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

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

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

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

Acute disseminated intravascular coagulation (DIC) is a life-threatening condition that may be encountered in many situations, especially in cases of shock with uncontrollable hemorrhage. Anisodamine, an alkaloid extracted from a Chinese herb, is well known for its dramatic therapeutic effect on DIC. Sixty male rabbits were used to establish an acute DIC model. A total of 240 blood samples were taken for laboratory assays of changes in blood coagulation factors, platelet count, platelet adhesion, platelet aggregation, malondialdehyde (MDA), thromboxane B2 (TXB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Changes of the microcirculatory status and the rate of the blood flow in the conjunctival capillaries of 60 rabbits were observed with WXS-II microcirculation microscope. Pathological sections of the lungs and kidneys were studied. Our investigation showed the presence of microthrombi in the microvasculature. After treatment with anisodamine, the prothrombin time stayed in the normal range, fibrinogen consumption was lessened, adenosine-diphosphate-induced platelet aggregation was inhibited, thromboxane B2 and malondialdehyde concentrations were significantly lower than in the control group, and the elevated quantity of 6-keto-PGF1 alpha was spared. We concluded that the anti-platelet-aggregating, microcirculation-facilitating, thromboxane-B2-inhibiting, malondialdehyde-inhibiting, and 6-keto-PGF1 alpha-sparing effects of anisodamine are the important mechanisms of its dramatic therapeutic effect on DIC.
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PMID:Mechanism of the therapeutic effect of anisodamine in disseminated intravascular coagulation: study of platelet adhesion and aggregation, malondialdehyde, thromboxane B2, 6-keto-prostaglandin F1 alpha, and microcirculation. 378 Aug 90

The secretolytic agent bromhexine and its active metabolite ambroxol prevent the collagen- and ADP-induced decrease in circulating blood platelets in rabbits, while they do not inhibit the aggregation induced by ADP, collagen or arachidonic acid of human and rabbit blood platelets in vitro. Bromhexine was found to exert beneficial effects on the disturbances of pulmonary function that might be caused by a reduced surfactant production observed during thrombin-induced disseminated intravascular coagulation in rats. The results suggest that bromhexine has a protective effect on the acute impairment of pulmonary function due to microthrombosis.
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PMID:[Effect of bromhexine on microthrombosis in animal experiments]. 392 41

The effect of experimental trypanosomiasis on coagulation was studied because a patient in this hospital with Rhodesian trypanosomiasis developed thrombocytopenia with disseminated intravascular coagulation. Rats injected intraperitoneally with this strain of Trypanosoma rhodesiense consistently developed trypanosomiasis and severe thrombocytopenia without changes in hematocrit or concentration of fibrinogen or fibrin split products. At the time of 50% mortality (4-5 days) mean platelet counts per cubic millimeter of infected rats were 18,000+/-9,000 (+/-2 SEM) compared to 1,091,000+/-128,000 in uninfected controls. In vitro, concentrated trypanosomes and trypanosomefree supernates of disrupted organisms added to normal rat, rabbit, or human blood produced platelet aggregation within 30 min. This platelet aggregation was not blocked by inhibitors of ADP, kinins, or early or late components of complement. In vivo thrombocytopenia also occurred in infected rabbits congenitally deficient in C6 and in infected, splenectomized rats. Although the aggregating substance obtained from disrupted trypanosomes is heat-labile, it is active in the presence of complement inhibitors, suggesting that this trypanosomal product may be a protein enzyme or toxin. Since the phenomenon is independent of immune complexes, complement, ADP, and kinins, it appears to represent a new mechanism of microbial injury of platelets and the induction of thrombocytopenia.
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PMID:Thrombocytopenia in experimental trypanosomiasis. 420 22


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