fibrin has been researched along with Pain* in 15 studies
2 review(s) available for fibrin and Pain
Article | Year |
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[Malignant pleural effusions. Pathophysiology, diagnosis and therapy].
Topics: Absorption; Amylases; Antineoplastic Agents; Breast Neoplasms; Bronchial Neoplasms; Capillary Permeability; Carcinoembryonic Antigen; Catheterization; Drainage; Dyspnea; Fibrin; Filtration; Humans; Hydrogen-Ion Concentration; Lymphoma; Pain; Pancreatic Neoplasms; Pleural Effusion; Pleural Neoplasms; Pregnancy Proteins; Quinacrine; Talc; Tetracyclines; Tissue Adhesives; Ultrasonography | 1985 |
[Morphology of the liver in experimental shock].
The authors' and literature data on the liver changes at different types of shock are summarized with consideration of the role of etiology and pathogenetic factors. Three groups of similar liver alterations reflecting the severity of impairment of the reticulo-endothelial system (RES), microcirculation and parenchyma are distinguished. No clear-cut dependence between the liver morphological changes and the severity of shock is noted. At the same time the characteristic structural alterations for some forms of shock differing at their early stages by a predominance of neuro-reflectoral, hypovolemic or toxic component are revealed. A rapidly developing hydropic degeneration, the absence of the compensatory changes, signs of the RES deficiency with the progressing necrobiotic and necrotic processes in the liver are characteristic for a neuro-reflectoral shock. Endotoxic shock is associated with widespread intravascular thrombi, liver cell necrosis, combination of the destruction of reticuloendotheliocytes with the signs of their preceding activation, foci of a smooth cytoplasmic network hyperplasia of centrolobular hepatocytes; hypovolemic shock is characterized by activation of compensatory processes. Topics: Animals; Crush Syndrome; Disseminated Intravascular Coagulation; Energy Metabolism; Fibrin; Kupffer Cells; Liver; Microcirculation; Microscopy, Electron; Mitochondria, Liver; Pain; Phagocytosis; Platelet Aggregation; Rabbits; Rats; Shock; Shock, Hemorrhagic; Shock, Septic | 1985 |
13 other study(ies) available for fibrin and Pain
Article | Year |
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Fixation of platelet-rich plasma and fibrin gels on knee cartilage defects after microfracture with arthroscopy.
An investigation of arthroscopic surgery combined with coverage of the microfractured wound surface with platelet-rich plasma (PRP) and fibrin gels (FG) to treat knee cartilage defects.. Between February 2017 and February 2020, 145 patients with knee cartilage defects were treated. Only isolated full-thickness cartilage defects were included, and 28 patients (12 men and 16 women) were included in this study. They were all treated with arthroscopic surgery on subchondral bones, filled with PRP and thrombin, and sealed with FG. The knee pain visual analogue scale (VAS) scores were measured after the patients climbed ten stairs up and down, and the Western Ontario and McMaster Universities osteoarthritis index and the area of cartilage defects were measured through the pre-operative and post-operative follow-up. The complication incidences were also observed.. All patients were followed up for ten to 15 months (median 12 months). The knee pain VAS scores decreased from 6.57 ± 1.07 pre-operatively to 2.09 ± 1.35 at the last follow-up. The WOMAC osteoarthritis index decreased from 44.32 ± 3.95 (mean ± sd) pre-operatively to 16.57 ± 2.20 by the last follow-up. The cartilage defect decreased from 2.93 ± 0.65 cm. The combination therapy of arthroscopic surgery and covering the microfractured wound surface with PRP and FG can repair knee cartilage defects, relieve pain, and improve function, and is a safe and effective treatment. Topics: Arthroscopy; Cartilage Diseases; Cartilage, Articular; Female; Fibrin; Fractures, Stress; Gels; Humans; Magnetic Resonance Imaging; Male; Osteoarthritis, Knee; Pain; Platelet-Rich Plasma; Treatment Outcome | 2022 |
The role of spinal thrombin through protease-activated receptor 1 in hyperalgesia after neural injury.
OBJECTIVE Painful neuropathic injuries induce blood-spinal cord barrier (BSCB) breakdown, allowing pro-inflammatory serum molecules to cross the BSCB, which contributes to nociception. The goal of these studies was to determine whether the blood-borne serine protease thrombin also crosses a permeable BSCB, contributing to nociception through its activation of protease-activated receptor-1 (PAR1). METHODS A 15-minute C-7 nerve root compression, which induces BSCB breakdown and painful behaviors by Day 1, was administered in the rat (n = 10); sham operation (n = 11) and a 3-minute compression (n = 10) that does not induce sensitivity were administered as controls. At Day 1 after root compression, spinal cord tissue was co-immunolabeled for fibrin/fibrinogen, the enzymatic product of thrombin, and IgG, a serum protein, to determine whether thrombin acts in areas of BSCB breakdown. To determine whether spinal thrombin and PAR1 contribute to hyperalgesia after compression, the thrombin inhibitor hirudin and the PAR1 antagonist SCH79797, were separately administered intrathecally before compression injuries (n = 5-7 per group). Rat thrombin was also administered intrathecally with and without SCH79797 (n = 6 per group) to determine whether spinal thrombin induces hypersensitivity in naïve rats through PAR1. RESULTS Spinal fibrin(ogen) was elevated at Day 1 after root compression in regions localized to BSCB breakdown and decreased in those regions by Day 7. Blocking either spinal thrombin or PAR1 completely prevented compression-induced hyperalgesia for 7 days. Intrathecal thrombin induced transient pain that was prevented by blocking spinal PAR1 before its injection. CONCLUSIONS The findings of this study suggest a potent role for spinal thrombin and its activation of PAR1 in pain onset following neuropathic injury. Topics: Animals; Antithrombins; Capillary Permeability; Central Nervous System Agents; Cervical Vertebrae; Disease Models, Animal; Fibrin; Hirudins; Hyperalgesia; Injections, Spinal; Male; Pain; Pain Measurement; Peripheral Nervous System Diseases; Pyrroles; Quinazolines; Radiculopathy; Rats, Sprague-Dawley; Receptor, PAR-1; Spinal Cord | 2017 |
The potential for salmon fibrin and thrombin to mitigate pain subsequent to cervical nerve root injury.
Nerve root compression is a common cause of radiculopathy and induces persistent pain. Mammalian fibrin is used clinically as a coagulant but presents a variety of risks. Fish fibrin is a potential biomaterial for neural injury treatment because it promotes neurite outgrowth, is non-toxic, and clots readily at lower temperatures. This study administered salmon fibrin and thrombin following nerve root compression and measured behavioral sensitivity and glial activation in a rat pain model. Fibrin and thrombin each significantly reduced mechanical allodynia compared to injury alone (p < 0.02). Painful compression with fibrin exhibited allodynia that was not different from sham for any day using stimulation by a 2 g filament; allodynia was only significantly different (p < 0.043) from sham using the 4 g filament on days 1 and 3. By day 5, responses for fibrin treatment decreased to sham levels. Allodynia following compression with thrombin treatment were unchanged from sham at any time point. Macrophage infiltration at the nerve root and spinal microglial activation were only mildly modified by salmon treatments. Spinal astrocytic expression decreased significantly with fibrin (p < 0.0001) but was unchanged from injury responses for thrombin treatment. Results suggest that salmon fibrin and thrombin may be suitable biomaterials to mitigate pain. Topics: Animals; Cervical Vertebrae; Densitometry; Fibrin; Hyperalgesia; Immunohistochemistry; Male; Pain; Radiculopathy; Rats; Salmon; Spinal Nerve Roots; Thrombin | 2011 |
The role and mechanism of the up-regulation of fibrinolytic activity in painful peripheral nerve injury.
Peripheral nerve injury is followed by Wallerians degeneration (WD) and degradation and regeneration of the extracellular matrix (ECM) are very important events in these processes. We tested fibrinolytic activities and the expression level of tPA and uPA levels in chronic constriction injury (CCI) model. The presented data demonstrates that in the injury nerve of CCI model, the fibrinolytic activities is upregulated and main caused by the upregulation of tPA expression. We also find that the activities of tPA and MMP-9 are co-upregulated post-CCI, both at CCI site and proximal site. These results indicate that tPA activity may regulate the MMP-9 activity in injury nerve post-CCI. Topics: Animals; Constriction, Pathologic; Fibrin; Male; Matrix Metalloproteinase 9; Pain; Rats; Rats, Sprague-Dawley; Sciatic Nerve; Tissue Plasminogen Activator; Up-Regulation; Urokinase-Type Plasminogen Activator | 2009 |
BDNF contributes to animal model neuropathic pain after peripheral nerve transection.
The outcome of peripheral nerve injury is often impaired by neuropathic pain, which is resistant to most analgesics and presents a serious clinical problem. The mechanisms underlying post-traumatic neuropathic pain remain unclear, but they are likely associated with the regeneration processes. Brain-derived neurotrophic factor (BDNF) is known to enhance peripheral nerve regeneration and is also considered to be an endogenous modulator of nociceptive responses following spinal cord lesion. The aim of this work was to examine the local effect of BDNF in a neuropathic pain model. Sciatic nerves of adult male rats were transected and supplied with connective tissue chambers filled with (1) fibrin only, (2) fibrin with BDNF, or (3) fibrin with antibodies against BDNF. In control animals the nerve was transected and no chamber was applied. During follow-up, autotomy behavior was assessed. Seven weeks after the operation, the number of surviving and regenerating neurons in dorsal root ganglia was counted and the neuroma incidence was examined. We found that local inactivation of BDNF decreased the incidence as well as severity of autotomy and neuroma formation, but did not influence neuron regeneration into the chambers. These results indicate that BDNF plays a locally crucial role in neuropathic pain development after peripheral nerve injury. Topics: Amputation, Traumatic; Animals; Antibodies, Blocking; Behavior, Animal; Brain-Derived Neurotrophic Factor; Fibrin; Fibrinogen; Ganglia, Spinal; Male; Nerve Regeneration; Neuroma; Neurons; Pain; Peripheral Nervous System Diseases; Peripheral Nervous System Neoplasms; Rats; Rats, Wistar; Sciatic Neuropathy; Thrombin | 2007 |
Genetic polymorphism in the fibrinolytic system and endometriosis.
Although most women experience retrograde menses during their reproductive life, endometriosis develops only in a small percentage. We hypothesized that persistence of a fibrin matrix in peritoneal pockets, as a result of hypofibrinolysis, could allow menstrually deposited endometrial fragments to initiate endometriosis. Fibrinolysis is modulated by several factors, and polymorphisms in the plasminogen activator inhibitor-1 (PAI-1) gene are considered to be one of the important determinants. The objective of this study was to evaluate PAI-1 genotypes in a group of women with or without endometriosis.. In 118 women (75 with laparoscopically confirmed endometriosis and 43 controls), genomic DNA was extracted from blood and the PAI-1 promoter genotype was determined by polymerase chain reaction amplification of DNA using specific primers for the 4G or 5G allele followed by gel electrophoresis. A portion of the polymerase chain reaction product was purified and sequenced to confirm the gel electrophoresis results.. Endometriosis was more likely in patients with 4G/5G (odds ratio 38; 95% confidence interval [CI] 6-229) or 4G/4G (odds ratio 441; 95% CI 53-3,694) compared with 5G/5G PAI-1 genotype. Fifty-two of 75 women with endometriosis (69 %, 95% CI 58-79%) had the 4G/4G genotype compared with only 5 of 43 (12%; 95% CI 4-25%) controls. In contrast, the 5G/5G genotype associated with normal fibrinolysis was found in 2 of 75 (3%; 95% CI 0-9%) women with endometriosis compared with 24 of 43 (56%; 95% CI 40-71%) controls.. Hypofibrinolysis, associated with the 4G allele of the PAI-1 gene, was found significantly more often in women with endometriosis compared with controls. Persistence of fibrin matrix could support the initiation of endometriotic lesions in the peritoneal cavity, explaining why some women with retrograde menstruation develop endometriosis while others do not.. II-2. Topics: Adult; Alleles; Endometriosis; Female; Fibrin; Fibrinolysis; Genetic Variation; Genotype; Humans; Infertility; Multivariate Analysis; Pain; Plasminogen Activator Inhibitor 1; Polymerase Chain Reaction; Polymorphism, Genetic | 2006 |
Pre-degenerated peripheral nerve extracts applied to the proximal stump of transected sciatic nerve enhance both regeneration and autotomic behavior in rats.
Peripheral nerve regeneration after traumatic injury and standard repair with a nerve autograft is often incomplete and results in neuropathic pain. Peripheral nerve extracts applied to the proximal nerve stump by means of autologous, dead-ended connective tissue chambers (deCTC) are known to accelerate the rate of axon regeneration. This study tested if such extracts would influence autotomy, which is a behavioral measure of neuropathic pain in animal models.. The study was performed on Wistar rats. DeCTCs, filled with postmicrosomal fraction obtained from 7-day-predegenerated nerves (7D group) or fibrin (F group), were implanted into transected sciatic nerve. In the control group (C), sciatic nerve was transected and its distal part was removed. The self-mutilation behavior in rats was assessed daily for seven weeks after sciatic nerve transection. The onset as well as intensity of autotomy was measured. The progress of regeneration was assessed under light microscopy and histochemistry.. The earliest onset and greatest severity of autotomy were found in the 7D group. Regeneration progress was also highest in this group. In the F group, we found weaker regeneration and less autotomy. The control group showed no regeneration, but more autotomy than the F group.. Intensified autotomy may be the price paid for enhanced peripheral nerve regeneration after application of growth-promoting substances. Topics: Animals; Behavior, Animal; Denervation; Fibrin; Male; Nerve Regeneration; Pain; Peripheral Nerves; Random Allocation; Rats; Rats, Wistar; Sciatic Nerve; Self Mutilation; Tissue Extracts; Transplants | 2002 |
Platelet activation and prostacyclin supporting capacity in the loin pain hematuria syndrome.
The loin pain hematuria syndrome has been characterized as a constellation of severe recurrent flank pain and hematuria, occurring predominantly in young women. We studied a 17-year-old woman who had recurrent right flank pain, gross hematuria, and fever, without evidence of urinary tract infection. Her physical exam was remarkable for right costovertebral angle tenderness and a normal BP. Her urinalysis showed blood and protein but her creatinine clearance and 24-hour urinary calcium excretion were normal. A kidney biopsy was remarkable for arteriolar subintimal fibrous thickening and fibrin deposition, but no glomerulonephritis. Her peripheral hemostasis evaluation was normal except for circulating platelet aggregates and elevated fibrinopeptide A levels. On two occasions, her serum was unable to normally support prostacyclin (PGI2) production by cultured human umbilical endothelial cells, as measured by radioimmunoassay (RIA) of its stable metabolite 6-keto-PGF alpha. Blood samples from the right renal vein and inferior vena cava revealed a selective elevation of fibrinopeptide A in the right renal venous effluent. The presence of circulating platelet aggregates and elevated levels of fibrinopeptide A (a cleavage product of fibrin) suggests that platelet activation and fibrin deposition may play a role in the pathogenesis of this disorder. The inability of her serum to normally support the production of the potent antiplatelet and antithrombotic substance, PGI2, could represent a primary renovascular endothelial cell defect. Topics: Adolescent; Epoprostenol; Female; Fibrin; Hematuria; Humans; Kidney; Pain; Platelet Aggregation; Syndrome | 1988 |
Abdominal pain associated with IgA nephropathy. Possible mechanism.
A 36-year-old man presented with IgA nephropathy (Berger's disease) and acute abdominal pain. Surgical biopsy of the ileum revealed deposits of IgA, C3, and fibrin in segments of the wall of submucosal arteries. The immune deposits appeared associated with areas of fibrinoid necrosis. These findings support the hypothesis that Berger's disease is a systemic disease, and provide a possible explanation for the abdominal pain associated with IgA nephropathy. Topics: Abdomen; Adult; Arteries; Biopsy; Complement C3; Fibrin; Fluorescent Antibody Technique; Follow-Up Studies; Glomerular Mesangium; Glomerulonephritis, IGA; Histocytochemistry; Humans; Ileum; Immunoglobulin A; Male; Necrosis; Pain | 1984 |
Is dry socket preventable?
Topics: Blood Coagulation; Costs and Cost Analysis; Dry Socket; Erythrocytes; Fibrin; Fibrinolysis; Humans; Ontario; Pain | 1977 |
A new haemorrhagic disorder with defective fibrin stabilization and cryofibrinogenaemia.
Topics: Abdomen; Antibodies; Blood Coagulation Tests; Blood Protein Disorders; Chromatography; Cold Temperature; Diagnosis, Differential; Ecchymosis; Electrophoresis; Factor XIII; Female; Fibrin; Fibrinogen; Hematuria; Hemorrhagic Disorders; Humans; Immunoglobulin G; Isoniazid; Middle Aged; Pain; Sarcoidosis | 1974 |
[Therapeutic defibrination with ancrod (author's transl)].
Topics: Adult; Aged; Animals; Anticoagulants; Arterial Occlusive Diseases; Blood Flow Velocity; Blood Viscosity; Enzyme Therapy; Female; Fibrin; Foot; Hemolysin Proteins; Humans; Injections, Intravenous; Leg; Male; Middle Aged; Necrosis; Pain; Regional Blood Flow; Snakes; Venoms | 1973 |
Cutaneous manifestations in capillary dilatation and endovascular fibrin deposits.
Topics: Angiomatosis; Anticoagulants; Arm; Biopsy; Blindness; Blood Coagulation Disorders; Capillaries; Chronic Disease; Factor V; Factor VIII; Female; Fibrin; Fibrinolysin; Humans; Leg Dermatoses; Middle Aged; Pain; Prednisolone; Skin Manifestations; Skin Ulcer; Thrombosis | 1968 |