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)

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.
 ...
PMID:[Physiological and pathological significance of plasma prekallikrein in obstetrics]. 692 84

Thromboembolism of minor vessels in the lungs is almost constantly seen in posttraumtic lung insufficiency. Many investigators consider it as the primary factor in the pathogenesis of this condition. The present paper deals with screening of the coagulation system as part of a more extended project also investigating changes in the fibrinolytic system and the kallikrein-kinin system. The data are also to be compared with morphological findings during the development of experimental posttraumatic lung insufficiency. The experimental syndrome was evoked in Labrador retriever dogs by haemorrhagic hypotension combined with clamping of the portal triad. The surgical procedure was extended to additional thoracotomy in one group of dogs. Group I, without thoracotomy, were followed for 12 hours. Group II, with thoracotomy, were followed until they succumbed (3-14 hours). Thrombotest (TT) showed a steady prolongation of clotting time in both groups, whereas Cephotest did not reveal any alterations, except for a significant prolongation in group II just before collapse. Fibrinogen was markedly reduced in both groups. Platelets and leucocytes were significantly reduced, but only in group II. It is concluded that the present data are indicative of disseminated intravascular coagulation. The involvement of the intrinsic coagulation system is questioned.
 ...
PMID:Blood cells and coagulation during experimental lung insufficiency in dogs. 693 93

From the viewpoint of fetal distress related disseminated intravascular coagulation (DIC), the Hageman Factor, kinin-kallikrein system were investigated and on the other hand the adaptation of the normal newborn to extrauterine life was also evaluated. (1) The Kininogen volume of the cord venous blood was approximately 1/2-1/3 or there abouts and was remarkable in serious cases of asphyxiated newborn. (2) In a similar manner the Hageman factor decreases in asphyxiated newborn. On the other hand, SFMC increases in aspyxiation as well as FDP. According to these results, there seems to be a coagulation obstruction due to consumption. Or it may be interpreted as an inhibition of kinin separation. In any event it may be considered as a rational contribution to the living body. (3) Based on the above, in cases of serious asphyxiation, DIC may possibly play a role and in these cases and the kininkallikrein system may be one of the mediators.
 ...
PMID:A biochemical study on the kinetics of kininogen in asphyxiated newborn. 706 58

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.
 ...
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

A total of 83 patients with chronic renal failure (CRF) at azotemia stage (S. I. Riabov's classification) complicating pyelonephritis were treated: 19 patients received symptomatic standard therapy (group 1), 29 patients received combined therapy with enterosorption (group 2), 35 patients received combined treatment with plasmapheresis (group 3). The efficacy of the treatments was controlled by platelet tests (platelet, coagulative hemostasis, fibrinolytic plasma activity) and parameters of kallikrein-kinin system. Treatment results in group 1 are characterized as poor: insignificant improvement of uremia, DIC syndrome against unchanged inhibition of kallikrein-kinin system. Group 2 patients achieved moderate response: uremia reduced to normal azotemia values, DIC syndrome and inhibition of kallikrein-kinin system reduced. Patients of group 3 got disappeared DIC syndrome and normal kallikrein-kinin system against high azotemia.
 ...
PMID:[Changes in the hemostatic system indices of patients with chronic kidney failure under the influence of enterosorption and plasmapheresis]. 798 57

C1-Inhibitor (Berinert, C1 INH), a 104 kDa protein, inhibits complement components (C1 esterase) as well as enzymes of the contact phase of coagulation (Factor XII, Factor XI) and kallikrein, thus regulating kinin generation. C1 INH is used for the treatment of the hereditary angioneurotic edema. This paper will give a survey about the evidence in recent literature concerning the potential efficacy of the compound on other diseases associated with shock, capillary leakage and inflammation as well. In our own experiments we evaluated whether the compound could influence acute inflammatory reactions or the severe systemic inflammatory response syndrome (SIRS) as a consequence of an experimental septic shock. To prevent the sepsis-induced DIC we co-infused the thrombin inhibitors AT III or rec. hirudin in combination with C1 INH. Coinfusion of C1-inhibitor (50-200 U/kg x h) with either rec. hirudin or AT III significantly improved survival rate compared to thrombin inhibitor alone.
 ...
PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80

Biochemical observations during clinical sepsis using functional and immunological measurements of enzymes, cofactors and inhibitors of the kallikrein-kinin system indicate that activation of these proteases occur during hypotensive gram-negative septicemia and adult respiratory distress syndrome. Using animal models of septicemia, we demonstrated that protease inhibitors or neutralizing monoclonal antibodies to proteins of the contact system inhibit or prevent the formation of kallikrein and the decrease in kininogen. In addition, the irreversible phase of hypotension can be prevented and survival prolonged. Thus, bradykinin is one of the important mediators of hypotension. In contrast, the contact system plays little role in the associated DIC. In cardiopulmonary bypass, the formation of kallikrein leads to neutrophil degranulation and release of elastase. Selective inhibitors of kallikrein not only block its activation but play a predominant role in inhibiting elastase release.
 ...
PMID:Factor XII activation and inhibition in inflammation. 835 19

DIC is an acquired disorder in which intravascular coagulation may lead to microvascular fibrin formation and a hemorrhagic diathesis. If DIC is acute and severe, fibrin formation may lead to microvascular thrombosis, and consumption of coagulation factors and platelets may result in a hemorrhagic diathesis. Secondary to or simultaneously with coagulation, the fibrinolytic system may be activated, accentuating the bleeding tendency. All the systems involved in DIC, such as coagulation, fibrinolysis, kallikrein-kinin, complement, and possibly other systems are regulated. Coagulation is the central event of DIC. The different coagulation factor derivatives may be generated that can be determined and used as markers for the degree of DIC and for effective control of therapy. Some of the procoagulant and anticoagulant factors are converted in the course of coagulation to their active forms and activation peptides. The active factor is subsequently neutralized by forming a complex with an inhibitor. Hemostatic molecular markers, D-dimer of cross-linked fibrin degradation products (D-dimer), thrombin-antithrombin III complex (TAT), and plasmin-alpha 2-plasmin inhibitor complex (PIC) have all been used for the diagnosis of DIC.
 ...
PMID:[Progress in diagnosis of disseminated intravascular coagulation (DIC)--diagnostic criteria of DIC]. 843 27

In accordance with the proposed methodics the state of Hageman factor (HF) system was studied, i.e. intimate connection of callicrein-kinine, coagulation and fibrinolytic blood systems in various clinic and hemostasiological forms of DIC-syndrome, acute and chronic arterial thromboses, thrombembolisms, post-operative and thrombolytic hemorrhages in 1118 patients. The author describes the principles of diagnosis, prophylaxis and correction of the disorders in blood coagulation, fibrinolysis and kinogenesis in this pathology. The article contains data concerning the structure of researches, index and HF coefficients, as well as reference hemostasiological criteria, classification and medical tactics in various forms of DIC-syndrome.
 ...
PMID:[New principles in the prognosis, diagnosis, prevention and treatment of the DIC syndrome]. 857 10

We found a new, highly selective plasma kallikrein inhibitor, trans-4-aminomethyl-cyclohexanecarbonylphenylalanine 4-carboxymethylanilide hydrochloride, called PKSI-527 in our laboratories. This study was conducted to evaluate PKSI-527, on thromboplastin (TP)- and endotoxin (LPS)-induced disseminated intravascular coagulation (DIC) in rats. PKSI-527 was infused intravenously at 0.1 mg/kg/min for 250 min. Three of the parameters of the coagulation and fibrinolysis system, fibrinogen level, platelet counts and fibrin(ogen) degradation products (FDP) level were assayed. PKSI-527 prevented the change in the coagulation and fibrinolysis system in LPS-induced DIC, however it was not clearly effective in TP-induced DIC. The parameters of organ failure, such as serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), creatine phosphokinase (CPK), lactate, blood urea nitrogen and beta-glucuronidase, were assayed. Although the changes in the fibrinogen level, platelet counts and FDP level were almost the same in both models, the parameters of organ failure apparently increased in LPS-induced DIC more so than in TP-induced DIC. PKSI-527 significantly suppressed the increases in GOT and GPT in LPS-induced DIC. These results indicate that plasma kallikrein may play a significant role in LPS-induced DIC. Therefore, PKSI-527, as a synthetic plasma kallikrein inhibitor may be a valuable tool to explore the mechanism of DIC and the accompanying organ failure.
 ...
PMID:Effects of a highly selective synthetic inhibitor of plasma kallikrein on disseminated intravascular coagulation in rats. 874 31


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