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)

Ischaemia of the bowel may arise from a number of causes affecting the arterial and venous compartments of the vascular tree. This article addresses the causes and consequences of arterial obstruction, which may compromise the supply of oxygenated blood to the bowel. These events may occur as an acute phenomenon, or they may present in a chronic fashion. The therapeutic options available to treat this condition are largely dependent on the mode of presentation and the amount of time that is available before irreversible damage occurs to the bowel integrity. In the acute phase, the viability of the bowel is in doubt, and this necessitates an open operative approach to assess the amount of bowel infarction which has already occurred. A variety of operative procedures are then available to limit this bowel loss and to secure the viability of the remaining bowel. In the more chronic phase there are alternative, less invasive procedures that may be appropriate for the patient, who may have suffered a prolonged period of undernourishment and dehydration. In such cases the immediate bowel viability is not in doubt, but the medium/long-term survival is compromised. Treatment options appropriate to each clinical scenario are discussed, along with the major technical issues associated with these treatments. A team approach to the most appropriate management plan is stressed, and the published outcomes reviewed.
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PMID:Mesenteric arterial ischaemia: diagnosis and therapeutic options. 1271 Aug 47

Abdominal pain frequently occurs after long-distance running. The cause of the pain may be due to dehydration, diaphragmatic ischemia, muscular spasm, or myonecrosis. However, data regarding the frequency of these purported causes are currently lacking. Pancreatitis can also occur after long-distance running, but few cases have been reported, and the etiology is controversial. We report a case of pancreatitis in a thin, muscular marathon runner. We suggest the etiology in this case may be traumatic as the pancreas may have suffered repetitive injury against the posterior abdominal wall and spine.
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PMID:Marathon pancreatitis: is the etiology repetitive trauma? 1521 17

The serum and glucocorticoid inducible kinase (SGK) 1 is expressed in brain tissue and upregulated by ischemia, neuronal excitation, and dehydration. The present study has been performed to elucidate the expression of SGK1 in cerebellar Purkinje cells and to explore whether it influences the colocalized glutamate transporter EAAT4. Intense SGK1 staining was observed in Purkinje cells following 48h of water deprivation. The kinase activates glutamate induced current (I(GLU)) in Xenopus oocytes heterologously expressing EAAT4, an effect mimicked by its isoforms SGK2, 3 and PKB. I(GLU) was decreased by the ubiquitin ligase Nedd4-2, an effect partially but not completely reversed by additional coexpression of the SGK kinase isoforms or PKB. According to immunohistochemistry EAAT4 protein abundance in the cell membrane was enhanced by SGK1 and decreased by Nedd4-2. In conclusion, SGK1 expression is upregulated by ischemia, excitation, and dehydration in cerebellar Purkinje cells. The upregulation of SGK1 may serve to stimulate EAAT4 and thus to reduce neuroexcitotoxicity.
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PMID:Stimulation of the EAAT4 glutamate transporter by SGK protein kinase isoforms and PKB. 1550 48

Thromboembolism is considered the inciting cause of many vascular disorders including acute coronary syndrome (ACS), ischemic stroke, pulmonary embolism (PE), deep vein thrombosis (DVT), and mesenteric ischemia. Adrenergia and inflammation are known to accompany these conditions, particularly among arterial thromboembolic disorders, but the teleologic basis of these associations remains poorly understood. We argue that thromboembolism may sometimes be the result, rather than the cause, of acute vascular events, and may be precipitated by underlying adrenergia. Thromboembolic events are most prone to occur during parts of the circadian, seasonal, lifespan, and reproductive cycles with sympathetic dominance, as well as during behavioral, exertional, physiologic, and iatrogenic activation of sympathetic stress. Molecular evidence suggests that adrenergia and inflammation can promote coagulation and lead to co-activation of the pathways. Acute vascular events that occur without angiographic evidence of occlusion suggest that some infarcts may be attributable to adrenergia alone. "Embolic" disorders may represent asynchronous systemic phenomena rather than clot migration. During acute thromboembolism, downstream tissue hypoxia can activate maladaptive self-propelling cycles of sympathetic bias, inflammation, and coagulation. The counterproductive co-activation of these pathways may reflect a maladaptive interlink forged during the primordial evolution of trauma physiology. Their rapid co-mobilization enables rapid control of hemorrhage, microbial defense, and perfusion maintenance during trauma, but the pathways may behave maladaptively in the setting of modern diseases where endothelial injury may be more often precipitated by smoking, diabetes, dyslipidemia, or hypertension. Sympathetic blockade is already employed in ACS, and beta-blockers are used as antihypertensives to prevent stroke. Our hypothesis suggests that the benefits of beta-blockers in stroke may be independent of antihypertensive effects, and that adrenergia may represent a target for managing all thromboembolic disorders, independent of anti-coagulative and thrombolytic therapies. Perhaps reducing adrenergia, rather than maintaining high cerebral perfusion pressure, may represent a counterintuitive strategy for treating stroke and for reducing reperfusion injury. Plausible mechanisms by which autonomic dysfunction may induce venous thrombosis are discussed, especially in those with baroreceptor dysfunction, immobilization, or dehydration. Unexplained hypercoagulability of cancer may also operate through tumor-induced adrenergia and inflammation.
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PMID:Can thromboembolism be the result, rather than the inciting cause, of acute vascular events such as stroke, pulmonary embolism, mesenteric ischemia, and venous thrombosis?: a maladaptation of the prehistoric trauma response. 1569 86

Natural freezing survival by the wood frog, Rana sylvatica, involves multiple organ-specific, freeze-responsive changes in gene expression. The present study provides the first report of freeze-responsive genes in brain. Differential screening of a cDNA library made from brain of frozen wood frogs revealed a freeze-responsive clone encoding a protein of 315 amino acids that was identified as the acidic ribosomal phosphoprotein, P0 (GenBank Accession No. AF176302). The amino acid sequence showed 91-92% identity with the protein from other vertebrates. Thirteen unique amino acid substitutions occurred as compared with mammalian or avian P0 sequences; these may represent structural differences that support protein function at low body temperature. Transcripts of P0 rose by 8-fold in brain of frogs frozen for 24 h at -2.5 degrees C, compared with controls at 5 degrees C, and reached 12-fold higher in 24 h thawed frogs. Immunoblotting showed that P0 protein increased by approximately 3-fold in brain during freezing and remained high after thawing. Freeze up-regulation of P0 was largely brain-specific; transcript levels were unaffected in skeletal muscle and skin and, although transcripts rose approximately 2-fold in liver of frozen frogs, liver P0 protein was unchanged (although P0 protein was much higher overall in liver than in brain). P0 transcripts in wood frog brain were also elevated during anoxia exposure (by approximately 4-fold), but did not change under dehydration stress. The gene was similarly up-regulated under anoxia in brain of the freeze intolerant leopard frog, Rana pipiens. This suggests that P0 expression responds to anoxia stress during freezing. Changes in P0 content in ribosomes may contribute to altered patterns of protein synthesis under anoxia or ischemia.
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PMID:Up-regulation of acidic ribosomal phosphoprotein P0 in response to freezing or anoxia in the freeze tolerant wood frog, Rana sylvatica. 1571 Mar 71

Ischemic bowel disease exhibits a complex spectrum of clinical presentations and in the athlete the disease may be superimposed on dehydration, hyperthermia, and exhaustion. Physicians caring for athletes should be aware of the manifestations of ischemic bowel disease and the optimum methods of diagnosis and treatment. Abdominal pain and diarrhea are typical initial symptoms of ischemia and these symptoms generally limit further damage. However, symptoms may be overridden in cases of extreme athletic competition or other significant endurance events such as combat. Athletes and coaches should be aware of the danger of ischemic bowel disease. Patients or athletes with recurrent symptoms of abdominal pain and diarrhea during exercise may be at increased risk for ischemic damage. However, no underlying anatomic abnormalities have been noted. Ischemic hemorrhagic gastritis is generally reversible and may be controlled with effective acid blockade. Ischemic colitis generally presents with pain, diarrhea, and bleeding. It is usually mild but may require volume and transfusion support, rarely progressing to need for resection or stricture. Severe presentations with intestinal infarction are rare but potentially life threatening. The athlete is usually able to ultimately resume his or her activities without restriction.
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PMID:Exercise-associated intestinal ischemia. 1576 45

The wood frog, Rana sylvatica, survives weeks of whole body freezing during winter hibernation, expressing numerous metabolic adaptations that deal not only with freezing but with its consequences including organ ischemia and cellular dehydration. The present study analyzes the 20s multicatalytic proteinase (MCP) complex from skeletal muscle to determine how protein degradation is managed in the ischemic frozen state. MCP was partially purified and assayed fluorometrically using three AMC-labeled substrates to compare multiple states: control (5 degrees C acclimated), 24 h frozen at -2.5 degrees C, 4 or 8 h thawed at 5 degrees C, 8 h anoxia, and 40% dehydration. MCP from frozen frogs showed significantly different K(m) and V(max) values compared with controls; e.g., K(m) Z-LLE-AMC increased by 45% during freezing and 52% under anoxia whereas V(max) decreased by 40%. After thawing, K(m) was restored and V(max) rose by 2.2-fold. Incubations promoting protein kinase or phosphatase action on MCP showed that phosphatase treatment strongly increased V(max) implicating reversible phosphorylation in MCP regulation during freeze-thaw. Western blotting showed a 36% decrease in MCP protein in muscle from frozen frogs. The 20s MCP preferentially degrades oxidatively-damaged proteins and evidence of impaired function during freezing came from a 1.4-fold increase in protein carbonyl content in muscle and liver during freezing. Ubiquitin and ubiquitin conjugate levels were unchanged in muscle but changed markedly in liver during freeze-thaw.
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PMID:Vertebrate freezing survival: Regulation of the multicatalytic proteinase complex and controls on protein degradation. 1644 58

Acute mesenteric ischemia frequently results in bowel necrosis, which necessitates laparotomy to assess bowel viability. Reduction in mortality requires a high index of suspicion and prompt diagnosis. Bowel resection should be preceded by visceral artery revascularization. Medical management includes the use of anticoagulation, vasodilators, and the use of inhibitors of reperfusion injury. The management of chronic mesenteric ischemia largely depends on the general condition of the patient, who is often affected by malnutrition and dehydration. Surgery, although associated with greater morbidity and mortality, is more durable and effective in relieving the symptoms of chronic mesenteric ischemia. Endovascular treatment options for chronic mesenteric ischemia include percutaneous balloon angioplasty and stenting. This treatment is more likely to be successful in dealing with stenotic rather than occlusive lesions and offers a minimal invasive approach but is associated with a smaller primary success rate and a higher recurrence rate.
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PMID:Surgical and medical management of mesenteric ischemia. 1653 88

We report a case of nonocclusive mesenteric ischemia (NOMI) which occurred in a patient with torsion of gallbladder. A 91-year-old woman was admitted to the hospital and was diagnosed of acute cholecystitis. The next day, she went into shock. Then, we diagnosed her illness as torsion of gallbladder by computed tomography and ultrasonography, and performed an emergency operation. After cholecystectomy, it was recognized that the wide range of the small intestine had become necrotic sporadically. We diagnosed it as NOMI, and performed the wide resection of the small intestine followed by making double stomas. There is no previous report of NOMI associated with torsion of gallbladder. We guess the cause of NOMI in this case would be dehydration because of gallbladder torsion. NOMI has high mortality. Early diagnosis and early treatment are of great importance in NOMI.
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PMID:[A case of nonocclusive mesenteric ischemia (NOMI) which occurred in a patient with torsion of gallbladder]. 1740 65

Following the generation of transgenic mouse models of sickle cell disease, pre-clinical trials have shown the beneficial effects of various potential therapeutic molecules for the acute or chronic manifestations of the disease. Several molecules are upon evaluation in phase I to phase III clinical trials. These therapeutic approaches target: 1) membrane cation transport systems and channels involved in sickle cell dehydration; 2) adherence of erythrocytes to endothelium; 3) activation of circulating and endothelial cells participating in the vasoocclusive events and local ischemia. The Gardos channel (calcium activated potassium channel KCNN4) is inhibited by the clotrimazole metabolite ICA17043, in phase III trial. The K-Cl co-transport (KCC1/3/4) activated by the depletion of erythrocyte magnesium is inhibited by Magnesium pidolate; dipyridamole inhibits ion transports upon deoxygenation. Sulfasalazyne (inhibitor of the NF-jB pathway) inhibits the abnormal activation of endothelial cells. Nitric oxide (NO) is the most potent vasodilator. It prevents the activation of leucocytes, platelets and endothelial cells in patients with sickle cell disease and vascular remodelling. The L-arginine, the NO precursor, provides could be beneficial in sickle cell patients.
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PMID:[Clinical trials of new therapeutic pharmacology for sickle cell disease]. 1744 60


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