Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Frog muscles were shown to contain thromboplastin, antiheparin factor and activators of fibrinolysis. The thromboplastin activity was distinctly increased in exhausted muscles. At the same time the activity of fibrinolytic agents was increased less significantly. It was proposed that stimulation of cell structures was related to liberation of thromboplastin from membranes both into an extracellular environment and into the cell. The latter effect caused structural alteration in protoplasm, which resembled blood coagulation. The exhaustion is considered as a result of absence of suitable "spreading out" of protoplasm or as a process caused by decrease in content of structural biopolymers.
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PMID:[Activities of coagulation factor and fibrinolysin in muscles before and after exertion]. 12 93

A breach in the inactivation of thrombin activity by antithrombin III following numerous repeated intravenous injections of tissue thromboplastin to albino rats was established. Seven injections of tissue thromboplastin to animals (at 30-40 min-interval) caused functional exhaustion of anticoagulation system and increased thrombin blood circulation level.
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PMID:[Formation of thrombin and its inactivation by antithrombin III following repeated intravenous injections of tissue thromboplastin in animals]. 370 29

Thrombocytopenia is characteristically associated with septicemia and hemolytic uremic syndrome (HUS), a subset of which has been shown to be associated with endotoxemia and shigellosis. An experimental model that closely resembles these clinical conditions is the generalized Shwartzman reaction modified with a continuous intravenous infusion of endotoxin for 5 hr in rabbits. In addition to exhibiting the triad of HUS (thrombocytopenia, hemolytic anemia, and azotemia), these animals also had circulating platelet aggregates, leukocytosis, lipidemia, hemoglobinemia, hyperfibrinogenemia, and prolonged partial thromboplastin time. Platelets that remained in circulation were chemically exhausted in serotonin content and functionally impaired in aggregation activities. Plasma from animals during thrombocytopenia and platelet functional deficiency had no effect of the aggregation responses of normal platelets. Although the single triggering event of endotoxin infusion was stopped at hour 5, recovery from abnormalities was only partial on day 2 and within normal limits by day 3. In vitro studies supported platelet exhaustion as a mechanism for decreased platelet function after endotoxin infusion. The presence of circulating platelet aggregates and exhausted platelets suggested that the process of platelet activation took place at as long as 24 hr after the cessation of LPS infusion. Endotoxin and other mechanism(s) are likely to be operative in the pathogenesis leading to platelet activation. Further studies to reveal the mechanism of platelet exhaustion in the experimental model may help our understanding of corresponding events in clinical endotoxic injury and HUS associated with endotoxemia.
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PMID:Impaired and exhausted platelets in modified generalized Shwartzman reaction: an analogue of hemolytic uremic syndrome associated with endotoxemia. 664 55

Hyperthrombinogenesis due to bacterial septicemia may aggravate the risk of irreversible septic shock. In 22 patients with septicemia complicating urinary or alimentary infections, daily assessment of hemostasis was performed throughout 1 week. Standard screening of hemostasis revealed significantly increased mean values of prothrombin time, fibrinogen, and fibrinogen degradation product (FDP) concentration. However, platelet counts, activated partial thromboplastin times (APTT), thrombin times, ethanol gelation tests, and antithrombin activity remained within the normal range. By contrast, except for insignificant changes in protein C activity and activated factor VII content, specific markers of plasma hypercoagulability, that is, thrombin-antithrombin (TAT) complexes, prothrombin activating factor F 1+2, activated factor XII (XIIa), and dimer D were all markedly increased. Pathologic levels of TAT and Xlla were found in 82% and 73% of all plasma samples, respectively. The augmentation of TAT correlated with prolongation of thrombin time and increases in F 1+2 levels. The increase in XIIa correlated with thrombocytopenia, prolongation of APTT, exhaustion of antithrombin, and accumulation of F 1+2 and FDP in the plasma. Moreover, a significant increase in XIIa, stronger positivity of the ethanol gelation test, a greater increase in FDP, and a more pronounced decrease in protein C activity were observed in 8 patients with fatal septic shock. This study suggests the usefulness of TAT and XIIa measurements in the early recognition of plasma hypercoagulation in serious infections.
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PMID:Plasma markers of hypercoagulability in patients with serious infections and risk of septic shock. 1236 Nov 99

The contrastive analysis of the indices of cellular and vascular, coagulatory haemostasis and fibrinolysis in arterial hypertension (AH) was held among the patients of different age groups. 69 patients with AH were researched. The average age of afflicted people in the first blockette is 50,9+/-0,7 years, in the second blockette - 70,7+/-1,5. In order to evaluate the condition of haemostasis the afflicted people were researched in the following indices: amount of thrombocytes, hemolysate-aggregative test (HAT), leukocytic-thrombocytic aggregation (LTA), activity of Villebrand factor (FV), inactivation index of thrombin (IIT), activated partial thromboplastin time (APTT), prothrombin index (PTI), fibrinogen, antithrombin III (AIII), Hageman-dependent fibrinolysis (HDF), lupous anticoagulants (LA), autocoagulatory test (ACT). All the examined patients with AH showed considerable abnormalities in cellular and vascular and coagulatory links of haemostasis and the system of fibrinolysis. It is observed, that aged afflected people with AH have progressive hyperaggregation of thrombocytes, the activity of Villebrand factor increases, the rise of coagulatory link activity of haemostasis and the exhaustion of anticoagulants' products is more considerable, the subsequent fibrinolysis depression is observed, but hyperfibrinogenemia accrues. The received results show the heterogeneity of AH in different age groups.
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PMID:[The indices of cellular-vascular, coagulatory haemostasis and fibrinolysis in arterial hypertension of patients of different age groups]. 1854 35

Systemic infusion of bone marrow-derived mesenchymal stem cells (BMSCs) has become a promising strategy for disease treatment and tissue regeneration. Strategies to enhance the efficiency of BMSC cell therapy are crucial to promote its clinical application. Here, we aimed to improve BMSC cell therapy by inhibiting the BMSC-induced coagulation reaction. Intravenous injection of gradient BMSCs into mice showed that BMSCs were not fully compatible with blood. Large doses of BMSCs induced a series of symptoms of respiratory failure and heart failure. Histological and homeostasis analysis confirmed that large doses of BMSCs induced disseminated intravascular thrombosis, exhaustion of platelets and coagulation factors, and prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT). Similar to mouse BMSCs, goat and human BMSCs also induced coagulation reactions in vitro and in vivo. The coagulation was induced mostly by tissue factor, the overexpression of which enhanced the procoagulant activity of BMSCs during in vitro culture. Notably, clinical doses of BMSCs in cell therapy also induced mild and reversible coagulation, which increased BMSC lung embolism and clearance. Anticoagulation treatment by heparin (400 U/kg) prevented BMSC-induced coagulation and the acute adverse effects of large-dose BMSCs infusion efficiently. Importantly, heparin treatment led to decreased BMSC lung embolism and enhanced migration and maintenance of BMSCs to target organs in cell therapy. Based on an experimental colitis model, we confirmed that heparin treatment enhanced the effect of BMSC therapy efficiently to reduce mortality, prevent weight loss, suppress inflammation reaction and alleviate tissue injury. In conclusion, BMSCs possess procoagulant activity that could induce disseminated coagulation and thrombosis in recipients. Anticoagulation treatment by heparin is a practical strategy to improve both the safety and therapeutic effect of BMSC therapy.
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PMID:Heparin improves BMSC cell therapy: Anticoagulant treatment by heparin improves the safety and therapeutic effect of bone marrow-derived mesenchymal stem cell cytotherapy. 2804 20