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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemostasis is initiated by injury to the vascular wall, leading to the deposition of platelets adhering to components of the subendothelium. Platelet adhesion requires the presence of von Willebrand factor and platelet receptors (IIb/IIIa and Ib/IX). Additional platelets are recruited to the site of injury by release of platelet granular contents, including ADP. The "platelet plug" is stabilized by interaction with fibrinogen. In this review, I consider laboratory tests used to evaluate coagulation, including prothrombin time, activated partial thromboplastin time, thrombin time, and platelet count. I discuss hereditary disorders of platelets and/or coagulation proteins that lead to clinical bleeding as well as acquired disorders, including disseminated intravascular coagulation and acquired circulating anticoagulants.
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PMID:Coagulation and bleeding disorders: review and update. 1092 20

Oxidative stress results from an oxidant/antioxidant imbalance, an excess of oxidants and/or a depletion of antioxidants. A considerable body of recent evidence suggests that oxidant stress plays a major role in several aspects of septic shock and disseminated intravascular coagulation (DIC), and it is the subject of this review. Immunohistochemical and biochemical evidence demonstrate the significant role of reactive oxygen species (ROS) in endotoxic and hemorrhagic shock, and in endothelial injury associated with DIC syndrome. Initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3-phosphate dehydrogenase, inhibition of membrane Na+/K+ ATP-ase activity, inactivation of membrane sodium channels, and other oxidative protein modifications contribute to the cytotoxic effect of ROS. In addition, reactive oxygen species are potent triggers of DNA strand breakage, with subsequent activation of the nuclear enzyme poly-ADP ribosyl synthetase, with eventual severe energy depletion of the cells. Pharmacological evidence suggests that the peroxynitrite-poly-ADP ribosyl synthetase pathway contributes to the cellular injury in shock and endothelial injury. Treatment with superoxide dismutase mimetics (SODms), which selectively mimic the catalytic activity of the human superoxide dismutase enzymes, have been shown to prevent in vivo shock and the cellular energetic failure associated with shock.
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PMID:Oxidative stress in septic shock and disseminated intravascular coagulation. 1239 25

Higenamine (HG) is a potent cardioactive benzylisoquinoline alkaloid isolated from Aconiti tuber which has long been used as a cardiotonic in traditional Chinese medicine. HG exerts various effects on the cardio-circulatory system inotropic and chronotropic in isolated rat atria. It also relaxes isolated rat aorta. It inhibits epinephrine, ADP or collagen-induced platelet aggregation in platelet rich plasma. HG inhibits LPS-induced nitrate accumulation and the expression of iNOS mRNA in RAW 264.7 cells. HG lowers blood pressure in rats and increases the recovery rates in acute thrombosis model of mice, and lower the weight of thrombus formed in the arterio-venous shunt model of rats. Higenamine also has ameliorative effects in the LPS-induced DIC model.
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PMID:[Effects of higenamine on the cardio-circulatory system]. 1562 Jan 76

A study was conducted on the changes in platelet function and platelet count in the Sprague-Dawley rat induced by a bends-producing N2-O2 compression-decompression cycle. In those instances where mild to moderate cases of decompression sickness were produced, a decrease in platelet reactivity to ADP-induced aggregation occurred immediately postdive along with an increase in inhibition of aggregation by prostaglandin E1. Both effects returned to control levels 24 hours postdive. In moderately affected animals, platelet counts were lower than normal 24 hours postdive but were similar to control values 72 hours postdive. These results tend to support current hypotheses regarding the etiological relationship between disseminated intravascular coagulation and decompression sickness as a function of bubble nucleation.
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PMID:Supportive evidence for altered platelet function in the dived rat. 1562 36

The anti-thrombic properties of the Korean herbal medicine, Dae-Jo-Hwan (DJW), which is consisted of 11 herbs (indicated as concentrations) of Rehmanniae radix 24%, Hominis placenta 5%, Testudinis carapax 9%, Eucommiae cortex 9%, Asparagi radix 9%, Phellodendri cortex 9%, Achyranthis radix 7%, Liriopis tuber 7%, Angelicae sinensis radix 7%, Ginseng radix 6%, and Schizandrae fructus 3%, were investigated. The extracts of DJW and its 11 herbs, except G. radix, A. sinensis radix and S. Fructus, inhibited the endotoxin-induced hepatic venous thrombosis in high cholesterol diet-treated rats. Also the extract inhibited the endotoxin-induced decrease in blood platelets and fibrinogen, and endotoxin-induced increase in fibrin degradation products (FDP) on disseminated intravascular coagulation in normal rats. In in vitro experiments, the extract was shown to have inhibitory effect on collagen- and ADP-induced blood platelet aggregation, on thrombin-induced conversion of fibrinogen to fibrin and on the activity of plasminogen or plasmin. In conclusion, the protection of extracts of Korean herbs on the ischemic infarction induced artificially might be related to their inhibitory effects on DIC, platelet coagulation and thrombic action.
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PMID:Anti-thrombic activity of Korean herbal medicine, Dae-Jo-Whan and its herbs. 1622 22

Inappropriate platelet activation is a feature of acute and chronic diseases such as disseminated intravascular coagulation (DIC) and atherosclerosis. Since proinflammatory microbial-derived agonists can be involved in the pathogenesis of these diseases, we examined the potential role of TLR4 (mediating responses to LPS) and TLR2 (which responds to bacterial lipopeptides) in platelet activation. Our data suggested low-level expression of TLR2 and TLR4 on platelets, determined by flow cytometry, and we also observed expression of TLR4 on a megakaryocytic cell line by both flow cytometry and immunohistochemistry. Stimulation of the platelets with the TLR4 agonist LPS, and the synthetic TLR2 agonist Pam3CSK4, resulted in no platelet aggregation, no increase in CD62P surface expression and no increase in the cytosolic concentration of Ca2+. The TLR agonists were also unable to directly activate platelets primed with epinephrine, or pretreated with a low concentration of ADP or PAF. Pretreatment of platelets with LPS or Pam3CSK4 also failed to modulate the platelet response to submaximal concentrations of the classical platelet agonists ADP and PAF. We conclude that the TLR agonists LPS and Pam3CSK4 have no direct effect on platelet activation and that platelet TLRs may be a remnant from megakaryocytes. TLR2 and TLR4 agonists are thought to have a significant role in diseases such as atherosclerosis and DIC, but our research suggests that this is through a mechanism other than direct platelet activation or by modification of platelet responses to other agonists.
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PMID:Agonists of toll-like receptor (TLR)2 and TLR4 are unable to modulate platelet activation by adenosine diphosphate and platelet activating factor. 1627 Jun 39

Platelet aggregation was undertaken in platelet rich plasma in 34 heat-stroke patients during the Muslim pilgrimage (Haj) to Makkah; 18 were males and 16 were females; their ages ranged from 36 to 80 years (mean SD = 58 10). Platelet aggregability, on arrival at the Heatstroke Centres, was markedly inhibited in response to adrenaline, collagen, arachidonic acid and ristocetin but not to ADP. Responses to decreasing ADP doses (20.0, 2.0, 1.0 and 0.5 micromol/l) showed hyperaggregability in 12 patients, inhibited responses in 16 and normal responses in 6 patients. Aggregation responses were not significantly different when comparing patients with bleeding manifestations ( n = 10), with those without bleeding ( n = 24). Haemostatic parameters including plasma fibrinogen, ATIII and platelet count, were markedly reduced in the two patient groups who showed hyperaggrebable and depressed aggregation responses, but not in those with normal responses. These results lead us to conclude that: (1) platelet activation is a frequent feature of heatstroke; (2) in heatstroke altered aggregation responses, whether hyperaggregable or depressed, occur simultaneously with a consumption coagulopathy.
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PMID:The role of platelets in the coagulopathy of heatstroke- a study of platelet aggregation in heatstroke patients during the Makkah pilgrimage (Haj) to Makkah. 1679 31

Patients with sepsis often suffer from haemostatic disturbances such as haemorrhage and disseminated intravascular coagulation (DIC). Considering the pivotal role of platelets in haemostasis, we have investigated platelet function by flow cytometry in 16 patients with sepsis for a better understanding of their haemostatic function. We have also investigated whether platelet function correlates with the severity of disease assessed by multiple organ dysfunction (MOD) score and patient outcome. The platelet response ex vivo after stimulation with agonists, measured as platelet fibrinogen, binding was low in comparison with healthy volunteers ( n = 30). This could reflect a previous response to agonists in vivo , which lead to platelet activation and consumption and formation of microthrombi that could then participate in the development of M OD. The platelets that remain in the circulation might be the result of a selection process where the most active platelets have already been consumed, and the remaining population consists of less active platelets. Another explanation might be desensitization of the remaining platelets because of exposure to agonists in vivo . Platelet activation with the agonists ADP and arachidonic acid were predictive of subsequent development of MOD and final patient outcome.
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PMID:Impaired platelet function correlates with multi-organ dysfunction. A study of patients with sepsis. 1679 6

It is believed that platelets play a key role in the production of pre-eclamptic toxaemia and toxaemia of pregnancy. Toxaemia of pregnancy is described as a condition of chronic DIC where there is thrombocytopenia as well as raised fibrin degradation products. Since fibrinogen receptors are involved in the final stage of the platelet aggregation reaction, we wanted to investigate the platelet receptors for fibrinogen in normal and abnormal pregnancy. Thirty-six normal pregnant women (12 in their 2nd trimester, 24 in their 3rd trimester), 24 pregnant pre-eclamptic toxaemia cases and 16 non-pregnant controls were included in the present study. All patients with pre-eclamptic toxaemia had oedema, proteinuria and hypertension. Flow cytometric study of platelets was undertaken utilizing fluorescein isothiocyanate (FITC)-labelled anti-human fibrinogen antibody in unstimulated and ADP-stimulated (final concentration 0.02 M) platelets. The intensity of platelet fluorescence was classified into three groups and expressed in arbitrary units. The results indicate that there are a higher number of stimulated platelets expressing fibrinogen receptors in the circulation of patients with pre-eclampsia. Thus, it is possible to hypothesize that platelets showing increased fibrinogen receptors aggregate and form microthrombi in smaller vessels in women with pre-eclamptic toxaemia.
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PMID:Functional and fibrinogen receptor studies in platelets in pre-eclamptic toxaemia of pregnancy. 1680 Oct 92

Stromal cell-derived factor-1 (SDF-1) is a CXC chemokine that activates and directs the migration of leukocytes that have CXCR4, which is the unique receptor for SDF-1. Although SDF-1/CXCR4 interaction has been implicated in various inflammatory conditions, its role in modulating coagulation has not been determined. We studied the plasma SDF-1 levels in 90 patients with suspected disseminated intravascular coagulation (DIC) and we found that circulating SDF-1 was significantly increased in the overt DIC patients and was also increased in overt DIC patients who have a poor outcome. We then tested in vitro whether SDF-1 can affect the expression of monocyte tissue factor (TF) and endothelial thrombomodulin (TM), and both of these play important roles in coagulopathy. SDF-1 did not affect the expression of surface TF protein and its function and the TF mRNA level in both monocytes and the monocytic leukemia cell line THP-1. SDF-1 also did not change the surface TM expression of endothelial cells. SDF-1 could enhance low-dose ADP induced platelet aggregation, although it failed by itself to induce aggregation. These findings suggest that plasma SDF-1 might be closely associated with hypercoagulability though its action as a platelet activator.
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PMID:Plasma level of stromal derived factor-1 (SDF-1) is increased in disseminated intravascular coagulation patients who have poor outcomes: in vitro effect of SDF-1 on coagulopathy. 1723 27


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