Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of platelet activating factor antagonist (PAF-A) for sublethal endotoxemia after 70% or 84% hepatectomy in rats were studied. Endotoxin of 1mg/kg b.w. was intravenously given once on the first, third or fifth day hepatectomy. One week survival rates of 84%-hepatectomized rats with endotoxin injection on the third postoperative day was the lowest at 20%, and the lowest survival rate improved to 80% with PAF-A administration. Pathophysiology of PAF-A treated and nontreated rats with endotoxemia was investigated on the third day after 84% hepatectomy. There was no significant difference in SGOT, SGPT and blood glucose level between the two groups. PAF-A nontreated rats' prothrombin time was prolonged (p < 0.05) and serum fibrinogen level significantly decreased (p < 0.01), compared to treated rats. Platelet count distinctly decreased in both groups. Fibrin was pathologically proved in the glomeruli of the kidney in both groups. However, single cell necrosis of hepatocytes was significantly reduced by PAF-A administration. Rats without PAF-A had bloody ascites in 75% of cases and showed shock and pathologically pulmonary congestion. PAF may be related to DIC, shock, bloody ascites and high mortality rate in sublethal endotoxemia after massive hepatectomy. PAF-A was significantly effective for endotoxemia after hepatectomy.
 ...
PMID:[Experimental studies on the relation of platelet activating factor (PAF) to high mortality in sublethal endotoxemia after massive hepatectomy and effects of its antagonist]. 833 21

Hemostatic studies found in the patients with Thrombotic thrombocytopenic purpura were discussed. Most of them showed normal routine hemostatic studies; normal prothrombin time, activated partial thromboplastin time, plasma level of fibrinogen. Fibrin degradation products are more consistently abnormal, with approximately to 70% having slight elevations, but less than 25% of titers are greater than 25 micrograms/ml. Although some cases concerning of complication of disseminated intravascular coagulation in the patient with TTP are found in the literature, laboratory and clinical finding suggest that TTP and DIC are separate entities.
 ...
PMID:[Changes in molecular markers in patients with thrombotic thrombocytopenic purpura]. 843 5

The changes in blood coagulation/fibrinolysis and intestinal microvasculature after acute portal vein occlusion were studied in adult mongrel dogs. All five dogs that underwent portal vein ligation with resultant portal system thrombosis died within 81-130 min following the procedure. Fibrin deposition occurred in the small-intestine mucous-membrane capillaries within 10 min after ligation. Before ligation, high levels of tissue plasminogen activator activity were noted in small vessels, mainly those of the small-intestine submucosa. However, this activity decreased significantly after portal vein ligation, suggesting progression into irreversible disseminated intravascular coagulation. After simultaneous portal vein and superior mesenteric artery occlusion, similar changes occurred, but later than with portal vein ligation alone. The five dogs who underwent this procedure died within 70-195 min. However, if portal blood was bypassed into the femoral vein through an anti-thrombogenic heparinized hydrophilic catheter, deterioration after complete portal vein ligation was not observed; the five dogs that underwent this procedure survived.
 ...
PMID:Disseminated intravascular coagulation (DIC) in the intestinal circulation by acute portal vein occlusion and the effectiveness of portal-venous bypass using an antithrombogenic catheter. 850 49

Thrombus formation and the sequential expression of tissue factor (TF), interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-1 ra) in several organs were examined immunohistochemically and morphometrically in a novel model of disseminated intravascular coagulation (DIC) developed by modifying the generalized Shwartzman reaction (GSR) in rabbits. The new model [carrageenan (CA)-lipopolysaccharide (LPS)] was induced by the administration of a priming dose of intraperitoneal CA, 10 mg/kg, followed 24 h later by a provocative dose of LPS 25 micrograms/kg, while GSR was induced by the intravenous injection of two doses of LPS 25 micrograms/kg. CA was detected predominantly within macrophages in the spleen and liver. Fibrin thrombi were formed as early as 1 h after the second LPS treatment in all examined organs reaching a peak at 3-9 h and their prevalence was higher in the CA-LPS group (p < 0.05). The sequential expressions of TF and IL-1 beta correlated well with each other in both groups reaching a peak at 3-9 h with the CA-LPS group showing a more pronounced expression than the GSR group. Macrophages in the liver, spleen and lungs, and Bowman's epithelial cells expressed both proteins, while IL-1 beta was also expressed by endothelial and epithelial cells. IL-1 ra was expressed by the same cells expressing IL-1 beta, however, its expression continued to increase gradually over 24 h. The mortality rate was lower (p < 0.05) and neutrophilic sequestration less prominent in the CA-LPS group than in the GSR group. These findings indicate that CA efficiently replaced the priming LPS treatment and the consequently enhanced production of IL-1 beta may have resulted in the upregulation of TF expression leading to the high level of thrombi in this new model which may provide a tool for further studies on the role of cytokines in DIC.
 ...
PMID:Expression of tissue factor and interleukin-1 beta in a novel rabbit model of disseminated intravascular coagulation induced by carrageenan and lipopolysaccharide. 873 72

Disseminated intravascular coagulation (DIC) syndromes can be defined as the formation of fibrin deposits within the microcirculation, occurring in definite clinical situations. Their biological counterpart is a consumption coagulopathy. The clinical profiles of DIC have been well known for decades, are multiform and range from latency to overwhelming haemorrhagic diatheses, including also characteristic but rare situations, such as purpura fulminans, acral cyanosis and pictures resembling thrombotic thrombocytopenic purpura or haemolytic-uraemic syndrome. Biological tests of DIC show a consumption coagulopathy, displayed on the standard haemostasis sheet; along with signs of paracoagulation and/or of secondary fibrinolysis (FDP). New tests have recently been introduced: D-dimers are specific and sensible; Antithrombin-III, protein C and alpha 2-antiplasmin also can sometimes be useful. The knowledge of the pathophysiology of DIC has made advances with passing years. Fibrin deposits may be non-occlusive, and indeed they are swiftly removed by a secondary fibrinolysis. Except in very rare situations, such as those leading to a cortical renal necrosis, and perhaps in some ARDS, there is little evidence relating DIC to organ failure syndromes. Moreover, there is no clear relationship between the severity of the consumption coagulopathy and the prognosis. For instance, the mortality is much lower in abruptio placentae, where the coagulopathy is very severe, than in septic shock, where it is usually moderate. In septic shock, the disorders of haemostasis were related initially to a platelet activation, then to an activation of the contact system (releasing kinins and triggering complement cascade), and nowadays to the activation of the extrinsic coagulation system. The treatment of DIC is mainly the treatment of its cause. Indications for heparin therapy should be strictly limited to a few exceptional circumstances. When haemorrhagic diathesis threatens, FPC and/or platelet transfusion may be indicated. Aprotinin can be useful in rare cases of overwhelming secondary fibrinolysis. Trials with antithrombin-III or C1-esterase inhibitors are in progress.
 ...
PMID:[Disseminated intravascular coagulations]. 900 11

Endotoxin infusion (lipopolysaccharide from Escherichia coli 120 micrograms kg-1 i.v.) was titrated to produce hypercoagulability in rabbits and the effects of prostacyclin (PGI2) treatment (continuous infusion of 6 ng kg-1 min-1 i.v.) on coagulation variables, cardiorespiratory variables, and fibrin deposition in the microcirculation of vital organs were studied. PGI2 infusion did not influence the concentration of soluble fibrin, thrombelastographic variables, or systemic platelet aggregability. Fibrin deposition in the microcirculation of the liver and the lungs was reduced to 50% of that observed in untreated animals (p < 0.01). The antiplatelet properties of PGI2 were unable to reduce experimental endotoxin-induced systemic procoagulant turnover but improved organ perfusion during the initial phase of disseminated intravascular coagulation.
 ...
PMID:Effects of prostacyclin substitution on systemic procoagulant turnover and cardiorespiratory variables in experimental hypercoagulability. 909 82

An animal model of gram-positive septicemia was developed to evaluate the effects of antithrombin (AT) concentrates on morbidity, mortality, and laboratory consequences of disseminated intravascular coagulation (DIC). DIC was induced in guinea pigs by infusing Staphylococcus aureus (SA) isolated from blood cultures of patients with DIC (DIC-SA) or without DIC (non-DIC-SA). The non-DIC-SA animals and animals infused with sterile saline served as controls. Varying doses of AT were administered either 30 minutes or 24 hours after infusion of SA. DIC was confirmed within 4 hours by changes in prothrombin time, activated partial thromboplastin time, fibrinogen, fibrinogen-fibrin degradation products, and AT activity. Clinical bleeding was also evident. Mortality of untreated DIC-SA animals was 36% within 24 hours and up to 75% by 72 hours. Intervention with any dose of AT between 125 and 1,000 IU/kg 30 minutes after DIC-SA infusion was associated with 100% survival (P < or = .05 in the 250 IU/kg group) and sustained increases in AT activity and fibrinogen concentrations (P < or = .05). When AT was administered in combination with low molecular weight heparin (LMWH) or if LMWH was adminstered alone, mortality from DIC-SA was slightly, but not significantly reduced compared with untreated DIC-SA. Gross hemorrhage was observed premortem and at autopsy in all of the DIC-SA animals but in substantially fewer animals that received AT (P < or = .001 in the 250, 500, and 1,000 IU/kg groups). In contrast, groups treated with LMWH, alone or with AT, experienced hemorrhage and appeared to develop pathologic DIC. Fibrin formation in end-organs was detected in all guinea pigs in the untreated DIC-SA group and in the groups treated with 125 IU/kg AT and LMWH alone. AT doses between 250 and 1,000 IU/kg administered 30 minutes after DIC-SA infusion prevented fibrin formation in end-organs (P < or = .001 in the 250 and 1,000 IU/kg groups). AT administered 24 hours after DIC-SA could not reverse pre-existing histopathologic evidence of DIC but favorably affected survival, which reached statistical significance in the 1,000 IU/kg AT group (P < or = .025). In summary, suprapharmacologic doses of AT concentrate significantly decreased morbidity and mortality and ameliorated adverse changes in laboratory measures induced by DIC-SA in this guinea pig model and were not associated with untoward hemorrhagic complications. These findings provide justification for studying the use of AT therapy in patients with DIC-SA.
 ...
PMID:The suprapharmacologic dosing of antithrombin concentrate for Staphylococcus aureus-induced disseminated intravascular coagulation in guinea pigs: substantial reduction in mortality and morbidity. 919 63

Pooled plasma from 40 patients with severe disseminated intravascular coagulation (DIC) secondary to septic conditions was subjected to gel permeation chromatography on Sephacryl S-500 HR after sample pretreatment with KSCN for dissociation of non-covalent fibrin complexes. Fibrin antigen in eluates was detected by an array of ELISA tests, using two monoclonal antibodies against fibrin degradation product D-dimer, a monoclonal antibody against an epitope generated by plasmin cleavage of the D-domain, and an antibody against the neo-N-terminus of the alpha-chain of fibrin exposed by cleavage of fibrinopeptide A. Tag antibodies were a polyclonal antibody against the fibrinogen/ fibrin D-domain, a POD-conjugated version of the monoclonal antibody against fibrin alpha-chain neo-N-terminus, and a polyclonal antibody against fibrinopeptide A. Most fibrin-related material present in the pooled DIC plasma was of higher molecular mass than fibrinogen. Fibrin polymers were reactive with antibodies against D-dimer, plasmin cleaved D-domain, and fibrin alpha-chain neo-N-terminus. Part of the polymers reacted with antibodies against fibrinopeptide A, indicating presence of fibrinogen or desA-fibrin monomer within the covalently linked complex. In conclusion, the primary analytes detected by monoclonal antibodies for D-dimer, plasmin-specific epitopes of fibrin degradation products, as well as sites exposed by fibrinopeptide cleavage in plasma from patients with disseminated intravascular coagulation are high molecular weight factor XIIIa-crosslinked fibrin complexes, containing plasmin-cleaved D-domains, intact fibrin monomer units, and fibrinogen or desA-fibrin monomer.
 ...
PMID:Fibrin detected in plasma of patients with disseminated intravascular coagulation by fibrin-specific antibodies consists primarily of high molecular weight factor XIIIa-crosslinked and plasmin-modified complexes partially containing fibrinopeptide A. 930 56

We investigated fibrin(ogen)-related antigens in liver tissues of rabbits infected with rabbit haemorrhagic disease (RHD) virus. Fibrin(ogen)-related antigens were detected in the sinusoids of liver at six hours post infection (pi). At 18 hours pi, the antigens were clearly detected in the hepatocytes infiltrated with heterophils rather than in the sinusoid. In the rabbits that spontaneously died (30 hours pi), fibrin(ogen)-related antigens were detected in both degenerating and some intact hepatocytes. They were also expressed in the necrotic foci of hepatocytes infiltrated by heterophils. By immunoprecipitation fibrin(ogen)-related antigens were extracted from the infected liver homogenates and analysed by sodium dodecyl sulphate polyacrylamide gel electrophoresis and Western blot analysis. There was an increase in fibrinogen and A alpha polypeptide chains in the liver homogenates from rabbits sacrificed at 18 and 24 hours pi, including those that died. Disseminated intravascular coagulation developed after progress of degeneration and necrosis of hepatocytes in RHD. It is assumed that the resultant consumption of fibrinogen triggers replenishment of fibrinogen by hepatocytes.
 ...
PMID:Fibrin(ogen)-related antigens in rabbits experimentally infected with rabbit haemorrhagic disease virus. 942 44

We report on a 64-year-old patient with a recurrent endometrial carcinoma which was associated with disseminated intravascular coagulation (DIC) and excessive hyperfibrinolysis. The patient presented with severe bleeding due to hypofibrinogenemia. Fibrin degradation products were excessively elevated and there were also increased levels of activation markers of coagulation. Free plasmin was demonstrated in the circulation and alpha 2-antiplasmin was almost completely depleted. No increase in t-PA or u-PA level was demonstrated. Antifibrinolytic treatment led to a decrease of fibrin degradation products, but to an increase of activation markers of coagulation and was not associated with an increase of fibrinogen. Combination chemotherapy led to a rapid decrease of activation markers of coagulation and a sustained increase of fibrinogen. The beneficial effects on DIC/hyperfibrinolysis occurred despite the absence of any measurable effect of chemotherapy on the tumour. The patient finally died due to progression of the tumour, but without recurrence of the DIC/hyperfibrinolysis.
 ...
PMID:[Disseminated intravascular coagulation (DIG) with massive hyperfibrinolysis in metastatic uterine cancer. Observations on the effects on the coagulopathy of various treatments (a case report)]. 953 80


<< Previous 1 2 3 4 5 6 7 8 Next >>