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)

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99

Although alien to man, the ability to endure the freezing of extracellular body fluids during the winter has developed in several species of terrestrially hibernating frogs and turtles as well as in many species of insects and other invertebrates. Wood frogs, for example, can endure freezing for at least 2 weeks with no breathing, no heart beat or blood circulation, and with up to 65% of their total body water as ice. Our studies are providing a comprehensive view of the requirements for natural freezing survival and of the physical and metabolic protection that must be offered for effective cryopreservation of vertebrate organs. Molecular mechanisms of natural freeze tolerance in lower vertebrates include: 1) control over ice crystal growth in plasma by ice nucleating proteins, 2) the accumulation of low molecular weight cryoprotectants to minimize intracellular dehydration and stabilize macromolecular components, and 3) good ischemia tolerance by all organs that may include metabolic arrest mechanisms to reduce organ energy requirements while frozen. Cryomicroscopy of tissue slices and magnetic resonance imaging (MRI) of whole animals is revealing the natural mode of ice propagation through an organism. MRI has also revealed that thawing is non-uniform; core organs (with high cryoprotectant levels) melt first, facilitating the early resumption of heart beat and blood circulation. Studies of the production and actions of the natural cryoprotectant, glucose, in frogs have shown its importance in maintaining a critical minimum cell volume in frozen organs and new work on the metabolic effects of whole body dehydration in 3 species of frogs has indicated that adaptations supporting freeze tolerance grew out of mechanisms that deal with desiccation resistance in amphibians. Studies of the regulation of cryoprotectant glucose synthesis by wood frog liver have shown the role of protein kinases and of alpha and beta adrenergic receptors in regulating the glycemic response, and of changes in membrane glucose transporter proteins to facilitate cryoprotectant distribution.
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PMID:Biochemistry below 0 degrees C: nature's frozen vertebrates. 873 22

A case of a female patient who was admitted urgently with intestinal obstruction, peripheral shock, hypovolemia and acute ischemia of the lower extremities is presented. The ischemia of the lower extremities had developed due to low cardiac output following extensive dehydration caused by a prolonged intestinal obstruction from a cholelith. Although this pathogenetic mechanism of acute ischemia of the lower extremities is well known, this characteristic case is, nevertheless, presented to alert the clinician of this situation.
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PMID:Acute arterial thrombosis of the lower extremities due to prolonged intestinal obstruction. 897 88

The gene Aat coding for ADP/ATP translocase (AAT) was cloned from liver of the freeze-tolerant wood frog, Rana sylvatica, via differential screening of a cDNA library from liver of frozen frogs and using probes from control versus frozen frogs. Sequence analysis showed that clone pBfFR07 bearing the AAT cDNA contained a 1318-bp insert with one full-length open reading frame. The deduced amino acid sequence included 317 residues, with 81-86% identities to mammalian AAT. A 1750-nt transcript from the Aat gene was detected using pBfFR07 probe and a putative frog AAT of over 30 kDa was visualized by immunoblotting using a polyclonal antibody raised against chicken AAT. Analysis of liver samples from a time course of freezing showed a maximal 4.5-fold increase in mRNA after 8 h with AAT protein peaking in 24-h frozen frogs. Freezing also induced Aat expression in bladder and lung. In liver, mRNA expression also responded positively to anoxia stress but not to experimental dehydration of the animals. These results suggest that AAT induction during freezing may be stimulated by the ischemia that develops when plasma freezes; changes in AAT may contribute to stabilizing energetics in mitochondrial versus cytosolic pools over freeze/thaw cycles.
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PMID:Differential regulation of the mitochondrial ADP/ATP translocase gene in wood frogs under freezing stress. 925 66

Recovery of the brain after a period of cerebral ischemia depends greatly on the restoration of nutritive blood flow, which, however, may be severely disturbed. Early post-ischemic deficits (no-reflow) multiply with increasing duration of ischemia. The pathophysiology is multifactorial and includes vascular factors (endothelial blebs, compression by swollen glial cells), blood factors (viscosity changes due to erythrocyte sludging, platelet aggregation, blood dehydration), and general cardiovascular factors (post-ischemic hypotension, venous congestion). Treatment of no-reflow requires a combination therapy (e.g., hypertensive flush, small volume hypertonic solutions, fibrinolysis) for interfering with as many of these factors as possible. Delayed post-ischemic hypoperfusion develops after a preceding phase of post-ischemic hyperemia and is characterized by increased vasotonus. Hypoperfusion is associated with a disturbed coupling between brain function, metabolism, and blood flow, and may lead to secondary stimulation of anaerobic metabolism. Causal factors include disturbed blood/vessel wall interactions (expression of adhesion molecules, generation of free radicals) and possibly down-regulation of endothelial nitric oxide synthase. Treatment of post-ischemic hypoperfusion includes neutrophil elimination and free radical scavengers but is still unsatisfactory. Improvement of reperfusion deficits is a challenging task that must be solved before proceeding to specific molecular interventions for the treatment of ischemic cell injury.
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PMID:Reperfusion of the brain after global ischemia: hemodynamic disturbances. 926 98

Acute mesenteric ischemia is a rare but severe complication after open heart surgery. Its incidence (0.2-0.4%) is quite low, but mortality rates are ranging between 70% and 100%. From October 1992 to December 1996, 4,640 patients underwent open heart surgery with cardiopulmonary bypass: 74.6% coronary artery bypass graft (CABG) operations, 23.2% valve replacement including aortic repairs, and 2.2% corrections of congenital heart diseases or tumors of the heart. The overall mortality rate (30 days) was 3.4%, and after CABG, 2.9%. Twelve patients (0.26%), following CABG (one combined with aortic valve replacement, one with mitral reconstruction, and one with carotid disobliteration) developed signs of acute mesenteric ischemia in the early postoperative period (day 1 to 5). In all patients various abdominal symptoms, leukocytosis, acidosis, hyperlactatemia, hyperosmolality, renal failure, and, finally, hemodynamic instability were observed. Eleven patients underwent emergency laparotomy. Mesenteric angiography was done if possible in still stable patients (n=7); it showed severe stenosis or occlusion prior to the operation in each case. Other diagnostic methods were not reliable. In six patients (55%) during the first look, extensive bowel necrosis was found and in five patients an ischemic intestine but no necrosis was detected. Of these, three patients were affected by extensive bowel gangrene at the second look. In the fourth patient a disseminated peripheral ischemia of the entire small intestine was found intraoperatively. After mechanical release and stimulation normal bowel function could be reestablished. One patient underwent percutaneous transluminal angioplasty prior to the laparotomy. Bowel perfusion was still deteriorated but no necrosis was found intraoperatively. These patients were the only survivors in the investigated group; 10 of 12 patients (83.3%) died in the early postoperative period (day 1 to day 6). Predisposing factors for mesenteric ischemia are: arteriosclerotic patients after CABG (100%), age >70 years (91.7%), hyperosmotic dehydration (100%), and cardiac ischemia in 25%. Mesenteric ischemia is a fatal complication with high mortality rates after open heart surgery, especially in older, dehydrated patients with generalized atherosclerotic vessel disease. As the acute mesenteric ischemia usually starts during anesthesia or in the early postoperative period, setting of immediate diagnosis is very difficult. With the occurrence of typical symptoms diagnostic and therapeutic procedures (angiography and laparotomy) must be done very urgently owing to the life-threatening mesenteric process. When mesenteric gangrene already has taken place, the prognosis is very poor, despite extensive resection. Prevention can be exercised by avoiding perioperative hyperosmotic dehydration of patients at high risk.
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PMID:Acute mesenteric ischemia after open heart surgery. 955 29

Frostbite causes injury to the tissue by direct ice-crystal formation at the cellular level with cellular dehydration and microvascular occlusion. Muscle that initially appears viable on reperfusion may subsequently become necrotic because of microcirculatory collapse. Since muscle is a sensitive tissue in frostbite injury, we used technetium-99m-sestamibi limb scintigraphy to assess tissue viability in an experimental rabbit model. Twelve rabbits were used for this investigation. The right hind limb of the rabbits was immersed to the ankle joint in a container filled with 90% ethanol at -25 degrees C for 10 min. Frostbitten limbs were allowed to thaw in air at room temperature. Imaging and pathological examination of the affected limbs were performed 2 h, 24 h, 48 h and 72 h after freezing. In 2-h images, initial hypoperfusion was seen that corresponded to circulatory collapse. In 24-h images, there was hyperperfusion (so-called period of temporary reperfusion), corresponding to circulatory restoration. In 48-h images, a second hypoperfusion corresponded to viable but ischaemic tissue. In 72-h images, there was non-perfusion of the limb that correlated with the pathologically determined diagnosis of necrosis. All scintigraphic patterns correlated with pathological findings. We suggest that these scintigraphic patterns in soft tissue may be helpful in distinguishing between frank infarction and reversible ischemia and therefore may be useful in selecting early therapeutic or surgical interventions to salvage bone and soft tissue. Further studies are needed to show the usefulness of 99mTc sestamibi scintigraphy in clinical frostbite cases.
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PMID:Assessment of tissue viability after frostbite injury by technetium-99m-sestamibi scintigraphy in an experimental rabbit model. 1065 45

The aim of the present experimental research was to study brain oxygenation parameters in relation to tissue water movement and brain cortex oedema caused by focal brain ischemia. It has been demonstrated that local osmotic dehydration of the parietal brain cortex, mercury compounds (aquaporin inhibitors) and brain cortex oedema resulting from focal brain ischemia all influence extra-capillary oxygen transport lowering tissue respiration rates and oxygen transfer coefficients. The changes of brain oxygenation parameters in case of cortex ischemic oedema are reflected in the gas composition (oxygen and carbon dioxide partial pressure) of the blood in v. jugularis. A short course of hyperbaric treatment results in normalization of water content in the brain. The results are interpreted in terms of the functioning of tissue microcirculation that might participate, at the extra-capillary level, in brain oxygenation.
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PMID:Experimental study on brain oxygenation in relation to tissue water redistribution and brain oedema. 1145 25

This hypothesis is that some crewmen on prolonged space flights may develop permanent myocardial injury despite the absence of coronary atherosclerosis and even without the hazards of radiation beyond orbit. This may resuIt from atrophy of skeletal muscle and bone resulting in magnesium ion deficiency predisposing to a vicious cycle with catecholamine elevations, with the latter aggravated by stress, dehydration-provoked angiotensin elevations, unremitting endurance exercise, and in turn a second vicious cycle with severe ischemia. Toxic free radicals can develop complicating ischemia and potential high radiation, with magnesium ion deficiency and high vascular catecholamines playing contributing roles. These free radicals may lead to inactivation of endothelium-derived relaxing factor (EDRF) causing coronary endothelial injury by a third vicious cycle, increased peripheral resistance and coronary vasospasm intensifying ischemia. Local and systemic thrombogenesis could contribute ultimately to focal fibrosis of the myocardium, if the ischemia is not recognized. Sufficient magnesium and time for repair are vital.
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PMID:Interplanetary travel and permanent injury to normal heart. 1154

The wood frog Rana sylvatica survives for weeks during winter hibernation with up to 65% body water frozen as ice. Natural freeze tolerance includes both seasonal and freeze-induced molecular adaptations that control ice formation, deal with long-term ischemia, regulate cell volume changes, and protect macromolecules. This report identifies and characterizes a novel freeze-inducible gene, li16, that codes for a protein of 115 amino acids. Northern blot analysis showed that li16 transcript levels rose quickly during freezing to reach levels 3.7-fold higher than control values after 24 h; immunoblotting showed a parallel 2.4-fold rise in Li16 protein. Regulatory influences on gene expression were assessed. Nuclear runoff assays confirmed that freezing initiated an increase in the rate of li16 transcription, and analysis of signal transduction pathways via in vitro incubation of liver slices implicated a cGMP-mediated pathway in li16 expression. Gene and protein expression in liver was also strongly stimulated by anoxia exposure, whereas the gene was less responsive to dehydration stress. The strong response of li16 to both freezing and anoxia, and the rapid down-regulation of the gene when oxygen was reintroduced, suggest that the Li16 protein may play a role in ischemia resistance during freezing.
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PMID:Identification and characterization of a novel freezing inducible gene, li16, in the wood frog Rana sylvatica. 1203 74


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