Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue factor (TF), formerly known as thromboplastin, is the key initiator of the coagulation cascade; it binds factor VIIa resulting in activation of factor IX and factor X, ultimately leading to fibrin formation. TF expression and activity can be induced in endothelial cells, vascular smooth muscle cells, and monocytes by various stimuli such as cytokines, growth factors, and biogenic amines. These mediators act through diverse signal transduction mechanisms including MAP kinases, PI3-kinase, and protein kinase C. Cellular TF is present in three pools as surface, encrypted, and intracellular protein. TF can also be detected in the bloodstream, referred to as circulating or blood-borne TF. Elevated levels of TF are observed in patients with cardiovascular risk factors such as hypertension, diabetes, dyslipidemia, and smoking as well as in those with acute coronary syndromes. TF may indeed be involved in the pathogenesis of atherosclerosis by promoting thrombus formation; in addition, it can induce migration and proliferation of vascular smooth muscle cells. As a consequence, therapeutic strategies have been developed to specifically interfere with the action of TF such as antibodies against TF, site-inactivated factor VIIa, or recombinant TF pathway inhibitor. Inhibition of TF action appears to be an attractive target for the treatment of cardiovascular diseases.
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PMID:Tissue factor in cardiovascular diseases: molecular mechanisms and clinical implications. 1646 45

A 66-year-old man with hypertension and hyperlipidemia developed a hemorrhagic stomal ulcer and massive hematoma of the face at 4 and 7 months, respectively, after fundusectomy for early gastric cancer. The diagnosis of acquired hemophilia A was made based on the marked prolongation of activated partial thromboplastin time, an extremely low factor VIII activity, and a very high-titer factor VIII inhibitor. After admission, oral prednisolone and cyclophosphamide were started. In addition, activated prothrombin complex concentrates and recombinant activated factor VII were intravenously administered which successfully controlled his hemorrhage. Only 1 week after the episode of bleeding, however, he complained of abdominal pain accompanied by watery stool with fresh blood. The diagnosis of ischemic colitis was made based on the clinical course and the findings on both CT-scan and colon fiberoscopy. The colitis spontaneously and quickly resolved with conservative observation. To the best of our knowledge, this is the first reported case of ischemic colitis that occurred in an acquired hemophilia patient without simultaneous administration of coagulation factors or antifibrinolytic agents. We should thus pay attention to the possible occurrence of thrombotic events even in acquired hemophilia patients in the presence of risk factors for thrombosis.
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PMID:[Ischemic colitis following the treatment of acute hemorrhage in a patient with acquired hemophilia A]. 1671 66

To evaluate the association of inherited coagulopathies and acquired conditions (e.g. hypertension, aspirin use) with emergency department admission due to epistaxis. Patients admitted to the emergency department with epistaxis were included. A questionnaire for personal and family history of any bleeding disorder was used. Physical examination including ear, nose and throat examination was performed. Platelet counts, International Normalized Ratio, activated partial thromboplastin time, factors VIII, IX and XI, von Willebrand factor and ristocetin cofactor activity levels were determined. Nineteen patients were included in the study. Personal history of mucocutaneous bleeding was present in four cases and family history in two cases. Only one case (5%) had a decreased von Willebrand factor level (45%), and also had a personal and family history of bleeding tendency. Ten patients (53%) had a history of aspirin use. Thirteen (68%) patients had hypertensive values on admission. Aspirin use and hypertension were the leading causes of emergency service admission in adults due to epistaxis in this study, although the number of the patients was relatively low. Regarding the low prevalence of inherited coagulopathies, detailed coagulation tests should be reserved for adult patients with positive personal and/or family history of bleeding.
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PMID:Research for bleeding tendency in patients presenting with significant epistaxis. 1717 25

Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord blood-derived CD34+ cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34- or CD34+ cells (1 x 10(5)-5 x 10(5)/mL/kg body weight) i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-alpha levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34- cell-treated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34+ cells significantly improved survival time (duration, 63-291 min). As compared with normothermic controls, all CD34- cell-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34+ cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34+ cell therapy during heatstroke. Our data indicate that CD34+ cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure.
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PMID:Human umbilical cord blood-derived CD34+ cells cause attenuation of multiorgan dysfunction during experimental heatstroke. 1750 7

Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.
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PMID:Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress. 1750 57

We investigated the antihypertensive effect and safety of alpha-linolenic acid (ALA) in human subjects. In Experiment 1, subjects with high-normal blood pressure and mild hypertension ingested bread containing 14 g of common blended oil (control oil) or ALA-enriched oil for 12 weeks. The test oil contained 2.6g/14 g of ALA. The subjects ingested strictly controlled meals during the study period. Systolic blood pressure was significantly lower in the ALA group than in the control group after ingestion of the test diet for 4, 8 and 12 weeks. Diastolic blood pressure was significantly lower in the ALA group than in the control group after ingestion of the test diet for 12 weeks. In Experiment 2, we evaluated the safety of high intake of ALA (7.8 g/d), particularly its effects on oxidation in the body and blood coagulation. Normotensive, high-normotensive and mildly hypertensive subjects ate bread that contained 42 g of the control oil or the test oil for 4 weeks. No significant difference was noted in the lipid peroxide level, high-sensitive C-reactive protein level, plasma prothrombin time or activated partial thromboplastin time between the two groups. No abnormal changes were noted after test diet ingestion on blood test or urinalysis, and no adverse event considered to have been induced by the test oil was observed in Experiment 1 and 2. These results suggest that ALA have an antihypertensive effect with no adverse effect in subjects with high-normal blood pressure and mild hypertension.
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PMID:Antihypertensive effect and safety of dietary alpha-linolenic acid in subjects with high-normal blood pressure and mild hypertension. 1789 1

We examined 62 women with three or more recurrent adverse pregnancy outcomes where we excluded the other well known causes of this state. We detected lupus anticoagulant (LAC) in three (5%), with the use of set of coagulation tests: activated partial thromboplastin time (APTT), APTT ratio, kaolin clotting time ratio (KCT), APTT of the 50:50 mixture of the patients and control plasmas, APTT ratio of the 50:50 mixture, phospholipid correction test and heat stability test. We excluded connective tissue disorders. Therapy was started between 12th and 14th gestational week. Efficacy was monitored in intervals of 2-6 weeks with following tests: APTT ratio, KCT and plateled count. Patient A, with strong LAC activity and thrombocytophenia, reacted weakly to therapy with Pronison 40 mg/day and Aspirin 80 mg/day. The activity of LAC was slightly diminished but was present all the time. Patient expressed hypertension and gestational diabetes mellitus. The outcome of pregnancy was adverse and placenta had typical pathological changes. Patient B, with moderate LAC activity, reacted quickly and completly on therapy with Pronison 20-40 mg/day and Aspirin 80 mg/day. The course of pregnancy was regular. The outcome was successful and placenta had no pathological changes. Patient C, with mild LAC activity, was treated only with Aspirin 80 mg/day. LAC activity rapidly disappeared, the course of pregnancy was regular and outcome was successful. On the basis of the first results we concluded that applied set of tests was sensitive for LAC of different intensity and that dissapeparance of LAC activity with the use of therapy anticipates successful pregnancy outcome.
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PMID:[Lupus anticoagulant in pregnancy--first experiences in detection and therapy]. 1797 56

Atrial fibrillation (AF) is an epidemic, affecting 1% to 1.5% of the population in the developed world. Projected data from the population-based studies suggest that the prevalence of AF will grow at least 3-fold by 2050. The health and economic burden imposed by AF and AF-related morbidity is enormous. Atrial fibrillation has a multiplicity of causes ranging from genetic to degenerative, but hypertension and heart failure are the commonest and epidemiologically most prevalent conditions associated with AF as both have been shown to create an arrhythmogenic substrate. Several theories emerged regarding the mechanism of AF, which can be combined into two groups: the single focus hypothesis and the multiple sources hypothesis. Several lines of evidence point to the relevance of both hypotheses to the mechanism of AF, probably with a different degree of involvement depending on the variety of AF (paroxysmal or persistent). Sustained AF alters electrophysiological and structural properties of the atrial myocardium such that the atria become more susceptible to the initiation and maintenance of the arrhythmia, a process known as atrial remodeling. Angiotensin II has been recognized as a key element in atrial remodeling in association with AF opening the possibility of exploitation of "upstream" therapies to prevent or delay atrial remodeling. The clinical significance of AF lies predominantly in a 5-fold increased risk of stroke. The limitations of warfarin prompted the development of new antithrombotic drugs, which include anticoagulants, such as direct oral thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban). Novel mechanical approaches for the prevention of cardioembolic stroke have recently been evaluated: percutaneous left atrial appendage occluders, minimally invasive surgical isolation of the left atrial appendage, and implantation of carotid filtering devices.
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PMID:Update on atrial fibrillation: part I. 1825 25

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

In patients with arterial hypertension (AH) accompanied by abdominal obesity (AO) increase in platelets adhesive and aggregation functions was noted in vitro and in vivo. The cause of these disturbances is blood serum and platelets lipid peroxidation activation, increase in synthesis of Willebrand's factor in a vascular wall, and intensification of thromboxane production in platelets. Activation of thromboplastin production is the main cause of increase in blood coagulation in patients with AH and AO.
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PMID:[Aggregation function of platelets in persons with arterial hypertension and abdominal obesity]. 1858 11


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