Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Colonic ischemia is one of the more common disorders of the colon in elderly people; the ischemic colitis can affect young people too. The splenic flexure, the descending colon and the sigmoid are the parts most commonly involved. Only in some cases it is possible to identify the specific cause of colonic ischemia. We report a case of ischemic colitis associated with antithrombin III deficiency.
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PMID:[Ischemic colitis associated with antithrombin deficiency]. 1038 13

The adherence of activated neutrophils to endothelial cells during ischemia/reperfusion injury is mediated by inside-out signal transduction. Subsequently, outside-in signal transduction occurs following ligation of adhesion molecules with their ligands triggering respiratory bursts of neutrophils. In addition, neutrophil elastase enhances CC- and CXC-chemokine production by monocytes and macrophages. MCP-1, a CC-chemokine, enhances tissue factor production by macrophages and increases ICAM-1 expression on endothelial cells. Chemotaxis and respiratory bursts of neutrophils are augmented by CXC-chemokines. Furthermore, neutrophil elastase inactivates anticoagulants including antithrombin III, heparin cofactor II, and thrombomodulin, suggesting that neutrophil elastase aggravates microcirculatory disturbance after ischemia/reperfusion. Thus neutrophil elastase modulates the interation of neutrophils and endothelial cells during ischemia/reperfusion injury. Taken together with these observations, a therapeutic regimen with antibodies against adhesion molecules in combination with neutrophil elastase inhibitor and anticoagulants may attenuate ischemia/reperfusion injury.
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PMID:[Interaction between neutrophils and endothelial cells following ischemia/reperfusion]. 1041 50

Myocardial stunning is characterized by transient contractile dysfunction occurring subsequent to an episode of ischemia followed by reperfusion. Platelet activation and hemostatic abnormalities have been described in patients with unstable angina and acute myocardial infarction, however, their role in the pathogenesis of myocardial stunning is unknown. The purpose of this study was to determine if platelet aggregation and certain hemostatic factors change during myocardial stunning following brief coronary arterial occlusion. Nine Yorkshire swine underwent left anterior descending coronary artery occlusion for 8 minutes followed by 90 minutes of reperfusion. Blood samples were obtained at baseline, at 4 and 8 minutes of occlusion, and at 60 and 90 minutes of reperfusion. Platelet aggregability and concentrations of antithrombin III, protein C, protein S, fibronectin, endothelin 1, and the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1a) were measured in systemic circulation. The occlusion phase was associated with a decline of endothelin 1 (-13.6%), and TxB2 (-19.6%), and elevation of antithrombin III (+40.2%) and protein C (+22.9%). Mild myocardial stunning was associated with a significant increase in platelet aggregation (+33.7%), endothelin-1 (+24.7%), 6-keto-PGF1a (+41.5%), TxB2 (+11.9%), and protein C (+42.3%) during the reperfusion phase. There were no changes in plasma fibronectin and total protein S. Thus, mild myocardial stunning following brief coronary artery occlusion is associated with substantial dynamic changes in platelet aggregability and certain hemostatic factors. These results may be relevant to understanding the mechanisms determining myocardial stunning and coronary arterial patency following reperfusion.
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PMID:Mild myocardial stunning affects platelet aggregation and certain hemostatic factors in swine. 1072 20

The discovery of the resistance to activated protein C (APCR) has provoked a new insight into the etiopathogenesis of venous and arterial thrombosis. APCR is determined in 95% genetically by point mutation in the gene for factor V resulting in substitution of arginine in the position 506 by glutamine. This change makes the activated form of factor V (factor Va) resistant to the cleavage by protein C in the place, where the cleavage takes place most quickly under normal conditions. The mutant factor V is known as factor V Leiden. Factor V Leiden preserves its procoagulation activity for a longer period, resulting thus into thrombophilia with all its negative consequences. The inherited deficiencies of antithrombin III, protein C and protein S occur in 10% of patients suffering from venous thrombosis, whereas factor V Leiden is present in as many as 20 to 60%. Thus, it seems that factor V Leiden is the most important inherited risk factor of venous thrombosis. The results of several trials did not indicate the participation of APCR in the development of myocardial infarction. On the other hand, APCR seems to be a risk factor of cerebrovascular accidents, especially of stroke and transitory brain ischemia. Factor V Leiden is an important risk factor of abortions, especially those occurring in the second trimester of pregnancy. According to recent results, factor V Leiden is considered to play a role in the pathogenesis of venous and arterial thromboses in children. The significant risk potential of factor V Leiden with respect to venous thrombosis development and relatively simple diagnosis of this mutation predispose the investigation of this disorder to become the screening method in indicated groups of patients. The investigation of APCR is recommended in all patients with either first or reoccurring attacks of venous thrombosis or thromboembolism, in patients with positive family history of thrombosis and thromboembolism and in women with repeated abortions, particularly in the second trimester of pregnancy. The investigation of APCR in selected groups of patients and early prophylactic anticoagulation therapy may be important in thrombosis prevention in situations with an increased thrombotic potential. (Tab. 1, Ref. 78.)
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PMID:Resistance to activated protein C--frequent etiologic factor for venous thrombosis. 1172 76

An 8-year retrospective review of Indiana University Hospital records consisting of any patient age 18 to 40 years old who presented with arterial mesenteric ischemia was performed. Three patients were identified that met our criteria. The first patient was discovered to have a protein C deficiency. The second patient was afflicted with afibrinoginemia, a protein C and an antithrombin III deficiency. The third patient had been previously diagnosed with Takayasu's arteritis and had an elevated ESR. Each patient had a protracted course of symptoms before mesenteric disease was considered, confirmed by angiography, and treated by arterial bypass with/without bowel resection. All patients survived and are currently asymptomatic at an average of 2 years postoperatively. Mesenteric ischemia in patients under the age of 40, especially in the absence of cocaine use, is rare and often causes a delay in diagnosis and appropriate treatment. The high incidence of hypercoagulable states in our study cases suggests the need for a search for such disorders and the possible need for long-term anticoagulation therapy as a deterrent to recurrence.
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PMID:Mesenteric ischemia affects young adults with predisposition. 1271 70

It is well established that a condition of hypercoagulation due to deficiencies of antithrombin III, protein C and protein S may result in thrombo-embolism. To evaluate the possibility of hypercoagulation in acute mesenteric ischemia (AMI); clinical features, ECG changes, drug history, the length of intestine remaining after the resection and mortality of 15 consecutive patients were recorded and plasma levels of antithrombin III, Protein C and protein S were measured. Antihypertensive, antidiabetic and digitalis were the main drugs used by the patients. Atrial fibrillation was the main ECG finding (60%). AMI was attributed to thrombo-embolic phenomena because of atrial fibrillation in these patients. Levels of antithrombin III and protein S were lower in patients without atrial fibrillation compared to those with the condition (mean values 16.18 vs. 18.04 and 87.33 vs. 94.22 respectively) but the difference was not statistically significant. Levels of Protein C were lower and the length of intestine remaining after resection was shorter in patients without, compared to those with, atrial fibrillation (mean values 77.00 vs. 88.66, and 52.5 cm vs. 86.11 cm respectively). The difference was statistically significant (p < 0.05). Postoperative mortality rate was 33.3% (5 patients) and the length of intestine remaining after resection was the main determining factor in the prognosis of the patients. We conclude that a condition of hypercoagulation due to a deficiency of protein C has a significant role in the pathogenesis of AMI especially in patients without atrial fibrillation.
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PMID:Significance of antithrombin III, protein C and protein S in acute mesenteric ischemia patients. 1515 76

Liver graft function after transplantation is dependent on ischemia-reperfusion injury, toxicity of drugs (immunosuppression, antibiotics and other) and transplant rejection. Although routinely monitored with enzymatic tests (AST, ALT, GGT, ALP), bilirubin and coagulation parameters, differentiation between these pathologies is hardly possible without liver biopsy. Arginase (3.5.3.1) mostly exists in the liver and in trace amounts in extra-hepatic tissue. Thus, we hypothesized that activity of arginase could be a more specific test of liver function. Sera of 32 liver transplant recipients were tested for AST, ALT, ATIII, bilirubin and arginase. Samples were obtained daily in first 2 weeks after LTx and weekly afterwards. Correlation of arginase activity with other liver function markers was calculated. Serum arginase peaked at day 1 post LTx (mean 64,6+/-91 IU/L), and decreased more rapidly than other tests if good liver function was observed. The values showed strong and significant correlation with AST and ALT activities (Pearsons R 0,65 and 0,47 respectively). We conclude that activity of arginase in the serum is an exact test of liver function.
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PMID:Clinical significance of arginase after liver transplantation. 1575 50

For the first time it is proved, that patients with an acute virus myocarditis have statistically confirmed authentic reduction in quantity of thrombocytes, extention of parameters of a activated partial thrombin time, reduction in concentration of a heparin-antithrombin III (AT-III) complex against suppressed enzyme of antiradical protection - superoxide dismutase and it has led to activization of a malonic dialdehyde in erythrocytes, thrombocytes and blood serum. In case of the development of an acute virus infection especially caused cardiotrophic strain Consaki, virus CVB 1-CVB 4, thrombocytes, according to P. Nemetchek-Gansler, acquire not pertaining to them ability for phagocytosis of viruses with following reduction in quantity of thrombocytes and increase in aggregation abilities of thrombocytes what influence the state of duration index of contact aggregation of thrombocytes with the tendency to shorten this duration, and also it may develop hypoxia, an ischemia and the subsequent necrosis of cardiomyocytes, that is to an acute virus myocarditis that demands corresponding correction with medications.
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PMID:[Total index of thrombocyte aggregation in patients with an acute viral myocarditis]. 1866 37

Intestinal ischemia/reperfusion causes severe injury and alters motility. N-methyl-D-aspartate (NMDA) receptor antagonists have been shown to reduce ischemia/reperfusion injury in the nervous system, and in other organs. In this study, we set out to investigate the effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury. Male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group; (2) an intestinal ischemia/reperfusion group subjected to 45 min ischemia and 1h reperfusion; (3) a group treated with 10 mg/kg ketamine before ischemia/reperfusion; and (4) a group treated with 10 mg/kg memantine before ischemia/reperfusion. Intestinal samples were taken for histological evaluation. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), malondialdehyde (MDA), total antioxidant capacity, tumor necrosis factor alpha (TNF-alpha), P-selectin and antithrombin III (ATIII) were measured. Intestinal transit time was determined to evaluate intestinal motility. Fecal pellet output and animal weight were also registered daily for 7 days post-ischemia. After reperfusion, AST, LDH, TNF-alpha and P-selectin levels were elevated, ATIII levels were depleted, and ALT levels were unchanged in serum. Additionally, levels of MDA were increased and total antioxidant capacity was reduced in serum, indicating oxidative stress. Intestinal mucosa showed severe injury. Ketamine, but not memantine, diminished these alterations. Intestinal motility and fecal pellet output were also altered after ischemia/reperfusion. Both drugs abolished the alterations in motility. In conclusion, ketamine's protective effects over ischemia/reperfusion do not appear to be NMDA mediated, but they could be playing a role in protecting the intestine against ischemia-induced functional changes.
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PMID:The effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury in rats. 1975 22

The complex picture of inflammation and coagulation alterations comes to life in acute stroke phases. Increasing evidence points to a strong interaction and extensive crosstalk between the inflammation and coagulation systems: the interest towards this relationship has increased since recent experimental research showed that the early administration of antithrombin III (ATIII) decreases the volume of ischemia in mice and might be neuroprotective, playing an antiinflammatory role.We aimed to establish the extent of the relationship among markers of inflammation (S100B and IL-18) and procoagulant and fibrinolytic markers (ATIII, thrombin-antithrombin III complex (TAT), Fibrin Degradation Products (FDP), D-dimer) in 13 comatose patients affected by focal cerebral ischemia.Plasma levels of TAT, D-dimer and FDP, IL18 and S100B were increased. IL-18 and S100B high serum levels in ischemic patients suggest an early activation of the inflammatory cascade in acute ischemic injury.The basic principles of the interaction between inflammatory and coagulation systems are revised, from the perspective that simultaneous modulation of both coagulation and inflammation, rather than specific therapies aimed at one of these systems could be more successful in stroke therapy.
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PMID:Thrombin antithrombin complex and IL-18 serum levels in stroke patients. 2157 33


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