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

In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. During the DIC reaction increasing inhibition of aggregability of circulating platelets against collagen and ADP is observed. Furthermore, ASA prevents the increase in the plasma haemoglobin level caused by DIC.
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PMID:[Effect of ASS on platelet function in experimental DIC]. 9 74

Platelet number, spontaneous aggregation, ADP- and adrenaline-induced aggregation, fibrinogen, and factors 2, 5, 7, and 10, were investigated in a series of 40 consecutive patients admitted to the clinic following severe head injury. Data were evaluated daily during the first week after trauma. Platelets were significantly decreased, particularly in non-survivors; there was no pathological spontaneous aggregation, except in a group of 22.5% of cases who had a mean age of 23.5 years. ADP-induced aggregation was negative in 69% of cases, and adrenaline-induced aggregation was absent in only two non-survivors. Fibrinogen was markedly reduced during the first five days, thereafter normalizing or increasing towards the end of the week. The other investigated values remained within their normal range of 70--130%. The results give no evidence of disseminated intravascular coagulation as a generalized and frequent phenomenon in severely head injured patients. There are, however, signs of latent consumption coagulopathy, which support data from the literature that indicate focal microthrombosis in contused brain areas.
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PMID:Disturbances of the coagulatory system in patients with severe cerebral trauma II. Platelet function. 51 79

The effects of Russell's viper venom (RVV) on blood coagulation, platelts and fibrinolysis were studied in vivo and in vitro in rabbits and dogs as experimental subjects. RVV was shown to be a strong coagulant, and at the time of manifestation of bleeding due to consumption coagulopathy, the most striking hemostatic abnormalities were fall of fibrinogen level, reduction in platelet count, delayed ADP aggregation of platelets, increased fibrinolytic activity and presence of fibrin degradation products. These findings showed that RVV interfered with blood coagulation, caused abnormalities of platelet function and also activated the fibrinolytic enzyme system.
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PMID:Effects of Russell's viper venom on blood coagulation, platelets and the fibrinolytic enzyme system. 91 51

A patient with clinical and laboratory evidence of disseminated intravascular coagulation associated with deep-vein thrombosis and pulmonary embolism developed a qualitative platelet abnormality characterized by a defective release reaction. Second-phase aggregation induced by ADP and adrenaline was impaired, and reduced collagen-induced aggregation was accompanied by defective release of ADP and ATP. The decrease in total platelet ATP and ADP, the high ATP:ADP ratio in the presence of normal amounts of metabolic adenine nucleotides, and the low content of serotonin associated with abnormal uptake and metabolism of the exogenous amine suggested that the defective platelet function was due to lack of the platelet organelles in which serotonin and nonmetabolic adenine nucleotides are normally stored. Acquired storage pool disease is likely to be related to exposure of circulating platelets to aggregating agents, with their degranulation occurring during disseminated intravascular coagulation.
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PMID:Acquired storage pool disease in platelets during disseminated intravascular coagulation. 96 91

The therapeutic efficiency of two glucocorticoids (hydrocortisone and dexamethasone) on endotoxin-induced intravascular coagulation was investigated in the rat. Coagulation and platelet aggregation studies were performed and plaminogen was assayed. Our results indicate that pretreatment of the animals with large doses of these steroids within a few hours prior to endotoxin totally prevents the consumption in Hageman factor, measurable contact product activity, platelets, fibrinogen, plasminogen, and the loss in platelet aggregability and serotonin. In addition to this, the hypercoagulable state consecutive to endotoxin, characterized here by shortenings in the partial thromboplastin and recalcification times and by an increase in the availability of platelet procoagulant activity, was also totally prevented by the steroid pretreatment. On the other hand, it is shown that these glucocorticoids do not interfere in the normal rat with platelet aggregation (tested with thrombin,adenosine diphosphate, and collagen), but with the availability of platelet procoagulant activity. This last phenomenon, in addition to that of an interference in vivo with the mechanism of activation of Hageman factor, are believed to be responsible for prevention by glucocorticoids of endotoxin-induced disseminated intravascular coagulation.
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PMID:Prevention by glucocorticoids of disseminated intravascular coagulation induced by endotoxin: mechanisms. 109 78

A prospective evaluation of the haemostatic mechanism was undertaken in 15 normal primigravidas and in 12 primigravidas with mild to moderately severe pre-eclampsia in order to further examine the possibility that disseminated intravascular coagulation may occur in this clinical syndrome. The only coagulation abnormality demonstrated was a prolongation of bleeding time. The data do not support the suggestion that significant disseminated intravascular coagulation is associated with pre-eclampsia. The addition of the heparinoid drug sodium pentosan polysulphate to the therapeutic regimen resulted in a significant fall in platelet factor 3 availability and in decreased aggregation against ADP but conferred no objective clinical improvement. We conclude that the drug has no place in the management of established pre-eclampsia.
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PMID:Pregnancy, pre-eclampsia and disseminated intravascular coagulation. 115 76

Increased blood loss is a major contributory factor to postoperative short- and longterm outcome in orthotopic liver transplantation (OLT). Hyperfibrinolysis, occurring mainly in the anhepatic phase, and disseminated intravascular coagulation (DIC), starting immediately after reperfusion, have been observed to parallel increased bleeding tendency. However, other factors may also contribute. For the first time we investigated platelet aggregation during the course of 10 OLTs and found a marked reduction of adenosine diphosphate-, collagen-, and ristocetin-induced platelet aggregation immediately after reperfusion. Since this is the point at which increased bleeding tendency is known to occur, it would seem that, apart from DIC and hyperfibrinolysis, an intermediate dysfunction of platelet aggregation may be a major cause of intraoperative bleeding.
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PMID:Decreased platelet aggregation after reperfusion in orthotopic liver transplantation. 154 50

Five antiplatelet agents have been isolated from Chinese herbs. Apigenin and magnolol are inhibitors of thromboxane synthesis, while osthole, protopine and norathyriol are inhibitiors of phosphoinositide breakdown. Thirty min after intraperitoneal (i.p.) administration of these drugs, tail bleeding time of mice was prolonged markedly in a dose-dependent manner by norathyriol, protopine, osthole and magnolol, but not by apigenin. However, the antiplatelet agents (up to 200 mg kg-1, i.p.) could not prevent acute thromboembolic death in mice. In endotoxin-induced experimental disseminated intravascular coagulation in rats, norathyriol (50-100 mg kg-1, i.p.) prevented the decrease in platelet counts and fibrinogen, and the prolongation of plasma prothrombin time. Norathyriol (100 mg kg-1, i.p.) also suppressed ex-vivo platelet aggregation induced by collagen and ADP in rat plasma.
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PMID:Antihaemostatic and antithrombotic effect of some antiplatelet agents isolated from Chinese herbs. 168 29

A left ventricular assist device (VAD) with a smooth surface of segmented polyurethane was implanted in five goats for 10-55 days, and plasma levels of fibrinogen (Fg), prekallikrein (PK), fibrinogen, fibrin degradation products (FDP), antithrombin III (AT III), prothrombin time (PT), partial thromboplastin time (PTT), platelet (Pl) count, and platelet aggregation (PlAg) induced by adenosine diphosphate were measured during the experiment. Heparin was administered during surgery and no systemic antithrombotic therapy was given thereafter. Before the third postoperative day (POD), plasma levels of Fg and PK were at their lowest, and increased afterward. Between the second and fifth POD PT and PTT increased to 130-160%, and returned to normal gradually. Plasma FDP appeared on the second POD and reached peak values of 10-40 micrograms/ml on the sixth POD. Platelet and AT III levels showed no uniform tendency, but the rate of PlAg decreased to levels of 6-77% before the fifth POD and remained low at approximately 80%, influenced by the pumping even after the 25th POD. In summary, VADs themselves activated coagulation and induced consumption coagulopathy to some degree. However, most of the parameters returned to normal within 2 weeks.
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PMID:Influences of ventricular assist device pumping on blood coagulation. 259 87

This paper describes changes in the circulating platelets of 25 patients with acute malaria within 2 to 6 days of onset of illness. Thrombocytopenia was observed in 10 out of 15 patients with Plasmodium falciparum infection, and in 4 out of 9 patients with P. vivax infection. One patient with a mixed infection of both species had a disseminated intravascular coagulation. Platelet antibody was detected in the sera of 8 out of 11 cases by the complement lysis inhibition technique and indirect immunofluorescence. The mean platelet antibody concentrations in the sera of 11 patients and 53 control subjects were 122.70 +/- 80.25 ng/10(7) platelets and 36.69 +/- 18.72 ng/10(7) platelets, respectively. An inverse relationship between the platelet count and platelet antibody levels in serum supported the view that thrombocytopenia in malaria may be partly immune-mediated. Platelet aggregation responses to agonists such as ADP, adrenaline, collagen and ristocetin revealed hyperactivity. Ultrastructural study of unstimulated platelets from patients revealed several changes such as centralization of dense granules, glycogen depletion, and formation of pseudopods and microaggregates, indicating in vivo activation of the platelets, which may also lead to thrombocytopenia.
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PMID:Functional and ultrastructural changes of platelets in malarial infection. 306 47


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