Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isovolemic exchange perfusion of conscious normal and splenectomized rats to a Hct of +/- 3% with the perfluorocarbon based oxygen transport fluid, Fluosol-DA 20%, is characterized by: 1) a greater than projected depression of fibrinogen and the plasma globulins and 2) a rapid regeneration of these and certain other plasma proteins. Similar responses were observed in a study of PFC resuscitation of hemorrhagic shock in splenectomized dogs in which there was a selective depression of the platelets, the plasma globulins, IgG and fibrinogen. In the rats, the red cells and platelets required 14-21 days to return to control levels while the leukocytes returned to normal in 1-2 days. The globulins and fibrinogen exhibited a transient rebound response at 3 and 12 hours post exchange respectively with total protein levels restored to control levels at 48 hours. In the shock study, the leukocytes, which remained at control levels throughout the shock period and for 1 hour post resuscitation were 2.5x control levels at 24 hours. The platelets which were depressed to 20% of control levels following resuscitation remained depressed through the 24 hour time course of the study. Implicit in these results is the possibility that; A) thrombosis and B) immunosuppression may be caused by some component(s) of the perfusion/resuscitation fluid.
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PMID:Regenerative responses to exchange perfusion. 317 90

The changes in the blood level of fibrin-fibrinogen degradation products (FDP) have been studied in 62 patients with myocardial infarction. 30 healthy donors served as the control. FDP was determined using solid-phase immunoenzyme assay. Acute and subacute phases of myocardial infarction were characterized by an increase in FDP blood level. However, in severe cases a possible low FDP blood level in conditions of fibrinolysis depression may be associated with an increased risk of severe thromboembolic complications.
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PMID:[Immunoenzyme determination of fibrin-fibrinogen degradation product levels in acute myocardial infarct patients]. 330 Jun 97

Disturbances of blood coagulation were studied in 32 consecutive patients with typhoid fever on their admission to hospital. Estimations of prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation products (FDPs), factors VII, VIII and XII, alpha I antitrypsin, plasminogen, CI esterase inhibitor, and platelet counts were performed as well as liver function tests and blood counts. Five patients had laboratory evidence of disseminated intravascular coagulation (DIC) and two had a generalised bleeding disorder which in the other three was inapparent. The platelet count in the group as a whole was low (P less than 0.05) and the FDPs in most cases were mildly elevated. The pre-kallikrein values were depressed in three of the five with DIC, whereas factor XII was not reduced. These results indicate that bleeding disorders in typhoid fever are uncommon. The depression of pre-kallikrein indicates that the DIC is probably triggered by activation of the intrinsic coagulation pathway. Most patients had lymphopenia and monocytopenia but only two had neutropenia.
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PMID:Disturbances of blood coagulation associated with Salmonella typhi infections. 335 16

Blood coagulation and lipid levels were studied in 60 depressive female patients (schizophrenia--14 patients, manic-depressive psychosis--22 patients, involutional depression--24 patients) and 20 healthy women. The depressive patients showed elevated blood levels of lipids, cholesterol, and fibrinogen, as well as increased antiheparin activity and fibrinolytic depression. The above alterations are regarded as activation of blood coagulation.
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PMID:[Changes in various indices of the blood-clotting system and lipid levels in patients with depression]. 359 Nov 38

The purpose of this study is to analyze the relationship between occurrence of hemorrhagic complications, kinetic of fibrinogen degradation-regeneration and the changes of prothrombin time (PT), partial thromboplastin time (PTT), after intravenous administration of Streptokinase (SK), 1.500.000 U., in acute myocardial infarction. 45 selected patients with acute myocardial infarction had pretreatment analysis and serial post-SK measurement of fibrinogen levels, PT, PTT (for 48 hours). Basal fibrinogen levels were 3.2 g/l and displayed significant depression for 18 hours (0.30-0.46 g/l) and normalization after 30 hours from SK infusion. Similar behaviour showed PT and PTT. Minor bleeding was identified in 25 patients. In bleeders mean fibrinogen levels, PT, PTT before and maximum changes after SK were not significantly different compared with non bleeders. We conclude that SK infusion produces important and prolonged changes of fibrinogen levels, PT, PTT; hemorrhagic risk is not related, however, to the extent of lytic state, but probably to pre-existent vascular derangement, predisposing to bleeding complications during fibrinolytic therapy. Therefore we believe to be prudent to delay the infusion of heparin for 12-18 hours after SK administration, when fibrinogen levels are beginning to increase.
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PMID:[Fibrinolysis and hemorrhage after streptokinase in acute myocardial infarct]. 367 11

Adhesion, phagocytosis, chemotactic and random migration, nitroblue tetrazolium dye reduction of peritoneal exudate neutrophils and macrophages, fibrinogen level, gelation of soluble fibrin and serial dilution protamine sulfate test were investigated in 115 New Zealand white rabbits with experimentally induced Shwartzman phenomenon in the colon, and in control animals. The results presented in this report demonstrated impairment of chemotactic migration of phagocytes in the presence of endotoxin. The depression was dose-dependent and less marked when neutrophils were stimulated with monocyte-derived chemotactic factor or with casein, than with complement-derived chemotactic factor. The prolonged depression of chemotactic migration of neutrophils and macrophages in rabbits with colitis, however, did not affect the healing time of the ulcers in the colon.
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PMID:Function of phagocytes in experimentally induced colitis in rabbits. II. The Shwartzman phenomenon in the colon. 372 94

The rabbits with CCl4-induced hepatic failure have revealed changes in hemostasis responses to streptokinase administration. The main distinction of hepatic dystrophy was the depression of plasma fibrinolytic activity accompanying the decrease in fibrinogen and antiplasmin concentrations. Streptokinase administration to rabbits with productive inflammatory liver disorders produced changes in hemostasis identical to those observed in intact rabbits, fibrinogen levels, however, remained unchanged. The common feature of all the toxic liver disorders is the increase of antithrombin III levels after streptokinase administration, whereas the antithrombin levels in the control animals were decreased.
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PMID:[Action of streptokinase on the hemostatic indices of rabbits with a toxic lesion of the liver due to carbon tetrachloride]. 381 94

To determine whether or not the timing of heparin infusion affects either bleeding or reocclusion following intracoronary streptokinase for acute myocardial infarction, heparin was infused immediately after streptokinase in 89 patients and was delayed for 12 hours in the subsequent 93. Bleeding occurred in 22 immediate-heparin patients and was major in five (one fatal); there were 14 hemorrhages in the delayed-heparin group, all minor. At discharge, reocclusions were observed in 18% (12/68) of immediate-heparin patients, and 11% (3/27) of the latter. Bioassayed fibrinogen levels displayed sustained depression regardless of bleeding for 20 hours after streptokinase; however, defibrinogenation measured by immunoassay was much less striking. This suggests that high levels of fibrinogen degradation products spuriously affect the bioassay of fibrinogen. We conclude that bleeding is related to the anticoagulant effects of fibrinogen degradation products interacting with heparin, and may be largely independent of hypofibrinogenemia. Delaying heparin for 12 hours may decrease the risk of bleeding while little affecting the risk of reocclusion.
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PMID:Hemorrhage vs rethrombosis after thrombolysis for acute myocardial infarction. 396 47

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
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PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

Endotoxin administered intravenously to a group of four calves resulted in disseminated intravascular coagulation. A sublethal dose of piromen, a commercially available Pseudomonas spp endotoxin, was used. Serial measurements of total plasma fibrinogen, soluble fibrin levels, ethanol gelation tests, protamine sulfate tests, fibrinogen-fibrin-related antigen (FR-antigen) and prothrombin and thrombin times were done.Initial depression of plasma fibrinogen with a nadir of about 40% of pre-endotoxin levels at eight to 11 hours post-endotoxin (+8 to +11 hours) followed by an overcompensation to 180% at +60 to +108 hours was shown. Soluble fibrin was demonstrated in plasma from +2 to +22 hours with a peak of 100-114 mg/100 ml at +4 to +9 hours. Positive plasma ethanol gelation and protamine sulfate tests, as well as the presence of serum FR-antigen, occurred consistently following endotoxin administration. Significant increases in prothrombin times (PT) from +4 to +40 hours and in thrombin times (TT) from +4 to +16 hours were demonstrated. The peak increase of PT at +8 to +10 hours was 180%. The peak increase of TT at +6 to +9 hours was 260-290%.
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PMID:Endotoxin induced disseminated intravascular coagulation in cattle. 427 65


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