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)

Changes of high molecular weight kininogen (HMW-K) clotting activity, antigen and cleavage in the plasma in the health and various diseases were studied. In 20 healthy individuals clotting activity of HMW-K, as measured by APTT one stage method, was 99 +/- 12% (male) and 84 +/- 15% (female). Antigen as measured by Laurell method were 106 +/- 24% (male) and 91 +/- 21% (female). In 35 patients with disseminated intravascular coagulation (DIC), both activity (78 +/- 33%) and antigen (69 +/- 31%) were statistically lower than those in normal individuals (p less than 0.01). In DIC both activity and antigen of HMW-K was correlated with serum albumin level. These results suggest that the cause of the lower level of HMW-K in DIC especially with septicemia is the result of lower production rather than consumption. In vivo cleavage of HMW-K was detected in plasma of a patient with septicemia and DIC by immunoblotting. The change of HMW-K was also assessed in other pathological states including liver cirrhosis, collagen disease, cardiopulmonary bypass and pregnant women.
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PMID:[Changes of high molecular weight kininogen in various states]. 259 37

We studied contact factors and kinin-kallikrein in normal non-pregnant and pregnant women, FXII deficient toxemia and DIC. The results obtained are as follows: 1. The levels of plasma prekallikrein, high molecular weight kininogen, kallikrein inhibitor, and C-1 INA were gradually decreased at delivery, and the levels of kallikrein like activity and bradykinin were increased during pregnancy and at the time of parturition. These facts indicate that kinin kallikrein systems played important role in uterine contraction. 2. The levels of contact factors (FXII and FXI) were lower at delivery than those of term. 3. In rat uterus, specific binding of bradykinin was observed by the method of radio receptor assay in the pelet of 10,000 X g fetal membranes, and its activity was 38%. 4. A synthetic kallikrein inhibitor (OS-291, MS) and bradykinin antagonist inhibited completely spontaneous uterine contraction of Wistar rats during delivery. 5. In the case of FXII deficiency, the levels of plasma prekallikrein, high molecular weight kininogen were normal, but at delivery, these levels were lower than those of term. The levels of kallikrein like activity which was half of normal parturition level was increased at parturition. 6. In cases of DIC (17) and severe toxemia (22), plasma prekallikrein levels were lower than the normal controls. The decrease was due to consumption of plasma prekallikrein to kallikrein activation.
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PMID:[Physiopathology of kinin forming system in reproduction]. 259 38

Disseminated intravascular coagulation, thrombocytopenia, consumption of factors VIII and II, and antithrombin deficiency have been previously demonstrated in pre-eclampsia. However, the precise mechanism responsible for initiation of disseminated intravascular coagulation has not been elucidated. The present study documents activation of the intrinsic coagulation pathway in a patient with severe pre-eclampsia. The studies revealed marked reductions of plasma coagulant activities of all intrinsic pathway factors, i.e., XII, XI, IX, and VIII. In addition, the ratio of plasma factor XII activity to antigen concentration was markedly abnormal, and plasma high-molecular-weight kininogen concentration was diminished. It is suggested that activation of the intrinsic coagulation pathway may be operative in the genesis of disseminated intravascular coagulation in pre-eclampsia.
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PMID:Activation of intrinsic coagulation pathway in pre-eclampsia. 2870 53

Components of the kallikrein-kinin system of the blood and some hemostatic indices were studied in parallel in 32 patients with diffuse toxic goiter. A decrease in the levels of prekallikrein, kininogen, the activity of kallikrein and kininase inhibitors in the blood plasma of the examinees resulted in raised activity of the kallikrein-kinin system in decompensated thyrotoxicosis. Hemostatic changes were characterized by signs of chronic disseminated intravascular coagulation. It was shown that kinin formation and blood coagulation were correlated. A certain parallelism in the increment of the activity of the kinin system and disorders of hemocoagulation was noted with an increase in a degree of severity of thyrotoxicosis. A tendency to improved indices was also noted after thyrostatic therapy.
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PMID:[Several aspects of the pathogenesis of disturbances of hemostasis in patients with diffuse toxic goiter]. 321 79

In vitro effects of S-2441, H-D-Pro-Phe-Arg-NH-Heptyl, include potent anti-bradykinin activity and broad-spectrum inhibition of serine proteases involved in the coagulation cascade. In this study, rats infused with 7.8 X 10(8) viable Escherichia coli were treated either with saline (group A) or with intravenous (0.1 mg) and intraperitoneal (0.4 mg) doses of S-2441 (group B). Survival rates for groups A and B were 68% and 98%, at 12 hours (P less than 0.001), and 37% and 73% at 24 hours (P less than 0.001), respectively. Hematologic studies revealed that S-2441 significantly inhibited E. coli-induced prolongation of prothrombin time and partial thromboplastin time as well as a rapid decrease in the values of factor X, anti-thrombin III, and fibrinogen. In addition, S-2441 attenuated E. coli-induced hypoglycemia and a marked reduction of serum complement level. Ultrastructural evaluation of the liver demonstrated that S-2441 prevented the development of extensive sinusosoidal microthrombosis and hepatocellular necrosis. The results indicate that S-2441 affords protection in lethal gram-negative bacteremia owing in part to attenuation of disseminated intravascular coagulation and complement-mediated reactions. The findings are consistent with the concept that S-2441 and related oligopeptides modulate serine protease-mediated responses involving inhibition of active enzymes with competitive antagonism of pharmcologically active products formed during the activation of coagulation, fibrinolytic, kallikrein, and complement systems.
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PMID:Efficacy of S-2441, a synthetic oligopeptide, in a rat model for gram-negative bacteremia. 388 74

Levels of prekallikrein and HMW kininogen that had increased during pregnancy decreased with start of labor. The role of the kinin-forming system with oxytocin in the mechanism of labor was suggested from the results of decreased prekallikrein and HMW kininogen, appearance of a free kallikrein-like enzyme during labor, and from the case of arrested labor in which both prekallikrein and HMW kininogen were markedly decreased. Prekallikrein was markedly decreased in patients with acute obstetrical DIC and severe toxemia of pregnancy. The excessive activation of prekallikrein in DIC seemed to be of help for understanding such clinical signs as shock, abnormal labor, and increased permeability in obstetrical DIC.
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PMID:The kinin-forming enzyme system in pregnancy and obstetrical DIC. 642 Dec 72

Fibrin clots have been detected at sites of inflammation, and kinins have been implicated as mediators of the vascular phenomena of acute inflammation, systemic shock, and disseminated intravascular coagulation. It is now reported that both negatively and positively charged asbestos fibers shorten the partial thromboplastin time of human plasma, indicating coagulation of the plasma. A sample containing short (less than 5 micron in length) chrysotile fibers is ineffective. Only the negatively charged amphiboles (crocidolite and amosite) are able to activate factor XII (Hageman factor). This particular effect of the amphiboles is enhanced by high molecular weight kininogen and leads to kinin formation.
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PMID:Asbestos fibers, plasma and inflammation. 664 59

Prolonged hypotension and disseminated intravascular coagulation were seen in a patient after intravasation of barium sulfate contrast medium during a barium enema examination. High endotoxin levels were measured in the contrast material. In vitro, this material induced generation of bradykinin. The clinical features observed may be explained by contact activation of the Hageman factor-dependent pathways caused by the contrast material and/or by circulating endotoxins. Treatment of this rare but severe complication occurring during a barium enema procedure should be directed against the endotoxic shock.
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PMID:Disseminated intravascular coagulation and hypotension after intravasation of barium. 686 54

Plasma kallikrein acts as a chemical mediator of microcirculation and as a contracting agent of smooth muscle by liberating bradykinin from high molecular weight kininogen. In addition, prekallikrein relates to coagulation process of blood. It is, therefore, a intriguous problem to know the behavior of prekallikrein in obstetrics, especially as to the mechanisms of labor, edema of toxemia and DIC. The following results were obtained: 1) Plasma prekallikrein determined by chromogenic tripeptide substrate was increased with advance of gestational ages, and reached maximum (213.5 +/- 31.1%) at the term. At the beginning of labor, the prekallikrein level was suddenly decreased, and remained low during labor. Rapidly lowered plasma prekallikrein during labor seems to be result from consumption of prekallikrein due to conversion to kallikrein. The kallikrein probably relates to uterine contraction by forming bradykinin. 2) A lowered plasma prekallikrein level was observed in 29 cases of toxemia, especially in edema type. In toxemic cases, kallikrein may play an important role in producing edema by bradykinin. 3) In 16 cases of DIC, prekallikrein was significantly low (p less than 0.001) especially in cases of endotoxic shock, suggesting consumption of prekallikrein as in other various coagulation fibrinolysis factors in DIC.
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PMID:[Physiological and pathological significance of plasma prekallikrein in obstetrics]. 692 84

The hypotension and disseminated intravascular coagulation (DIC) in bacteremia is thought to be mediated by the combined actions of cytokines, prostaglandins, and complement. The contact system, via the release of bradykinin and the activation of Factor XI, has been postulated to be contributing to the observed hypotension and DIC. Using a mAb to Factor XII (C6B7), we blocked the activation of the contact system in an established experimental baboon model in which Escherichia coli was infused to produce lethal bacteremia with hypotension. The untreated group (n = 5) displayed contact activation, manifested by a significant decrease in high molecular weight kininogen (HK) and a significant increase in alpha 2 macroglobulin-kallikrein complexes (alpha 2M-Kal). The C6B7-treated group (n = 5) showed an inactivation of Factor XII and the changes in HK and alpha 2M-Kal complexes were prevented. Both groups developed DIC manifested by a decrease in platelet, fibrinogen, and Factor V levels. The untreated group developed irreversible hypotension. The treated group experienced an initial hypotension that was reversed and extended the life of the animals. This study suggests that irreversible hypotension correlates with prolonged activation of the contact system, and specific antibody therapy can modulate both the pathophysiological and biochemical changes.
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PMID:The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia. In vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons. 767 10


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