Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disseminated intravascular coagulation (DIC) secondary to colic was diagnosed in 23 horses. Each horse was categorized retrospectively as to the cause of the colic based on surgical and/or necropsy findings: group 1 consisted of 14 horses with compromised intestine that required resection and anastomosis; group 2 consisted of 3 horses with nonstrangulating intestinal displacement and/or impactions; and group 3 consisted of 6 horses with colic associated with enteritis and/or colitis. Horses were considered to be affected with DIC if at least three of five hemostatic parameters were significantly abnormal: decreased antithrombin III (AT III) values, increased level of fibrin degradation products (FDP), thrombocytopenia, prolonged activated partial thromboplastin time, and prolonged prothrombin time. The most consistent hemostatic abnormalities were decreased AT III activity, increased FDP titers, and thrombocytopenia. Clotting times were more variable and did not always correlate with the presence of excessive hemorrhage. Excessive hemorrhage was present during surgery in seven horses and occurred within 1 to 12 hours after surgery in nine other horses. In addition to treatment of the primary disease, 19 horses received treatment for DIC consisting of heparin and/or plasma or fresh whole blood transfusions. Heparin alone was used in 12 horses. Heparin, in addition to fresh whole blood transfusions or fresh plasma, was administered to four horses. Three horses were treated with plasma alone. Four other horses were not treated specifically for the DIC. Eight horses (34%) survived the acute coagulopathy. Although a greater proportion of the surviving horses received heparin therapy (87.5%; 7/8) than did those that died (60%; 9/15), the difference was not statistically significant (P = 0.345).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disseminated intravascular coagulation associated with colic in 23 horses (1984-1989). 154 23

Whole blood re-calcification times were evaluated as a measure of endotoxin-associated coagulopathy in horses. First, the effects of endotoxin concentration and duration of in vitro incubation of citrated whole blood with endotoxin on the whole blood re-calcification time of blood collected from healthy horses were determined. Increasing concentrations or incubation times of endotoxin accelerated the whole blood re-calcification time. This effect was attributed mainly to increased monocyte thromboplastin activity. Second, whole blood re-calcification time, a clotting profile, plasma factor VII activity and plasma endotoxin concentration on blood samples obtained from 35 equine colic patients and 10 healthy horses were determined. Compared with healthy horses, colic patients had a longer mean whole blood re-calcification and prothrombin time, lower per cent factor VII activity and higher mean fibrin degradation products concentration. Within the colic patient group, horses that did not survive had detectable endotoxin in plasma, longer whole blood re-calcification and prothrombin times, and lower plasma factor VII activity, compared with colic patients that survived. These data indicate that colic patients with endotoxaemia experience hypercoagulable states, followed by consumptive coagulopathy. Although the cause of endotoxin-associated coagulopathy is likely multi-factorial, increased expression of monocyte thromboplastin activity may be involved in the pathogenesis of coagulopathy. The whole blood recalcification time is a simple, fast and inexpensive way to detect coagulopathy during endotoxaemia and determine the prognosis for survival.
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PMID:Whole blood re-calcification time in equine colic. 191 33

Endotoxemia remains the leading cause of death in horses, being intimately involved in the pathogenesis of gastrointestinal disorders that cause colic and neonatal foal septicemia. Endotoxins, normally present within the bowel, gain access to the blood across damaged intestinal mucosa, or endotoxemia occurs when gram negative organisms proliferate in tissues. Endotoxins are removed from the circulation by the mononuclear phagocyte system, and the response of mononuclear phagocytes to these lipopolysaccharides (LPS) play an important role in determining the severity of clinical disease. Macrophages become highly activated for enhanced secretory, phagocytic and cidal functions by LPS. Macrophage-derived cytokines are responsible for many of the pathophysiologic consequences of endotoxemia. The arachidonic acid metabolites, prostacyclin and thromboxane A2 likely mediate early hemodynamic dysfunction and the leukotrienes may potentiate tissue ischemia during endotoxemia. Interleukin 1 (IL-1) induces fever and is responsible for the inflammatory cascade, which constitutes the acute phase response. Tumor necrosis factor (TNF), an important proximal mediator of the effects of LPS, acts to initiate events and formation of other molecules that affect shock and tissue injury. Systemic administration of TNF produces most of the physiologic derangements that are associated with endotoxemia and antibodies that are directed against TNF significantly reduce LPS-induced mortality in experimental animals. In response to endotoxins, mononuclear phagocytes express thromboplastin-like procoagulant activity (PCA), which initiates microvascular thrombosis. Both IL-1 and TNF induce PCA expression, creating a positive feedback loop for LPS-induced coagulopathy. A macrophage-derived platelet activating factor contributes to coagulation dysfunction and further stimulates arachidonic acid metabolism. The ultimate consequences of endotoxemia are multiple system organ failure and death. The numerous feedback loops and intertwining cascades of mediators during endotoxemia defy simplistic methods of treatment. The optimal therapy likely involves methods to alter the generation of inflammatory mediators by mononuclear phagocytes.
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PMID:Endotoxemia in horses. A review of cellular and humoral mediators involved in its pathogenesis. 192 Feb 54

Endotoxin-activated monocytes express a thromboplastin-like procoagulant activity on the cell surface that may serve as a focal point for formation of microvascular thrombi. Because coagulopathy is a common sequela to endotoxemia in the equine species, we investigated the ability of monocytes, isolated from horses with colic, to express procoagulant activity. On the day of admission, and on the third and fifth day of hospitalization, monocytes were isolated from 30 adult horses with colic. A coagulation profile, including prothrombin time, activated partial thromboplastin time, thrombin time, and plasma fibrinogen and serum fibrin degradation products concentrations, was determined at each sample collection. The concentration of endotoxin in the plasma was quantitated at the time of admission. Ten clinically normal adult horses served as controls. The procoagulant activity of monocytes isolated from horses with colic was significantly (P less than 0.05) greater than that of the monocytes isolated from clinically normal horses. On the first and third day of hospitalization, the mean prothrombin time was significantly (P less than 0.05) longer in horses with colic, compared with clinically normal horses, and was the most common abnormality in the coagulation profile on the day of admission (25/30; 83%). Mean fibrin degradation products concentration was significantly (P less than 0.05) greater in horses with colic on the day of admission and was the second most common abnormality in the coagulation profile on day 1 (23/30; 77%). In horses with colic, the mean prothrombin and activated partial thromboplastin times were significantly (P less than 0.05) longer in horses that did not survive, compared with horses that survived.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical relevance of monocyte procoagulant activity in horses with colic. 202 36

The incidence and nature of coagulation abnormalities in horses presented with colic and the possible prognostic value of these abnormalities was investigated. A coagulogram was performed on each of 24 adult Thoroughbred or Standardbred horses. A coagulogram consisted of measurements of eight parameters; platelet count, plasma fibrinogen, plasma antithrombin III (AT), partial thromboplastin time (PTT), prothrombin time (PT), thrombin clotting time (TCT), soluble fibrin monomer (SFM) and fibrin-fibrinogen degradation products (FDP). Retrospective determination of the cause of the colic and outcome (survival vs non-survival) was carried out. All patients examined had at least one abnormal parameter with the frequency being: Increased SFM 67 per cent; prolonged PTT 63 per cent; prolonged TCT 50 per cent; elevated plasma fibrinogen 46 per cent; reduced platelet count 29 per cent; reduced plasma AT 29 per cent; prolonged PT 25 per cent; and elevated serum FDP 21 per cent. When survivor and non-survivor groups were compared there was little difference in the frequency of abnormalities such as elevated SFM, elevated fibrinogen and prolonged PTT. The abnormalities which had the greatest frequency difference between non-survivors and survivors, and therefore the greatest prognostic value, were decreased AT greater than prolonged TCT = prolonged PT greater than elevated FDP greater than reduced platelet count. The frequency of these abnormalities in non-survivors compared to survivors was 8.6:1, 7.1:1, 5.7:1 and 3.6:1, respectively. The average number of abnormal parameters in non-survivors (five) was significantly greater than in survivors (two).
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PMID:Haemostatic abnormalities in horses with colic--their prognostic value. 375 3

Hemostatic profiles were determined in 30 horses with clinical colic. Blood samples were obtained at the time of the animal's admission, and the following hemostatic tests were done: blood platelet count, plasma fibrinogen, plasma antithrombin, prothrombin time, partial thromboplastin time, thrombin time, protamine sulfate test for soluble fibrin monomer, and fibrin-fibrinogen degradation products. The patients were categorized in retrospect, according to the cause of the colic: group 1--colic associated with colitis and/or severe diarrhea, group 2--colic associated with torsion or obstruction of the intestine, and group 3--colic associated with impaction of the intestine or the presence of enteroliths. Of the 30 horses with colic, 28 had at least 1 abnormality in their coagulogram--the most frequent abnormalities being high plasma fibrinogen concentration, high circulating soluble fibrin monomer, or a long partial thromboplastin time or thrombin time. The horses in group 1 seemed to have the most severe coagulopathies, as indicated by the average number of demonstrable abnormalities. The horses in group 3 showed the fewest abnormalities--usually a high plasma concentrations of fibrinogen and/or soluble fibrin monomer. The results indicated that hemostatic abnormalities are not uncommon in horses with gastrointestinal disease and colic--the degree of severity depending to some extent on the cause of the colic.
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PMID:Hemostatic abnormalities in equine colic. 395 19

In horses with large bowel disease, those with circulating endotoxins but no evidence of altered hemostasis had a good prognosis for survival. Those with circulating endotoxins and evidence of altered hemostasis (fibrin degradation products) had a poor prognosis. Portal vein infusion of endotoxins over 24 hours caused hoof discomfort, evidenced by shifting of weight and standing with all 4 feet together, and a decreased hoof temperature. Clinical signs appeared within 30 minutes of initiation of infusion and subsided within 4 hours despite continued infusion. Long-term heparin therapy results in rapid depletion of RBC but no detectable bleeding. Heparin therapy should be initiated before colic surgery is begun. Coagulation is monitored with the activated partial thromboplastin time. Heparin should initially be given IV, followed by SC or intrafat injections, and should never be given IM. The anticoagulative effects of heparin can be reversed with protamine sulfate.
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PMID:Heparin anticoagulant therapy in equine colic. 649 4

Components of the coagulation and fibrinolytic cascades, prothrombin and activated partial thromboplastin times, endotoxin activity, and albumin concentration were measured in blood and peritoneal fluid from 20 healthy horses and from 153 horses with acute gastrointestinal tract diseases at admission. Overall, 77% (117/153) of affected horses survived to discharge from the hospital, and 85% (82/97) of horses discharged were reported to be normal 9 to 14 months later. Significant differences in hemostatic factors were more common in peritoneal fluid than in blood. Tissue plasminogen activator, plasminogen, protein C, antithrombin III, and alpha 2-antiplasmin activities and concentrations of fibrinogen and fibrin degradation products were significantly (P < 0.05) greater in peritoneal fluid from horses with colic, and, with the exception of fibrinogen concentration, were associated with detection of endotoxin. Higher values for these variables, except tissue plasminogen activator activity, were significantly (P < 0.05) associated with survival. Plasminogen, antithrombin III, and alpha 2-antiplasmin activities were significantly (P < 0.05) greater in peritoneal fluid from horses with inflammatory or strangulating lesions, compared with those in horses with simple colic. Plasminogen-activator inhibitor type 1 activity, fibrin degradation products concentration, and prothrombin time were significantly (P < 0.05) greater in the blood of horses with colic. Survival was inversely associated with significantly (P < 0.05) greater intravascular concentrations of fibrin degradation products and fibrinogen and prothrombin time. This study revealed marked contrasts between peritoneal and intravascular coagulation and fibrinolysis in horses with colic, indicating that inferences regarding the peritoneal environment, particularly with respect to fibrinolytic capacity, should not be made on the basis of factors measured in blood.
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PMID:Intravascular and peritoneal coagulation and fibrinolysis in horses with acute gastrointestinal tract diseases. 759 47

Although tissue factor (TF) activity has been observed on the subendothelial surface of rabbit aorta and human umbilical cord, immunofluorescent and in situ hybridization methods have failed repeatedly to demonstrate TF in the intima of human blood vessels. In the present study, TF activity on everted, de-endothelialized arteries was studied by two methods. One utilized a flow system and measured fibrin deposition and fibrinopeptide A formation. The other utilized a newly developed rotating probe system and measured the conversion of factor X to factor Xa in the presence of factor VIIa and Ca+2. The study attempted to control, or assess, the possibility that functional TF could have been exposed on the vessel surface by the procedures used to prepare the arterial segments. By both methods, TF activity was detected on the subendothelium of rabbit aortae and human umbilical arteries, and was unaffected by the length of storage or by inclusion of actinomycin D in the storage buffer. TF activity was also observed in the subendothelium of adult human ileo-colic, internal mammary, and renal arteries, studied by the rotating probe method. The latter may underestimate TF activity, as some of the factor Xa formed appears to bind to the subendothelial surface. TF activity (Xa formation) was detected on the luminal surface (subendothelium) of non-everted arteries, but increased activity was observed after eversion of the vessel. The source of the subendothelial TF, and its presence in normal subendothelium in vivo, requires further study. In addition, if any of the TF activity observed in this study was derived from injured endothelial or myointimal cells during preparation of the everted vessel segments, the techniques described could serve as a useful model for studying TF-induced thrombosis and factor Xa formation on injured blood vessels, and for evaluating the anti-thrombotic properties of TF-inhibitors.
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PMID:Further studies on the presence of functional tissue factor activity on the subendothelium of normal human and rabbit arteries. 801 16

Eight tests of hemostasis were measured in 233 horses with colic. Blood samples were obtained at admission and for 4 consecutive days of hospitalization. Data were analyzed retrospectively by outcome, by broad-category diagnosis group, by small intestinal disorder, and by smaller categories for comparing specific diseases. Nonsurviving horses and horses with the most severe forms of intestinal ischemia had changes interpreted as hypercoagulative, the intensity of which was increased on the first and second mornings (sample times 2 and 3) after admission, when most significant differences for results of specific tests were detected. Nonsurvivors had decreased antithrombin III activity and prolonged prothrombin and activated partial thromboplastin times; those with strangulating obstructions also had decreased protein C and plasminogen activities. During hospitalization and with survival, these changes tended to reverse. In most horses, regardless of diagnosis or outcome, concentration of fibrin degradation products and fibrinogen, and alpha 2-antiplasmin activity increased over time. Whether these changes reflected specific effects of colic or of the acute-phase response was not determined. In comparisons of small intestinal disorders (proximal enteritis, strangulations, and impactions), diagnostically distinguishing features were not found. Likewise, in comparisons of specific diseases (small vs large intestinal impaction, proximal enteritis vs colitis, small vs large intestinal obstruction), diagnostically distinguishing features were not found.
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PMID:Analysis of hemostasis in horses with colic. 840 38


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