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)

Pregnant Wistar rats injected intraperitoneally on gestational day 12 with single doses (100-1,000 mg/kg) or 600 mg/kg of 4(5)-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (dic) were autopsied on day 21 (100-1,000 mg/kg) or at 24-hour intervals on days 13-20 (600 mg/kg). Controls received CMC on the same schedule. All fetuses were weighed and examined for urogenital system (UGS) malformations. Those given 600 mg/kg were also studied histologically. DIC produced significant growth retardation at all doses on day 21 (18-72%). UGS malformations occurred in 27-67% of the fetuses at 200-400 mg/kg and in 100% of those given 600 mg/kg or more of DIC. Abnormalities included renal growth inhibition, fusion, ectopia, and ureteropelvic dilatation. At 600 mg/kg renal and body weights were reduced 40 and 55%, respectively. Ureteropelvic dilation was common, and cortical glomeruli, nephric collecting tubules, and papillae were retarded in development. The juxtamedullary glomeruli were well developed. Proximal nephric tubular mitotic activity was 85% greater than in control animals (day 17). On the basis of pertinent morphological and physiological data, it is postulated that the dilated upper urinary tracts represent functional hydronephrosis incident to severe renal retardation and its resultant compensatory response.
Anat Rec 1976 Nov
PMID:Urogenital anomalies in fetal rats produced by the anticancer agent 4(5)-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide. 99 39

Rats which were infected with the gramnegative pathogen Klebsiella pneumoniae develop disseminated intravascular coagulation (DIC), multi-organ failure (MOF) and finally die in a septic shock. We investigated the therapeutic effect of antibiotic (tobramycin) treatment combined with the infusion of the highly specific thrombin inhibitor rec. hirudin. Although administration of 2 mg/kg tobramycin alone leads to a decrease of the bacterial burden, DIC could not be prevented. Infusion of rec. hirudin (0.25 mg/kg x h) for 4 h (start of treatment 1 h post infection), in addition to a bolus administration of tobramycin, led to an amelioration of DIC parameters as fibrinogen, thrombin-antithrombin complex (TAT) and platelets. Serum transaminase levels (GOT, GPT) as a marker of MOF were significantly improved by rec. hirudin, the T50 value increased from 17 h in the tobramycin group to 42 h in the tobramycin+rec. hirudin group, mortality rates were 90% or 60%, respectively. Combination of heparin (100 U/kg x h) and tobramycin was not effective on survival.
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PMID:Combination of antibiotic treatment with the thrombin inhibitor recombinant hirudin for the therapy of experimental Klebsiella pneumoniae sepsis. 797 45

An experimental disseminated intravascular coagulation (DIC) was induced in female CD rats by the intravenous administration of living bacteria (9.5 x 10(7) cfu Klebsiella pneumoniae), sublethal (5 mg/kg) or lethal (50 mg/kg) lipopolysaccharide (LPS), or tissue factor (1.5 micrograms/kg i.v. bolus or 0.4 micrograms/kg x hr i.v. infusion). We used a new fibrin monomer (FM) assay to follow the course of DIC. FM were detected by their ability to stimulate the tissue-type (t-PA) plasminogen activator dependent conversion of plasminogen to plasmin by a chromogenic assay. Miniplasminogen was used instead of plasminogen to avoid interference of the assay by alpha 2-antiplasmin. As a marker of DIC, elevated levels of FM were observed with all DIC-inducing agents (plasma levels were up to 90 micrograms/ml). The kinetics of FM formation were similar to the course of thrombin-antithrombin III (TAT) levels (maximal plasma levels 70 ng/ml); however, in the bacterial infection group, both parameters rose after a lag phase of about 1 hr. A 4 hr infusion of the highly specific thrombin inhibitor recombinant (rec.) hirudin (0.125 mg/kg x hr) resulted in a decrease of FM levels from 89.2 +/- 14.4 micrograms/ml in the LPS group (n = 10) to 27.4 +/- 11.2 micrograms/ml in the rec. hirudin group (n = 10; P < 0.001). The respective values for TAT levels were 73.1 +/- 19.7 micrograms/ml in the LPS group and 52.7 +/- 15.7 ng/ml in the rec. hirudin group (P < 0.001). Other coagulation parameters, such as platelets, fibrinogen, and fibrin(ogen) degradation products, were ameliorated accordingly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Formation of fibrin monomers in experimental disseminated intravascular coagulation and its inhibition by recombinant hirudin. 805 64

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.
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PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80

Three horses developed severe pulmonary infections while being treated with systemic corticosteroids for other diseases. Two of them had an immune-mediated skin disease, compatible with a diagnosis of pemphigus foliaceus, and one had severe chronic obstructive pulmonary disease. Case 1 developed diffuse pneumonia from which Streptococcus zooepidemicus and Bacteroides melaninogenicus were isolated, and it responded to antibiotic therapy. Case 2 developed septicaemia, pulmonary thrombosis and pneumonia associated with Escherichia coli, and died during a peracute illness with signs of disseminated intravascular coagulation. Case 3 developed focal pneumonia from which S zooepidemicus was isolated. This horse was destroyed at the owner's request and no treatment was attempted.
Vet Rec 1996 Mar 02
PMID:Bacterial pneumonia associated with corticosteroid therapy in three horses. 868 53

A dog whose major clinical signs suggested a coagulopathy, is described. The dog had a history of bleeding episodes and had a severe regenerative anaemia. By using specific factor assays, the coagulopathy was found to be due to a consumptive intravascular process that resembled chronic disseminated intravascular coagulation. Subsequent investigations identified Angiostrongylus vasorum as the cause.
Vet Rec 1996 Apr 13
PMID:Role of chronic disseminated intravascular coagulation in a case of canine angiostrongylosis. 873 63

A six-day-old Missouri foxtrotter colt was examined because it had had diarrhoea since it was 24 hours old. A diagnosis of colitis, septicaemia, and disruption of the arterial blood flow to the pelvic limbs was made on the basis of clinical and laboratory findings. Despite intensive medical therapy, the foal died 13 hours after being examined. Postmortem examination revealed diffuse fibrinous enteritis with lymphoid necrosis, multifocal fibrinonecrotic typhlocolitis, disseminated intravascular coagulation, and a large occluding thrombus at the aortic termination. The results of bacteriological culturing supported the diagnosis of septicaemia leading to activation of the clotting cascade, disseminated intravascular coagulation, aorto-iliac thrombosis and infarction of the pelvic limbs.
Vet Rec 1998 Apr 25
PMID:Aorto-iliac thrombosis in a foal. 960 15

Haemostasis was evaluated in 19 dogs with natural Leishmania infection, six of them with a history of epistaxis, and the results were compared with the results from 24 healthy dogs. In addition, the dogs' blood pressure was measured and biopsies were taken from the nasal mucosa. Buccal mucosa bleeding time was prolonged in the dogs with leishmaniasis (P < 0.002) and most significantly in those with epistaxis (P < 0.005). None of the Leishmania-infected dogs had thrombocytopenia, low levels of plasma von Willebrand factor antigen, a prolonged prothrombin time or activated partial thromboplastin time, a low plasma fibrinogen concentration or high serum fibrin degradation products. These results rule out defects of secondary haemostasis or disseminated intravascular coagulation as significant causes of epistaxis in non-complicated leishmaniasis. Histopathology of the nasal mucosa of 10 of the affected dogs, three of them with epistaxis, revealed ulcerative and inflammatory lesions in all of them.
Vet Rec 2001 Aug 11
PMID:Evaluation of the potential causes of epistaxis in dogs with natural visceral leishmaniasis. 1153 Sep 2

A 19-year-old horse that was one of a group of six horses infected experimentally with Anaplasma phagocytophilum for a study of the pathogenesis of equine granulocytic ehrlichiosis died suddenly two days after first showing clinical signs of disease. The clinical signs and laboratory findings observed before its death were similar to all those of the other infected horses, and to previous reports of this disease. A postmortem examination revealed widespread haemorrhaging in its internal organs, and vasculitis and thrombosis in the kidneys. These changes are consistent with disseminated intravascular coagulation, which has previously been reported in human beings infected with the presumably identical agent of human granulocytic ehrlichiosis.
Vet Rec 2007 Jan 27
PMID:Death of a horse infected experimentally with Anaplasma phagocytophilum. 1725 54

Eight hundred and seventy-one dogs with thrombocytopenia were divided into the following five categories: immune-mediated thrombocytopenia (49; 5.6 per cent), thrombocytopenia caused by disseminated intravascular coagulation (DIC) (52; 6.0 per cent), thrombocytopenia caused by miscellaneous disorders (222; 25.5 per cent), neoplasia-associated thrombocytopenia (244; 28 per cent) and inflammatory/infectious thrombocytopenia (304; 34.9 per cent). The incidence of thrombocytopenia among the hospital population was 6.7 per cent. The dogs with immune-mediated thrombocytopenia and thrombocytopenia caused by DIC had significantly (P<0.001) lower platelet counts (median 32.0 x 10(9)/l and 55.0 x 10(9)/l, respectively) than the dogs in the other three categories.
Vet Rec 2009 May 23
PMID:Retrospective study of 871 dogs with thrombocytopenia. 1946 53


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