fibrin and Respiratory-Insufficiency

Topics: Acute Disease; Aged; Chlamydophila Infections; Chlamydophila pneumoniae; Cryptogenic Organizing Pneumonia; Fatal Outcome; Female; Fibrin; Humans; Multiple Organ Failure; Pneumonia, Bacterial; Pulmonary Alveoli; Respiratory Insufficiency

Topics: Animals; Antifibrinolytic Agents; Autopsy; Blood Coagulation Factors; Dogs; Fibrin; Fibrinolysis; Fibrinolytic Agents; Heart Failure; Humans; Hypoxia; Kidney; Lung; Lymph; Plasminogen Activators; Plasminogen Inactivators; Prostaglandins; Pulmonary Embolism; Pulmonary Veins; Respiration; Respiratory Insufficiency; Syndrome; Thrombin; Wounds and Injuries

Topics: Birth Weight; Clinical Trials as Topic; Fibrin; Fibrinolysis; Humans; Hyaline Membrane Disease; Infant, Newborn; Injections, Intravenous; Placebos; Plasminogen; Pulmonary Alveoli; Respiratory Distress Syndrome, Newborn; Respiratory Insufficiency; Umbilical Veins

Topics: Bronchi; COVID-19; Fibrin; Humans; Respiratory Insufficiency; SARS-CoV-2

A circuit clot is one of the most frequent complications during extracorporeal membrane oxygenation (ECMO) support. We identify coagulation/fibrinolysis markers for predicting ECMO circuit exchange because of circuit clots during ECMO support. Ten patients with acute pulmonary failure who underwent veno-venous ECMO were enrolled between January 2014 and December 2016. ECMO support lasted 106 days. The 6 days on which the ECMO circuits were exchanged were considered as circuit clot (+) group, while the remaining 100 days were considered as circuit clot (-) group. The predictors of ECMO circuit exchange because of circuit clots were identified. The mean duration of ECMO support was 10 ± 13 days, and the mean number of ECMO circuit exchange was 0.6 ± 1.1 times per patient. Thrombin-antithrombin complex (TAT) and soluble fibrin (SF) were higher in the circuit clot (+) group than in the circuit clot (-) group (both P < 0.01). According to a multivariate analysis, SF was the only independent predictor of ECMO circuit exchange (P < 0.01). The odds ratio (confidence intervals) for SF (10 µg/ml) was 1.20 (1.06-1.36). The area under the curve and optimal cut-off value were 0.95 and 101 ng/ml for SF (sensitivity, 100%; specificity, 89%). SF may be useful in predicting ECMO circuit exchange because of circuit clots.

Topics: Aged; Antithrombin III; Biomarkers; Blood Coagulation; Extracorporeal Membrane Oxygenation; Female; Fibrin; Humans; Lung; Male; Middle Aged; Peptide Hydrolases; Respiratory Insufficiency; Retrospective Studies; Thrombosis

Sulfur mustard (SM) inhalation causes airway injury, with enhanced vascular permeability, coagulation, and airway obstruction. The objective of this study was to determine whether recombinant tissue factor pathway inhibitor (TFPI) could inhibit this pathogenic sequence.. Rats were exposed to the SM analog 2-chloroethyl ethyl sulfide (CEES) via nose-only aerosol inhalation. One hour later, TFPI (1.5mg/kg) in vehicle, or vehicle alone, was instilled into the trachea. Arterial O2 saturation was monitored using pulse oximetry. Twelve hours after exposure, animals were euthanized and bronchoalveolar lavage fluid (BALF) and plasma were analyzed for prothrombin, thrombin-antithrombin complex (TAT), active plasminogen activator inhibitor-1 (PAI-1) levels, and fluid fibrinolytic capacity. Lung steady-state PAI-1 mRNA was measured by RT-PCR analysis. Airway-capillary leak was estimated by BALF protein and IgM, and by pleural fluid measurement. In additional animals, airway cast formation was assessed by microdissection and immunohistochemical detection of airway fibrin.. Airway obstruction in the form of fibrin-containing casts was evident in central conducting airways of rats receiving CEES. TFPI decreased cast formation, and limited severe hypoxemia. Findings of reduced prothrombin consumption, and lower TAT complexes in BALF, demonstrated that TFPI acted to limit thrombin activation in airways. TFPI, however, did not appreciably affect CEES-induced airway protein leak, PAI-1 mRNA induction, or inhibition of the fibrinolytic activity present in airway surface liquid.. Intratracheal administration of TFPI limits airway obstruction, improves gas exchange, and prevents mortality in rats with sulfur mustard-analog-induced acute lung injury.

Topics: Administration, Inhalation; Airway Obstruction; Animals; Blotting, Western; Bronchoalveolar Lavage Fluid; Chemical Warfare Agents; Enzyme-Linked Immunosorbent Assay; Fibrin; Fibrinolysis; Immunoglobulin M; Immunohistochemistry; Indicators and Reagents; Lipoproteins; Male; Microdissection; Mustard Gas; Proteins; Prothrombin; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Respiratory Insufficiency

Topics: Female; Fibrin; Headache; Humans; Middle Aged; Pneumonia; Respiratory Insufficiency

Sulfur mustard (SM) inhalation causes the rare but life-threatening disorder of plastic bronchitis, characterized by bronchial cast formation, resulting in severe airway obstruction that can lead to respiratory failure and death. Mortality in those requiring intubation is greater than 80%. To date, no antidote exists for SM toxicity. In addition, therapies for plastic bronchitis are solely anecdotal, due to lack of systematic research available to assess drug efficacy in improving mortality and/or morbidity. Adult rats exposed to SM analog were treated with intratracheal tissue plasminogen activator (tPA) (0.15-0.7 mg/kg, 5.5 and 6.5 h), compared with controls (no treatment, isoflurane, and placebo). Respiratory distress and pulse oximetry were assessed (for 12 or 48 h), and arterial blood gases were obtained at study termination (12 h). Microdissection of fixed lungs was done to assess airway obstruction by casts. Optimal intratracheal tPA treatment (0.7 mg/kg) completely eliminated mortality (0% at 48 h), and greatly improved morbidity in this nearly uniformly fatal disease model (90-100% mortality at 48 h). tPA normalized plastic bronchitis-associated hypoxemia, hypercarbia, and lactic acidosis, and improved respiratory distress (i.e., clinical scores) while decreasing airway fibrin casts. Intratracheal tPA diminished airway-obstructive fibrin-containing casts while improving clinical respiratory distress, pulmonary gas exchange, tissue oxygenation, and oxygen utilization in our model of severe chemically induced plastic bronchitis. Most importantly, mortality, which was associated with hypoxemia and clinical respiratory distress, was eliminated.

Topics: Airway Obstruction; Animals; Chemical Warfare Agents; Disease Models, Animal; Fibrin; Fibrinolytic Agents; Humans; Mustard Gas; Rats; Rats, Sprague-Dawley; Respiratory Insufficiency; Tissue Plasminogen Activator

Assessing state of various hemostasis levels in patients having pulmonary diseases caused by dust, in accordance with respiratory failure severity, enables to diagnose early changes confirming hypoxia. The most reliable parameters are changes in vascular and platelet hemostasis and in fibrinolysis system.

Topics: Biomarkers; Bronchitis; Disease Progression; Early Diagnosis; Fibrin; Hemostasis; Humans; Hypoxia; Lung Diseases; Middle Aged; Occupational Exposure; Particulate Matter; Platelet Function Tests; Respiratory Insufficiency; Thrombin

Fat embolization following major trauma is reported to be a quite common event, while the clinical fat embolism syndrome (FES) seems to be a much rarer event. Fat embolism occurs in 2 up to 23% of patients with isolated femoral shaft fractures. This complication appears to be related not only to the fracture, but also to the timing of stabilization. Sometimes it may be impossible to perform histochemical reactions on frozen sections to detect fat emboli thus confirming diagnosis or suspicion of FES. The finding of fibrinogen and platelets around the apparently empty spaces in the blood vessels has been proposed as an evidence for vital reaction due to either a vital cellular reaction or a flotation mechanism, thus supporting an intravital fat embolism. We report a fatal case due to fat embolism syndrome in a young man hospitalized for a right femoral neck fracture, treated with orthopaedic surgery and subjected to an intra-surgery transesophageal echocardiography that revealed embolization of numerous highly echogenic bodies. Four hours after the onset of clinical symptoms the man died from respiratory failure. The autopsy confirmed the clinical diagnosis of fat embolism syndrome. The histological examination revealed a large amount of fat globules in cerebral and pulmonary arteries and in glomerular capillaries, as well as fibrin and platelet deposition confirmed by the positive results by Sudan III staining for lipids and immunohistochemistry with anti-CD61 and anti-fibrinogen antibodies. The quantitative classification of fat embolism was grade 3 of Sevitt's classification or grade 4 of Fineschi's quantification, according to the current quantitative microscopic methods used for grading fat embolism in pulmonary tissue.

Topics: Adult; Antibodies; Blood Platelets; Capillaries; Echocardiography, Transesophageal; Embolism, Fat; Femoral Neck Fractures; Fibrin; Fibrinogen; Forensic Pathology; Humans; Immunohistochemistry; Integrin beta3; Lung; Male; Microscopy, Confocal; Pulmonary Artery; Respiratory Insufficiency; Syndrome

Acid aspiration causes direct lung damage and secondary inflammatory response involving several cytokines and accumulation of neutrophils. Activated protein C (APC) exhibits antithrombotic and anti-inflammatory properties. We examined the effect and mechanism of pre-treatment APC on acid-aspirated lung injury in rats. Anesthetized rats were instilled intratracheally with normal saline (NS, 2 ml kg(-1)) or hydrochloric acid (HCl, 0.1 N, 2 ml kg(-1)). Thirty minutes before HCl instillation, APC (200 U kg(-1) h(-1)) was infused continuously into the right jugular vein. Animals were ventilated during the experiments. Five hours after HCl or NS instillation, bronchoalveolar lavage fluid (BALF) and lung tissue samples were obtained. Total and differential cell count, absorbance, albumin concentration, concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and cytokine-induced neutrophil chemoattractant (CINC) in BALF, wet and dry weight (W/D) ratio were measured. Platelet count and fibrin degradation product (FDP) in peripheral blood were also measured. HCl instillation markedly increased these values in BALF as well as W/D ratio. APC attenuated the parameters increased by HCl-induced lung injury in rats. However, HCl instillation and APC treatment did not cause significant changes in platelet count and FDP compared with the control. We conclude that APC treatment protected the rats against HCl-induced lung injury and that this action seemed to be due to the anti-inflammatory properties of this protein rather than its anti-coagulant effects.

Topics: Albumins; Animals; Anticoagulants; Cell Count; Cytokines; Fibrin; Hemorrhage; Hydrochloric Acid; Leukocyte Elastase; Lung; Male; Neutrophils; Organ Size; Platelet Count; Pneumonia, Aspiration; Protein C; Pulmonary Alveoli; Rats; Rats, Sprague-Dawley; Respiratory Insufficiency

In order to find some treatments for respiratory failure caused by pulmonary edema, we investigated the mechanism of neurogenic pulmonary edema. Previously, stimulation of sympathetic nerves caused an increase in pulmonary vascular permeability, possibly due to neuropeptide Y. Neuropeptide Y injected into the trachea increased lung vascular permeability dose-dependently, the ED50 of which was 0.3-1 nM. Such an effect remained even after treatment with reserpine, as well as in the presence of alpha- and beta-blockers. And norepinephrine enhanced the effect of neuropeptide Y on lung vascular permeability. These responses were almost similar to those obtained by stimulation of sympathetic nerves. Furthermore, neuropeptide Y, in fibrin-induced pulmonary edema, was localized in alveolar macrophages and alveolar spaces, amounting to approximately 200 nM in edema fluid. The value was significantly greater than that obtained in hydrostatic pulmonary edema by 10-30 times. Peptide YY, an analogue of neuropeptide Y, had no action on lung vascular permeability, whereas the effect of neuropeptide Y was inhibited by pretreatment with neuropeptide Y- 13-36, an antagonist for Y3-recetor subtype. These results suggested that neuropeptide Y enhances the lung vascular permeability via Y3-recetor subtype. Neuropeptide Y- 13-36, in fibrin-induced pulmonary edema, decreased a ratio of protein concentration in edema fluid to that in serum, indicating that neuropeptide Y actually acts a role in the development of neurogenic pulmonary edema, via an increase in lung vascular permeability.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Adrenergic Uptake Inhibitors; Animals; Capillary Permeability; Dose-Response Relationship, Drug; Fibrin; Neuropeptide Y; Norepinephrine; Peptide YY; Pulmonary Circulation; Pulmonary Edema; Rats; Receptors, Neuropeptide; Reserpine; Respiratory Insufficiency

The weight gain of IVOX devices removed from the first 49 human clinical trials patients after from 1 to 29 days of implantation into the venae caval blood stream has been assessed. Each patient had received sufficient systemic heparin to maintain activated clotting times between 150 and 200 s while the IVOX device was indwelling. The nature of the material accumulating on the IVOX device was documented histologically as being thrombus in various stages of development. The weight gain findings indicate that an average of 2.0 g of thrombus accumulates per 24 h on IVOX devices indwelling in the venous blood stream of moderately anticoagulated human acute respiratory failure patients. The rate of weight gain per 24 h of the IVOX device was more rapid during the first 96 h after its implantation than during its second, third, or fourth week of implantation. The accumulated thrombus on the IVOX hollow fibers was associated with a small but measurable decrease (approximately 1%/day) in gas transfer efficiency of the implanted device. The data support the conclusion that IVOX can function effectively and safely without major thrombus formation for up to 29 days in moderately anticoagulated human acute respiratory failure patients.

Topics: Acute Disease; Blood Platelets; Carbon Dioxide; Clinical Trials as Topic; Fibrin; Heparin; Humans; Oxygenators; Prostheses and Implants; Respiratory Insufficiency; Surface Properties; Thrombosis; Time Factors; Venae Cavae

Plasma proteins, in particular fibrinogen and its degradation products leaking into air spaces in various forms of lung injuries, can adversely affect surfactant function. Two types of interaction of pulmonary surfactant with plasma proteins have been described: (1) a reversible type of interaction of surfactant with plasma proteins, and (2) a coagulative type of surfactant inactivation. The physiological significance of the latter mode of surfactant inactivation remains controversial. The purpose of this study was to determine the relative importance of these two modes of surfactant inactivation in an alveolar model. Surfactant-fibrinogen mixtures were prepared by adding fibrinogen at various concentrations to a standard preparation of surfactant-TA (suspended in Tris buffered saline at the final concentration of 1.25 mg/ml). To one of the mixtures were added caCl2 and thrombin, and the resulting fibrin clot was removed from the mixture by passing through polyethylene telephthalate filter. The surface activity of surfactant-TA suspension and the mixtures of surfactant-TA and fibrinogen before and after fibrin formation was examined during adsorption and dynamic compression using a pulsating bubble surfactometer. The concentrations of total phospholipid and surfactant-associated proteins (SP-B and SP-C) were also measured in these samples. Similar studies were performed with natural surfactant and dipalmitoylphosphatidylcholine (DPPC). Retarded adsorption of surfactant-TA and an increased minimum surface tension were observed in fibrinogen concentrations exceeding 2(-5) mg/ml. The inhibitory effect of fibrinogen on surfactant function reversed completely by 10-min after dynamic bubble pulsations. The magnitude of retarded adsorption and a lessening the ability to lower the minimum surface tension during dynamic bubble compression were significantly greater in the surfactant-fibrinogen mixtures after removal of the fibrin clots than in those before fibrin formation in fibrinogen concentrations exceeding 2(-3) mg/ml. More than 90% of both phospholipid and SP -B, C of surfactant-TA was incorporated into the fibrin clot in fibrinogen concentrations of > 2(-3) mg/ml. Similar results were obtained with natural surfactant or DPPC. At a fixed fibrinogen concentration of 2 mg/ml the fibrin clot removal was accompanied by a 90% loss of surfactant-TA in its concentration range of 1.25-40 mg/ml. Scanning electron microscopic examinations showed that numerous particle

Topics: Fibrin; Fibrinogen; Humans; Phospholipids; Pulmonary Alveoli; Pulmonary Surfactants; Respiratory Insufficiency

Topics: beta-Thromboglobulin; Chronic Disease; Fibrin; Humans; Platelet Aggregation; Respiratory Insufficiency; Thrombosis

Topics: Adult; Antithrombin III; Chronic Disease; Female; Fibrin; Fibrinogen; Humans; Male; Middle Aged; Respiratory Insufficiency

Topics: Animals; Blood Pressure; Dogs; Fibrin; Humans; Models, Biological; Molecular Weight; Peptides; Pulmonary Edema; Pulmonary Embolism; Rats; Respiratory Insufficiency

Clinical and autopsy studies have shown an association between pulmonary microembolism and acute respiratory failure after trauma or sepsis. Prophylaxis and treatment with the aim of decreasing the fibrin deposition in the lungs were associated with a decrease in the incidence and death rate of this syndrome. Small fibrin degradation products (peptides) are accumulated in the lungs and are only slowly cleared from this organ, especially during states of fibrinolysis inhibition. These peptides may contribute to the pulmonary damage in several ways. They act by interfering with other vasoactive substances as bradykinin, histamine and products of the arachidonic acid cascade. Products of the cyclooxygenase pathways as thromboxane A2 play a major role in early microembolism whereas lipoxygenase products seem to be involved in delayed microembolism. Pulmonary microembolism thus seems to be one important, but certainly not the only pathogenetic factor in acute "idiopathic" respiratory failure. Other factors such as pulmonary contusion, aspiration of gastric contents or blood, or oxygen toxicity, might well be contributory in some cases. Pulmonary microemboli containing fibrin and leukocytes are probably also involved as contributory agents in some cases in the large group of acute respiratory failure due to "known factors".

Topics: Acute Disease; Animals; Disseminated Intravascular Coagulation; Dogs; Fibrin; Fibrinolysis; Humans; Lung; Pulmonary Embolism; Rats; Respiratory Insufficiency

Forty-two patients underwent open-lung biopsy during the early phase of acute respiratory insufficiency. Correlation between the gross appearance of the lung at operation and the microscopic findings was good. Although only fair correlation was found between lung and tracheal cultures, the findings of two positive cultures in the lung only was of utmost importance. Biopsying multiple areas from the same operation showed identical pathology in 86 per cent of cases. The mortality rate of open-lung biopsy was zero; the morbidity rate was 4 per cent. The over-all survival rate of acute respiratory insufficiency (ARI) due to trauma was 39 per cent; that of pneumonia, 11 per cent. In 17 (33 percent) patients specific diagnoses and/or specific therapies were employed as a direct result of the biopsy or the thoracotomy. The incidence and prognostic implications of fibrosis and microthromboembolism are presented and discussed. Open-lung biopsy has been extremely safe and valuable in characterizing and managing ARI.

Topics: Acute Disease; Biopsy; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Humans; Lung; Pulmonary Embolism; Pulmonary Fibrosis; Respiratory Insufficiency

Sufficient clotting factors to ensure coagulation and replacement of lost volume and oxygen-carrying capacity are necessary to obviate many of the complications that may occur when massive transfusions are used in patients with multiple injuries. A regimen that has been successful includes immediate infusion of plasma protein fraction, packed red cells, fresh-frozen plasma, and nonspecific platelets.

Topics: Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Blood Proteins; Blood Transfusion; Disseminated Intravascular Coagulation; Fibrin; Humans; Respiratory Insufficiency; Thrombocytopenia; Transfusion Reaction; Wounds and Injuries

Topics: Animals; Blood Coagulation; Capillaries; Endothelium; Epithelial Cells; Extracorporeal Circulation; Fibrin; Humans; Lung; Lung Diseases; Lymphatic System; Microcirculation; Microscopy, Electron; Oxygen; Positive-Pressure Respiration; Pulmonary Circulation; Pulmonary Surfactants; Respiratory Insufficiency; Shock

Topics: Blood Coagulation Factors; Carbon Dioxide; Disseminated Intravascular Coagulation; Fibrin; Fibrinolysis; Humans; Immunodiffusion; Lung Diseases, Obstructive; Oxygen; Pulmonary Embolism; Respiratory Insufficiency; Time Factors

Topics: Afibrinogenemia; Animals; Antifibrinolytic Agents; Blood Cell Count; Blood Platelets; Chromium Radioisotopes; Cyclohexanecarboxylic Acids; Dogs; Fibrin; Fibrinogen; Injections, Intravenous; Methylamines; Oxygen; Partial Pressure; Peptide Hydrolases; Respiratory Insufficiency; Serum Albumin, Radio-Iodinated; Snakes; Thrombin; Venoms

Topics: Accidents, Traffic; Adolescent; Adult; Aged; Asphyxia Neonatorum; Brain Abscess; Capillaries; Child; Child, Preschool; Fibrin; Heart Arrest; Heart Failure; Humans; Infant; Infant, Newborn; Lung; Macrophages; Meningitis; Microcirculation; Middle Aged; Myocardial Infarction; Pancreatic Diseases; Postoperative Complications; Proteins; Pulmonary Alveoli; Pulmonary Atelectasis; Pulmonary Circulation; Pulmonary Edema; Respiration, Artificial; Respiratory Insufficiency; Shock, Traumatic; Suicide; Tetanus