). Clot permeability coefficient and CLT correlated with apnoea-hypopnoea index (r = -0.46; P < 0.001 and r = 0.44; P < 0.001, respectively) as well with mean (r = 0.31; P = 0.003; r = -0.36; P = 0.001, respectively) and minimal oxygen saturation (r = 0.46; P < 0.001; r = -0.49; P < 0.001, respectively). After 3 months of CPAP treatment we observed an increase in clot permeability coefficient (5.95 vs. 7.60 10 cm; P = 0,001), shortened CLT (107.00 vs. 87.00; P = 0.006), a longer lag phase of fibrin formation (40.00 vs. 43.50 s; P = 0.013), and a trend toward lower maximum clot absorbency (0.86 vs. 0.81; P = 0.058).. In hypertensive patients at high cardiovascular risk, OSA was associated with unfavourable prothrombotic fibrin clot characteristics, including hypofibrinolysis, which significantly improve as early as after 3 months of CPAP treatment.

Topics: Adult; Aged; Carotid Arteries; Continuous Positive Airway Pressure; Echocardiography; Female; Fibrin; Fibrin Clot Lysis Time; Fibrinolysis; Humans; Hypertension; Male; Middle Aged; Oxygen; Permeability; Renal Artery; Severity of Illness Index; Sleep Apnea, Obstructive; Thrombosis; Ultrasonography, Doppler

To determine the fibrinoid necrosis and hyalinization extent in placenta observed in normal, diabetic and hypertensive pregnancies.. Comparative cross-sectional study.. Institute of Basic Medical Sciences, Dow University of Health Sciences, Karachi, from 2008-2010.. One hundred and fifty placentae were divided in three groups on the basis of their histories and clinical examination. Group A (control), Group B (Diabetic) and Group C (Hypertensive), each consisted of 50 samples. The samples were transferred to Dow Diagnostic Reference and Research Laboratory for histopathology and gross examination. The tissue samples were taken from different sites, processed and routine staining done. The slides were then examined under light microscope for hyalinization and fibrinoid necrosis. The data was analyzed by applying ANOVA and post-hoc Tukey at 95% confidence interval. Mean ± standard deviations (SD) were computed.. The mean number of hyalinized villi in control group was 0.54 ± 0.908, 1.18 ± 1.9540 in the diabetic group and 2.14 ± 1.863 in the hypertensive group. The difference in their average turned out to be statistically significant (p-value < 0.001). Mean number of villi having fibrinoid necrosis was statistically significant in both the diabetic and hypertensive groups as compared to the control group i.e. 13.98 vs. 4.02 and 10.08 vs. 4.02 respectively (p-value < 0.001).. There was significantly greater fibrinoid necrosis and hyalinization in placentae from mothers having diabetes and hypertension. The fibrinoid necrosis was seen more in diabetic group as compared to hypertensive and control, while hyalinization was observed more frequently in hypertensive group as compared to the other groups. Placental changes as seen in examination of delivered placentae will be helpful in preventing the adverse effects in successive pregnancies.

Topics: Analysis of Variance; Chorionic Villi; Cross-Sectional Studies; Diabetes, Gestational; Female; Fibrin; Gestational Age; Humans; Hypertension; Hypertension, Pregnancy-Induced; Microscopy; Necrosis; Organ Size; Pakistan; Placenta; Pregnancy; Pregnancy in Diabetics

An 85 year old male suffered vision loss in both eyes due to ruptured bilateral retinal arterial macroaneurysms.. We report this unusual case and show the importance of studying these types of patients in order to detect associated systemic diseases.

Topics: Aged, 80 and over; Aneurysm; Aneurysm, Ruptured; Atrial Fibrillation; Fibrin; Humans; Hypertension; Laser Therapy; Male; Retinal Artery; Retinal Hemorrhage; Tomography, Optical Coherence; Vision Disorders

Type 2 diabetes is an important risk factor for the development of coronary artery disease (CAD). Focal or diffuse inflammation is often present in the vessels of patients with CAD. Mast cells are frequently present in the plaques as well as in the inflammatory infiltrates in the atherosclerotic vessel wall. In the study we wanted to examine whether there are differences in the morphology, number and distribution of mast cells and in their ability to modify the atherosclerotic process in coronary arteries (CA) in the diabetic vs. the hypertensive population of patients with CAD.. Coronary artery endarterectomy specimens were obtained from patients with diabetes or hypertension as the only risk factor for CAD. The specimens were stained with haematoxylin-eosin and Sulphated Alcian Blue for mast cells and with immunofluorescent methods for fibrinogen-fibrin and IgG deposits in the vessel wall. Both morphological and stereological assessments were conducted for mast cells and mononuclear cell infiltrates.. The histological analysis of the vessel wall of diabetic patients in comparison with hypertensive patients showed a damaged endothelial cells layer and deposits of fibrin-fibrinogen and IgG in the tunica intima and media. The stereological count revealed a diminished numerical density of mast cells and a significantly higher volume density of the mononuclear cells. Mast cells displayed cytoplasmic vacuolization, extracellular extrusion of granule and pyknotic nuclei.. This preliminary study suggests that the impaired mast cells might be the reason for more extensive inflammatory and immunologic atherosclerotic changes in the CA vessel wall of CAD patients with type 2 diabetes.

Topics: Aged; Coronary Artery Bypass; Coronary Artery Disease; Coronary Vessels; Diabetes Mellitus, Type 2; Endarterectomy; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Humans; Hypertension; Immunoglobulin G; Male; Mast Cells; Middle Aged; Pilot Projects; Slovenia; Staining and Labeling

Individuals with hypertension, dyslipidemia or diabetes are at a higher risk to suffer cardiovascular disease than other people; while impaired fibrin structure/function may contribute to further raise the cardiovascular risk in the former. The purpose of this work was to study the fibrin network and fibrin degradation properties in hypertensive (HT) patients, pharmacologically treated, 124 +/- 11 mmHg, systolic blood pressure, and 70 +/- 10 mmHg, diastolic blood pressure, n = 12; metabolic dyslipidemic patients (DL), cholesterol: 5.7 +/- 1.5 mmol/L, n = 10; patients with type 2 diabetes mellitus (T2D), fasting plasma glucose: 8.8 +/- 2.2 mmol/L, n = 10; and a control group of healthy individuals, n = 9. The fibrinogen concentration was determined by the gravimetric method. Fibrin network formation and porosity were assessed by turbidity and permeation techniques, respectively; fibrin elastic properties were evaluated by compaction and fibrin lysis, by turbidity after addition of external tPA prior to plasma clotting. Fibrinogen concentration was significantly higher only in T2D patients (p = 0.004), compared to the control group. The fibrin polymerization and lysis processes were similar for all patient and control groups. Permeation was significantly slower in DL and T2D patients, p = 0.022 and 0.0002, respectively, whereas the compaction coefficient was significantly smaller in T2D patients, p = 0.0015. Our results suggest that the fibrin structure was altered in DL and T2D patients, probably due to the increased cholesterol and glycation, respectively.

Topics: Diabetes Mellitus, Type 2; Dyslipidemias; Female; Fibrin; Humans; Hypertension; Male; Middle Aged; Structure-Activity Relationship

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Aspirin; Coronary Disease; Diabetes Mellitus, Type 2; Female; Fibrin; Humans; Hypertension; Middle Aged; Platelet Aggregation

Collagen Type I and fibrin are polymeric proteins commonly used in the field of regenerative medicine as the foundational matrix of engineered tissues. We examined the response of vascular smooth muscle cells (VSMC) to both two-dimensional (2D) substrates as well as three-dimensional (3D) matrices of these biopolymers. Pure collagen Type I, pure fibrin and composite matrices consisting of 1:1 mixtures of collagen and fibrin were studied. Relative gene expression of three ECM molecules (collagen Type I and III, and tropoelastin) and three integrin subunits (integrins alpha1, beta1 and beta3) was determined over 7 days in culture using quantitative RT-PCR. Expression of all of these marker genes was up-regulated in 3D matrices, relative to 2D substrates. Tropoelastin, integrin alpha1 and integrin beta1 were highest in collagen matrices, while collagen III and integrin beta3 expression were highest in pure fibrin, and collagen I expression was highest in the collagen-fibrin composite materials. Both the compositional and temporal expression patterns of these specific ECM-related genes were suggestive of a wound healing response. These results illuminate the short-term responses of VSMC to 2D and 3D biopolymer matrices, and have relevance to tissue engineering and cardiovascular biology.

Topics: Animals; Atherosclerosis; Cells, Cultured; Collagen; Extracellular Matrix; Fibrin; Gene Expression Regulation; Hydrogels; Hypertension; Integrins; Male; Muscle, Smooth, Vascular; Rats; Tissue Engineering; Tropoelastin

Even though there are clinical studies emphasizing the diagnosis and the perinatal intercurrent diseases of the Hypertensive Syndromes in Pregnancy, few of these studies establish the clinical forms of the specific hypertensive syndromes with the associated morphological placental alterations. The lack of studies on placental morphology and the etiopathogenesis of the different clinical standards for HSP, together with the need to objectively characterize these morphological placental lesions justify this study.. A retrospective study was carried out with 91 placentas examined throughout the period from 2000 to 2003. All placentas from patients presenting HSP in this period were included in the study. These were classified according to features well established by the literature such as laboratory and clinical criteria into: gestational hypertension (GH), chronic hypertension (CH), pre-eclampsia (PE) and pre-eclampsia superimposed on chronic hypertension (PSCH).. The number of knots presented a positive correlation with the length of time and severity of the hypertension during gestation (Spearman correlation: 0.253; P = 0.0158). The fibrin deposit was greater in all HSP groups but the pattern of distribution changes in the most severe cases from perivillous to intravillous as in the PSCH group (P = 0.002). There was no statistically significant difference in the area of the stem vessel walls among the groups. The cases with PE and CH presented a larger number of terminal villi vessels (P < 0.001).. This report suggests, that although they could be different types of hypertension or an evaluation of the same disease, the final pathway that leads to microscopic lesions in the placenta is the same, with only different intensity due to the severity of the disease.

Topics: Case-Control Studies; Female; Fibrin; Gestational Age; Humans; Hypertension; Hypertension, Pregnancy-Induced; Placenta; Pregnancy; Premature Birth; Retrospective Studies; Severity of Illness Index

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

Topics: Brain; Brain Infarction; Brain Ischemia; Cerebral Arteries; Cerebrovascular Circulation; Corpus Striatum; Diagnosis, Differential; Endothelium, Vascular; Fibrin; Humans; Hypertension; Magnetic Resonance Imaging; Necrosis; Vasospasm, Intracranial

Microvascular rarefaction by an unbalanced angiogenesis could promote the onset of hypertension in spontaneously hypertensive rats and in hypertensive patients. We studied the angiogenic potency in the fibrin gel chamber model in prehypertensive spontaneously hypertensive rats and their controls, Wistar-Kyoto rats.. Four-week-old prehypertensive spontaneously hypertensive rats (n = 9) and Wistar-Kyoto rats (n = 9) were implanted with four fibrin gel chambers located in the dorsal subcutaneous space. After 14 days, vasculoconjunctive buds had invaded the fibrin gel through the 10 hole-perforated bottom slip of the chamber. The intact vascular buds were studied using optical microscopy, alpha-actin and von Willebrand factor stainings. Capillaries and arterialized vessels were counted in three peripheral and one central field in each bud. The immunodetection of vascular endothelial growth factor and fibroblast growth factor 2 was performed on the neovascular buds.. In fibrin chambers implanted in spontaneously hypertensive rats, the number of peripheral vessels was significantly higher than in Wistar-Kyoto rats. There were significantly more arterialized vessels in spontaneously hypertensive rats compared with Wistar-Kyoto rats. The number of immunostained cells for fibroblast growth factor 2 was significantly greater in spontaneously hypertensive rats compared with Wistar-Kyoto rats. There was no significant difference in vascular endothelial growth factor staining between the two strains of rats.. Angiogenesis and arteriogenesis are increased in fibrin chambers implanted in prehypertensive spontaneously hypertensive rats compared with Wistar-Kyoto rats. These results argue against microvascular rarefaction as a cause of hypertension using this model of angiogenesis.

Topics: Actins; Animals; Arteries; Drug Implants; Fibrin; Fibroblast Growth Factor 2; Gels; Hypertension; Immunohistochemistry; Models, Biological; Neovascularization, Physiologic; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Vascular Endothelial Growth Factor A; von Willebrand Factor

Hemostasis factors may influence the pathophysiology of stroke. The role of brain hemostasis in ischemic hypertensive brain injury is not known. We studied ischemic injury in spontaneously hypertensive rats in relation to cerebrovascular fibrin deposition and activity of different hemostasis factors in brain microcirculation. In spontaneously hypertensive rats subjected to transient middle cerebral artery occlusion versus normotensive Wistar-Kyoto (W-K) rats, infarct and edema volumes were increased by 6.1-fold (P < 0.001) and 5.8-fold (P < 0.001), respectively, the cerebral blood flow (CBF) reduced during middle cerebral artery occlusion (MCAO) by 55% (P < 0.01), motor neurologic score increased by 6.9-fold (P < 0.01), and cerebrovascular fibrin deposition increased by 6.8-fold (P < 0.01). Under basal conditions, brain capillary protein C activation and tissue plasminogen activator activity were reduced in spontaneously hypertensive rats compared with Wistar-Kyoto rats by 11.8-fold (P < 0.001) and 5.1-fold (P < 0.001), respectively, and the plasminogen activator inhibitor-1 antigen and tissue factor activity were increased by 154-fold (P < 0.00001) and 74% (P < 0.01), respectively. We suggest that hypertension reduces antithrombotic mechanisms in brain microcirculation, which may enhance cerebrovascular fibrin deposition and microvascular obstructions during transient focal cerebral ischemia, which results in greater neuronal injury.

Topics: Animals; Blood Gas Analysis; Brain Ischemia; Capillaries; Cerebrovascular Circulation; Disease Models, Animal; Endothelium, Vascular; Fibrin; Fibrinolysis; Gene Expression; Hemostasis; Hypertension; Intracranial Thrombosis; Male; Microscopy, Electron; Neurologic Examination; Plasminogen Activator Inhibitor 1; Protein C; Rats; Rats, Inbred SHR; Rats, Inbred WKY; RNA, Messenger; Stroke; Thromboplastin

Preeclampsia is characterized by maternal hypercoagulable state and intravascular coagulation, microthromboses in several organs, and impairment of uteroplacental circulation. Excessive fibrin deposition occurs in the placenta, suggesting that disorders of placental coagulation and fibrinolysis physiologic systems may have a role in hemostasis activation. Term placentas were collected from 17 hypertensive/preeclamptic women and from 17 healthy pregnant women, and processed for both histologic and hemostasis studies. Placental fibrinoid deposition was visualized by cresyl-violet staining and quantified by histomorphometric analysis. The content in hemostasis factors was measured on extracts from homogenized placentas treated by a nonionic detergent. The percentage of villi with fibrinoid deposits was higher in the diseased placentas than in controls: 13.2 +/- 11.2 versus 6.75 +/- 2.7% (p < 0.001) for the total amount of deposits; 4.8 +/- 6.7 versus 1.5 +/- 1.0% (p = 0.04) for perivillous fibrinoid deposits, which are considered as histologic markers of intraplacental fibrin. The content in type 2 plasminogen activator inhibitor (PAI-2) antigen was higher in the diseased placentas than in controls: 124 +/- 8 versus 104 +/- 6 ng/mg placental protein (p = 0.046); there was a negative correlation between PAI-2 antigen and thrombomodulin activity (r = -0.57, p = 0.02) in the diseased placentas. No significant differences were found between the two groups for placental procoagulant tissue factor and anticoagulant thrombomodulin activities, and for the content in plasminogen activators and PAI-1 antigens. Placental antifibrinolytic potential is increased in pregnancy-induced hypertension and preeclampsia. This change, and the association of the highest PAI-2 placental concentrations with the lowest concentrations of thrombomodulin, may contribute to the prethrombotic state and to the excessive placental perivillous fibrin deposition observed in these situations.

Topics: Adult; Female; Fibrin; Fibrinolysis; Hemostasis; Humans; Hypertension; Placenta; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Thrombomodulin

We tested the hypothesis that enhanced intravascular coagulation in pregnancy could produce clinical symptoms similar to those of preeclampsia, such as hypertension, proteinuria, and edema. Having confirmed this, we then examined whether the pathological changes caused by intravascular coagulation could be suppressed by administration of antithrombin III (AT III), an endogenous inhibitor active to thrombin and factor X a. Intravascular coagulation was induced in Wistar rats on day 16-20 of pregnancy by 1-h arterial infusion of tissue thromboplastin (TP) through the left ventricle of the heart. One hour after the end of the infusion period, organ blood flows were measured by the radioactive ((57)Co-labeled) microsphere method, and fibrin deposition in organs was measured by radiolabeling with [(125)I] fibrinogen injected before TP infusion. Infusion of TP produced fibrin deposition in the kidney, lung, and liver, but not in the myometrium and placenta, as well as an 80% decrease in renal blood flow (RBF), with oliguria and proteinuria. TP also caused an increase in blood pressure (BP) accompanied by an increase in plasma renin activity (PRA), both of which were suppressed by bilateral nephrectomy before TP infusion. The prophylactic administration of AT III concentrates (60 or 300 U/kg intravenously (i.v.), followed by infusion of 30 or 150 U/kg/2 h, respectively) prevented all pathological changes in a dose-dependent manner. AT III increased placental blood flow regardless of the state of coagulation. These findings suggest that intravascular coagulation plays a significant part in the pathophysiology of preeclampsia and that AT III concentrates may have therapeutic potential in the treatment of this condition.

Topics: Animals; Antithrombin III; Blood Coagulation; Female; Fibrin; Hypertension; Kidney; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Rats; Rats, Wistar; Regional Blood Flow; Renin; Serum Albumin; Thromboplastin

In the spontaneously hypertensive stroke-prone rat, it is unclear whether plasminogen activator plays a role in the development of stroke. The present study was undertaken to investigate brain levels of plasminogen activator activity in spontaneously hypertensive stroke-prone rats and Wistar-Kyoto rats.. Plasminogen activator was purified from the brains of rats of both strains. The purification involved used ammonium sulfate precipitation, gel filtration, a zinc chelate-Sepharose column, and a concanavalin A-Sepharose column. Fraction I (0.15 M KCl-soluble fraction) and fraction II (2 M KCl plus 6 M urea-soluble fraction) were purified from both strains.. Total plasminogen activator activity in the original homogenates for fractions I and II derived from spontaneously hypertensive stroke-prone rats was increased to twice the level found in Wistar-Kyoto rats. The final product purified from fractions I and II in both strains of rats revealed single bands of plasminogen activator activity on enzymatic analysis with a molecular weight of 72,000. The purified product had stronger S-2288 amidolytic activity than S-2444 amidolytic activity, and it also displayed fibrin-binding ability.. The study demonstrated that there is an increased content of plasminogen activator in the brains of spontaneously hypertensive stroke-prone rats that might be related to the development of stroke.

Topics: Animals; Brain; Cerebrovascular Disorders; Electrophoresis, Polyacrylamide Gel; Fibrin; Hypertension; Male; Plasminogen Activators; Rats; Rats, Inbred SHR; Rats, Inbred WKY

The sequence of the incorporation of the stable isotope 15N in plasma protein and fibrinogen has been followed by an 15N labelling test in 11 patients with arteriosclerosis and a control group of 7 persons. The investigation showed a higher turnover of plasma protein and especially of fibrinogen in the patients with arteriosclerosis.

Topics: Arteriosclerosis; Blood Proteins; Female; Fibrin; Fibrinogen; Humans; Hypertension; Male; Middle Aged; Nitrogen; Nitrogen Radioisotopes

Following Skelton's procedure with unilateral adrenonephrectomy, contralateral adrenal enucleation and application of 1% NaCl with drinking fluid, normal rats develop hypertension and generalized severe arteriosclerosis within 7 weeks, experimental group I. Thereby the mean systolic blood pressure increased from 108 +/- 10 to 223 +/- 12 mm Hg, and 90 arteriosclerotic blood vessels could be counted in 100 histological sections (10 from each animal) of the hearts. Following Skelton's procedure and admixture of flunarizine with the food (40 mg flunarizine per kg for 8 weeks, started 1 week before the operation; mean plasma flunarizine value: 336 +/- 136 ng/ml at the end of the experiment), experimental group II, all rats developed hypertension too, whereby the mean systolic blood pressure increased from 109 +/- 10 to 214 +/- 16 mm Hg, but in contrast to experimental group I, only one artery with sclerosis could be observed in 100 comparable histological sections of the hearts. The untreated control rats, experimental group III, remained normotensive, and no arteriosclerotic blood vessels could be observed. The findings presented show that the calcium-antagonist flunarizine with the dosage used does not reduce hypertension, but almost completely suppresses hypertension-induced arteriosclerosis of the myocardial blood vessels without lowering the high blood pressure.

Topics: Animals; Blood Pressure; Cardiomegaly; Coronary Artery Disease; Coronary Vessels; Endothelium, Vascular; Fibrin; Flunarizine; Hypertension; Male; Muscle, Smooth, Vascular; Organ Size; Rats; Rats, Inbred Strains

We have previously shown abnormalities of haemostasis suggestive of intravascular coagulation in patients with malignant hypertension, a condition associated with retinopathy and renal fibrin deposition. To determine whether such abnormalities are specific to malignant hypertension, we have measured several haemostatic and haemorheological variables in 18 patients with malignant hypertension (Group 1), 18 matched healthy controls (Group 2), and 18 patients with non-malignant hypertension (Group 3) matched for renal pathology, blood pressure and serum creatinine with Group 1. Both Groups 1 and 3 had increased mean levels of fibrinogen, factor VIIIc, beta-thromboglobulin, plasma viscosity and blood viscosity (corrected for haematocrit); and decreased mean levels of haematocrit, antithrombin III and platelet count. Mean levels of fast antiplasmin and alpha2-macroglobulin were elevated in Group 1 but not in Group 3. We conclude that most blood abnormalities are not specific to malignant hypertension; are also present in patients with non-malignant hypertension who have similar levels of blood pressure and renal damage; and might result from renal damage as well as promoting further renal damage by enhancing fibrin deposition. However increased levels of fibrinolytic inhibitors in malignant hypertension merit further investigation in relation to removal of renal fibrin.

Topics: Adult; beta-Thromboglobulin; Blood Viscosity; Factor VIII; Female; Fibrin; Fibrinogen; Hemostasis; Humans; Hypertension; Hypertension, Malignant; Male

The effect of long and short-term venous hypertension upon lymph fibrinogen concentrations was studied in an attempt to explain the peri-capillary deposition of fibrin reported in patients with post-phlebitic syndromes. The clearance of radioactive fibrinogen/thrombin clots from the subcutaneous tissues of rats and human volunteers was also studied. Both long- and short-term venous hypertension were found to increase fibrinogen transport across the interstitial space by more than 600%. Not only was there evidence of fibrinolytic activity in the lymph but after long-term venous hypertension alpha 2 antiplasmin activity was also detectable. Skin biopsies from the venous hypertensive ankles showed deposition of interstitial fibrin. The clearance of radioactive fibrinogen/thrombin clots from the subcutaneous tissues of the rat was found to be delayed if the rats were given epsilon amino caproic acid but it could not be increased with stanozolol. In human subjects it was found that patients with lipodermatosclerosis had delayed clot clearance and retarded blood fibrinolytic activity when compared with normal volunteers and patients with uncomplicated varicose veins. The principle cause why tall men are more subject to ulcers than short men, Dr Young conceived to be then length of the column of blood in their veins; which by its pressure, renders the legs less able to recover when hurt by any violence.

Topics: Aminocaproic Acid; Animals; Dogs; Extracellular Space; Fibrin; Fibrinogen; Fibrinolysis; Humans; Hypertension; Lymph; Male; Rats; Rats, Inbred Strains; Skin; Varicose Ulcer

Topics: Adult; Animals; Child; Dogs; Fibrin; Fibrinolytic Agents; Humans; Hypertension; Leg Ulcer; Oxygen Consumption; Stanozolol; Thrombophlebitis; Venous Pressure

The glomerular lesions of preeclampsia consist of swelling of endothelial cells, interposition of mesangial cells and matrix between the endothelial cells and the glomerular basement membrane, and organization of subendothelial deposits of incompletely characterized material. Fibrin and immunoglobulins have previously been localized to these deposits. Laminin, a large basement membrane glycoprotein, type IV collagen, fibronectin, and a basement membrane proteoglycan were found in moderate amounts in the mesangium and prominently in the thickened glomerular capillary walls of patients with preeclampsia or other hypertensive syndromes of pregnancy. Fibrin showed the same pattern of distribution as that of fibronectin. The material deposited in the subendothelial layer of the capillary loops thus consists not only of plasma-derived proteins but also structural components of the glomerular basement membrane and of the mesangial matrix. Type I collagen deposits were demonstrated only in mesangium of pregnant patients with chronic or recurrent hypertension. Glomerular epithelial and mesangial cells synthesize in vitro the basement membrane proteins that accumulate in glomeruli of pregnant hypertensive patients. We have tested the influence of some of the pathophysiologic changes occurring during preeclampsia on the biosynthesis of collagen by rat glomerular epithelial and mesangial cells. Addition of indomethacin to the cultures transiently inhibited the synthesis of prostaglandins (PGE2) and of collagen. Addition of exogenous fibronectin to the media stimulated the production of collagen by mesangial and epithelial cells. Alterations in the metabolism of prostaglandins and the increased deposition of fibronectin observed during preeclampsia could thus play a pathogenic role in the accumulation of basement membrane proteins in glomeruli of these patients.

Topics: Basement Membrane; Collagen; Female; Fibrin; Fibronectins; Glycoproteins; Humans; Hypertension; Indomethacin; Kidney Glomerulus; Laminin; Membrane Proteins; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Prostaglandins

Topics: Female; Fibrin; Fibrinogen; Humans; Hypertension; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Reference Values; Streptokinase

Arterial hypertension was evoked in pregnant rabbits by daily applications of 2.5 microgram/kg/min of CIBA hypertensin, beginning on the 16th day of pregnancy. The animals were sacrificed on the 30th day of pregnancy. Pathological changes were histological recorded from their pulmonary arterioles, particularly those between 100 and 400 micron in outer diameter. They were vascular contraction, hyperplasia of exterior and central vascular layers, oedema, elastosis as well as fibrinous and hyaline proliferation. Non-pregnant rabbits, which had received the same dose of hypertensin, died on the third day from application. Their pulmonary arterioles were found to have undergone contraction. No vascular changes were recordable from clinically intact pregnant rabbits.

Topics: Animals; Arterioles; Female; Fibrin; Fibromuscular Dysplasia; Hypertension; Muscle, Smooth, Vascular; Pregnancy; Pulmonary Artery; Rabbits

A 48-year-old man with accelerated hypertension developed right-sided ischemic colitis. There was no evidence of another cause of vascular inadequacy. Microscopically, the bowel showed ischemic alterations of different stages. The arterial alterations of different stages. The arterial vessels showed minimal changes. In older lesions, fibrosis was prominent and the mucosa was atrophic. In more recent lesions, some vessels of the submucosa were plugged with fibrin and the overlying mucosa was infiltrated by nonorganized hemorrhage and cellular elements.

Topics: Arteries; Atrophy; Colitis; Colon; Fibrin; Gastrointestinal Hemorrhage; Humans; Hypertension; Intestinal Mucosa; Ischemia; Male; Middle Aged

Whole-blood fibrinolytic activity was measured in 68 pregnant and 29 nonpregnant women with a sensitive, solid-state assay in which 125I-labeled fibrin was bound to polystyrene tubes. Antepartum fibrinolytic activity in 36 normotensive gravid women [234.5 +/- 29.2 (mean +/- standard error of the mean) ng fibrin lysed/30 min] was significantly (p less than 0.001) greater than that found in 28 nonpregnant normotensive women not taking oral contraceptives (63.61 +/- 7.66 ng fibrin lysed/30 min) and not different from the activity observed during the active phase of labor (198.50 +/- 16.5 ng fibrin lysed/30 min.) Normotensive pregnant patients had a significant (p less than 0.001) increase in whole-blood fibrinolytic activity (341.04 +/- 25.7 ng fibrin lysed/30 min) within the first 24 hours after delivery which persisted in measurements taken the second postpartum day. Fibrinolytic activity values before labor, in the active phase of labor, and in the first and second postpartum days in 17 patients with mild to moderate pregnancy-induced or pregd or pregnancy-aggravated hypertension were not different from those found in the normotensive group. However, patients with severe pregnancy-induced or pregnancy-aggravated hypertension had significantly (p less than 0.01) lower levels of fibrinolytic activity than normotensive patients before labor, during the active phase of labor, and on the first and second postpartum days. The placental 800 X g and 110,000 X g fractions of patients with severe hypertension had a significantly (p less than 0.001) greater capacity to inhibit "in vitro" urokinase-induced fibrinolysis than similar fractions obtained from placentas of normotensive women, and there was a significant inverse correlation (r = 0.61; p less than 0.01) between whole-blood fibrinolytic activity and urokinase inhibition by placental fractions. Our findings indicate that contrary to widely held views, fibrinolysis is extremely active in term pregnancies and during labor and that a derangement of this activity is present in cases of severe pregnancy-induced or pregnancy-aggravated hypertension.

Topics: Adolescent; Adult; Female; Fibrin; Fibrinolysis; Humans; Hypertension; In Vitro Techniques; Iodine Radioisotopes; Isotope Labeling; Labor, Obstetric; Placental Extracts; Postpartum Period; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Trimester, Third; Protease Inhibitors; Urokinase-Type Plasminogen Activator

Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12-24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

Topics: Animals; Arteriosclerosis; Cerebral Arteries; Cerebral Hemorrhage; Fibrin; Humans; Hypertension; Male; Mesenteric Arteries; Methoxamine; Muscle Contraction; Muscle, Smooth; Necrosis; Rats; Renal Artery

The arterial changes designated as "hyalinosis" in the vessels of spontaneously hypertensive rats were studied using light- and electron-microscopy. Such changes were classified into three types, hyaline, fibrinoid and atypical fibrinoid degeneration. Hyaline material consisted mainly of excessive lamellar thickening of the basement membrane synthesised by endothelial and smooth muscle cells and associated with cellular debris and electron-dense particles. Acid mucopolysaccharides were found to be one of the components of the hyaline material. The nature of fibrinoid material was primarily fibrin derived from polymerised fibrinogen which has permeated through the injured endothelial cell layer. Atypical fibrinoid material consisted of granular and fibrillar substances derived from blood plasma. In some cases, all three changes were encountered in the same artery.

Topics: Animals; Cerebral Arteries; Endothelium; Female; Fibrin; Hyalin; Hypertension; Mice; Mice, Inbred Strains; Microscopy, Electron; Muscle, Smooth; Rats

Topics: Chronic Disease; Coronary Disease; Fibrin; Glomerulonephritis; Humans; Hypertension; Pyelonephritis; Solubility

Topics: Animals; Aorta; Arteriosclerosis; Blood Platelets; Fibrin; Humans; Hypertension; Swine; Thrombosis

Topics: Animals; Cerebral Arteries; Disease Models, Animal; Fibrin; Hyalin; Hypertension; Rats

The clinical and renal biopsy findings from two patients in whom renal functional abnormalities developed in the late postpartum period are described. Both biopsies showed fibrin deposition in the renal vasculature, in one case marked and in the other mild. The patient with the more severely damaged kidney subsequently died, and the other is alive but with evidence of slowly progressing renal damage. The clinicopathological spectrum and pathogenesis of late postpartum renal failure are discussed.

Topics: Acute Kidney Injury; Animals; Biopsy; Blood Coagulation; Disseminated Intravascular Coagulation; Ergot Alkaloids; Female; Fibrin; Fluorescent Antibody Technique; Hemolytic-Uremic Syndrome; Humans; Hypertension; Ischemia; Kidney; Kidney Glomerulus; Pregnancy; Puerperal Disorders

Immunofluorescent studies were performed on 217 percutaneous renal biopsies on patients with various renal diseases, which were examined in detail to assess the amount, character, and distribution of fibrin deposits in the glomeruli. The fibrin deposits were classified into six different forms on immunohistologic grounds. These were adhesive, adhesive and occlusive, membranous, mesangial, crescent forming, and sclerotic types. The sclerotic type was further subdivided into 2 groups: periglomerular fibrosing, and sclerosis with occlusion types. In many instances, immunofluorescence may reveal a pattern which is commonly associated with a characteristic abnormality on light microscopy. Fibrin deposits were commonly correlated with the presence of glomerular immunoglobulin and betaIc/betaIa-globulin. These findings interpreted as the immune reaction within glomeruli leads to an initiation of the coagulation process. The patrular hyalinization are briefly discussed.

Topics: Adolescent; Adult; Aged; Antigen-Antibody Complex; Female; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Hypertension; Immunity; Immunoglobulins; Kidney Diseases; Kidney Glomerulus; Male; Middle Aged

Plasmorrhagia of the arterial wall of various organs in rats with ischemic renal, DOCA-saline, and genetic spontaneous hypertension was studied by the method of fluorescent antibodies according to Coombs with the use of pure antibodies to yamma-globudin of a rabbit. The most pronounced plasmorrhagia was observed in rats with DOCA-saline hypertension in the arterial vessels of the kidneys. In rats with genetic hypertension lesions of the heart vessels were noted.

Topics: Animals; Arteries; Blood Proteins; Brain; Coronary Vessels; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Hypertension; Immune Sera; Kidney; Male; Pancreas; Rats

Topics: Capillaries; Fibrin; Humans; Hypertension; Sclerosis; Skin; Varicose Ulcer; Venous Pressure

In view of the association between pre-eclampsia and disseminated intravascular coagulation, three patients presenting with severe pre-eclampsia before the 28th week of pregnancy were treated with heparin. In all three patients, there was deterioration of hypertension and proteinuria that necessitated the withdrawal of treatment after five to six days. During treatment, serum and urinary fibrinolytic degradation products (FDPs) continued to rise or remained unaltered, plasminogen levels showed a steady fall, and the platelet count remained at a reduced level. These data suggest that heparin was an ineffective form of treatment and did not prevent the intravascular fibrin deposition associated with severe pre-eclampsia.

Topics: Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Dipyridamole; Disseminated Intravascular Coagulation; Female; Fibrin; Heparin; Humans; Hypertension; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Second; Proteinuria

Topics: Arteriosclerosis; Blood Specimen Collection; Cardiac Catheterization; Coronary Disease; Coronary Vessels; Electric Countershock; Enzyme Activation; Enzyme Repression; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Heparin; Humans; Hypertension; Myocardial Infarction; Plasminogen; Radiography

Topics: Adolescent; Adult; Aged; Blood Coagulation Disorders; Blood Pressure; Female; Fibrin; Fibrinogen; Humans; Hypertension; Male; Middle Aged; Solubility

The urinary excretion of fibrin/fibrinogen degradation products (F.D.P.) of 81 human cadaver kidney transplants has been measured serially by the techniques of tanned red cell haemagglutination inhibition immunoassay and immunonephelometry. Acute rejection episodes in functioning transplants have been associated with increased F.D.P. excretion which in 80% of cases has preceded clinical diagnosis by periods of one to seven days. Recovery from these episodes has been associated with a rapid fall of F.D.P. excretion to undetectable levels. The level of F.D.P. excretion during a rejection episode is a guide to its ultimate outcome. Irreversibly rejected kidneys excrete high levels of F.D.P. for long periods. Viable kidney transplants with prolonged oliguric phases can be distinguished, while still oliguric, from rejected kidneys by their low F.D.P. excretion. F.D.P. cannot usually be detected in the urine of well-functioning transplants. Episodes of raised F.D.P. excretion in the absence of acute clinical rejection, however, occur occasionally and may be associated with permanent impairment of renal function.

Topics: Anuria; Cadaver; Creatinine; Fibrin; Fibrinogen; Graft Rejection; Hemagglutination Inhibition Tests; Humans; Hypertension; Kidney Transplantation; Transplantation, Homologous; Urea

Topics: Adult; Aged; Anemia, Hemolytic; Blood Cell Count; Creatinine; Erythrocytes; Female; Fibrin; Fibrinogen; Fluorescein Angiography; Humans; Hypertension; Iodine Isotopes; Kidney Diseases; Male; Middle Aged; Retinal Diseases; Retinal Vessels

Hyaline deposits in arterioles and arteries of spleen were studied immunohistochemically. Hyaline lesions in arteriosclerotic heart disease were characterized by significant deposits of IgG, IgM, beta1C-beta 1A-globulins and beta-lipoproteins. These corresponded to histochemically stained deposits of acid mucopolysaccharides and microscopic areas of musculoelastic tissue damage in the hyaline masses. While, in young adults and a few other cases of other diseases, an occasional granular to linear deposit of IgG, IgM, beta1C-beta 1A-globulin and beta-lipoprotein was noted, no localization of IgA, rabbit antihuman fibrin and rabbit antihuman fibrinogen was seen. A variety of other histochemical staining reactions were found to be negative. These findings suggest that: a) hyaline deposits in splenic arterioles and arteries occur with greater severity in patients with hypertensive and arteriosclerotic heart disease; b) a possible abnormality related to filtration defects in arteries and arterioles, resulting in the trapping of plasma proteins, appears likely; c) increased localization of acid mucopolysaccharides and destruction of musculoelastic tissue is not an uncommon feature in hyaline masses; d) fibrin is not a component of these deposits and e) further study of other organs is necesary to observe the composition of hyaline in arterioles and arteries.

Topics: Adolescent; Adult; Aged; Animals; Arteriosclerosis; Beta-Globulins; Child; Child, Preschool; Complement System Proteins; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Glycosaminoglycans; Histocytochemistry; Humans; Hyalin; Hypertension; Immunoglobulin G; Immunoglobulin M; Infant; Infant, Newborn; Lipoproteins, LDL; Middle Aged; Rabbits; Splenic Artery; Vascular Diseases

Topics: Animals; Binding Sites; Cell Membrane; Disease Models, Animal; Fibrin; Hypertension; Kidney; Male; Myocardium; Protein Binding; Rats

The coagulation and fibrinolytic mechanisms were investigated in a group of patients with severe pre-eclampsia and eclampsia and the findings were compared with those of healthy women in late pregnancy. In patients with pre-eclampsia the following significant differences were found: (1) greater depression of plasma fibrinolytic activity (euglobulin lysis time) than in normal pregnancy, (2) a higher level of inhibitor to urokinaseinduced lysis, (3) increased levels of serum fibrin degradation products, and (4) reduced platelet counts.In patients with eclampsia a progressive increase of the level of serum fibrin degradation products was found over the three days following eclamptic seizures. No such increase occurred after grand mal seizures in late pregnancy. The findings in this study support the view that intravascular clotting is taking place in pre-eclampsia and that this disturbance of the balance between coagulation and fibrinolysis may be localized to certain areas of the vascular compartment, particularly the placental and renal circulations. Fibrin deposition in the maternal vessels supplying the placenta would impair the placental blood flow, which may explain the placental insufficiency which occurs in pre-eclampsia. Likewise fibrin deposition in the renal vasculature will result in glomerular damage and proteinuria. Hypertension may be related to the renal ischaemic changes or a compensatory response to the presence of fibrin deposition in the vascular compartment. This evidence of intravascular fibrin deposition raises the question of the possible therapeutic value of antithrombotic agents to inhibit the clotting process. On a theoretical basis such treatment might be expected to improve blood flow to the placenta and thereby fetal growth.

Topics: Adult; Blood Coagulation; Blood Platelets; Eclampsia; Embryonic and Fetal Development; Epilepsy, Tonic-Clonic; Female; Fibrin; Fibrinolysis; Fibrinolytic Agents; Humans; Hypertension; Ischemia; Kidney; Kidney Diseases; Maternal-Fetal Exchange; Placenta; Pre-Eclampsia; Pregnancy; Proteinuria; Serum Globulins

Topics: Adenosine Diphosphate; Adult; Antithrombins; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Cold Temperature; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Humans; Hypertension; Placenta; Placenta Diseases; Plasminogen; Platelet Adhesiveness; Postpartum Period; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Thromboplastin

Topics: Albuminuria; Eclampsia; Edema; Female; Fibrin; Humans; Hypertension; Pre-Eclampsia; Pregnancy

Topics: Adult; Antigen-Antibody Reactions; Biopsy; Cardiovascular Diseases; Cesarean Section; Female; Fibrin; Humans; Hypertension; Kidney Diseases; Kidney Glomerulus; Kidney Tubules; Lysosomes; Obstetric Labor Complications; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Pyelonephritis; Serotonin

Topics: Animals; Aorta; Arteries; Female; Fibrin; Hypertension; Macrophages; Male; Necrosis; Rats

Topics: Aorta; Arteriosclerosis; Blood Coagulation Tests; Colonic Neoplasms; Fibrin; Fibrinogen; Fibrinolysis; Humans; Hypertension; Hypertension, Renal; Immunoassay; Kidney; Obesity; Pyelonephritis; Renal Veins; Staphylococcus

Topics: Animals; Arteries; Endothelium, Vascular; Fibrin; Histocytochemistry; Hypertension; Microscopy, Electron; Muscle, Smooth, Vascular; Rats

Topics: Basement Membrane; Female; Fetal Death; Fibrin; Humans; Hypertension; Hypoxia; Photomicrography; Placenta; Pre-Eclampsia; Pregnancy

Topics: Cesarean Section; Extraembryonic Membranes; Female; Fibrin; Humans; Hypertension; Labor, Induced; Necrosis; Placenta; Pregnancy; Pregnancy Complications, Cardiovascular; Trophoblasts

Topics: Animals; Blood Vessels; Dogs; Fibrin; Hydrochloric Acid; Hypertension; Necrosis; Norepinephrine; Rabbits; Vascular Diseases

Topics: Blood Proteins; Connective Tissue; Electrons; Fibrin; Hypertension; Hypertension, Renal; Mesenteric Arteries; Microscopy; Microscopy, Electron; Morphogenesis; Pathology; Rats; Renal Artery Obstruction; Research

Topics: Arteriosclerosis; Fibrin; Hyalin; Hypertension; Hypertension, Renal; Kidney; Microscopy; Pathology; Rats; Research; Vascular Diseases

Topics: Arterial Pressure; Arteries; Arteriosclerosis; Carotid Arteries; Fibrin; Hypertension; Necrosis; Pathology; Rats; Renal Artery; Research

Topics: Arteries; Arteriosclerosis; Blood Proteins; Fibrin; Fibrinogen; Gold Colloid; Gold Colloid, Radioactive; Hypertension; Iodine Isotopes; Mesenteric Arteries; Morphogenesis; Pathology; Rats; Renal Artery Obstruction; Research

Topics: Arteriosclerosis; Collagen; Diabetes Mellitus; Fibrin; Geriatrics; Humans; Hyalin; Hypertension; Hypertension, Malignant; Hypertension, Pulmonary; Mitral Valve Stenosis; Pathology; Pyelonephritis

Topics: Afibrinogenemia; Bone and Bones; Bone Diseases; Fibrin; Gastrointestinal Diseases; Humans; Hypertension; Hypertension, Portal; Lung Diseases; Male; Siblings

Topics: Fibrin; Hypertension; Lung; Pressure; Pulmonary Edema; Thrombin; Vasoconstriction; Vasodilation

Topics: Blood; Blood Pressure; Female; Fibrin; Humans; Hypertension; Pre-Eclampsia; Pregnancy; Serum; Thrombolytic Therapy; Toxemia