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)

The adult pelvis and hip contain extensive marrow space in which a variety of processes may occur. Evaluation of this space requires an understanding of normal maturation and recognition that the marrow of the pelvis (axial skeleton) and that of the proximal femurs (appendicular skeleton) contain variable amounts of red and yellow marrow. At magnetic resonance (MR) imaging, this variability yields patterns in normal marrow ranging from very uniform and homogeneous signal intensity to patchy and heterogeneous signal intensity. The marrow space serves as a reflection of patient health and may herald developing anemia with reconversion of inactive to active marrow. Pathologic processes to be considered include marrow edema related to trauma, tumors, or infection; marrow ischemia and infarction; marrow infiltration from primary or secondary neoplasms or from infection; or complete loss of normal myeloid tissue in the marrow space. Each process can be effectively studied with MR imaging.
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PMID:From the RSNA Refresher Courses. Radiological Society of North America. Evaluation of the marrow space in the adult hip. 1104 60

Ischemia-induced changes of diastolic leftventricular (LV) properties commonly precede corresponding ECG-changes. In the present experimental study the consequences of acute normovolemic hemodilution (ANH) induced dilutional anemia (hematocrit, hct 20%) for LV diastolic function were investigated. A total of 22 anaesthetized, splenectomized beagle dogs breathing room air were hemodiluted with isooncotic hydroxyethylstarch solution (6% HAES 200,000/0.5) until a hct value of 20% was reached. Before and after ANH intravascular blood volume (indocyaningreen dilution technique), global and regional myocardial blood flow (radioactive microspheres technique) and the following parameters reflecting LV diastolic properties were ascertained: 1) the maximum rate of LV pressure decrease (LVdp/dtmin), 2) slope and intercept of the enddiastolic pressure-volume relationship (EDPVR, conductance technique) and 3) the time-constant of isovolumic LV pressure decline "tau". After ANH to hct 20% diastolic LV function was found unchanged. Particularly the load-independent parameters (EDPVR-slope and tau) remained constant. The decrease of LV dp/dtmin (-2724 +/- 479 vs. -2388 +/- 408 mmHg.sek-1; p < 0.05) reflects ANH induced changes of LV pre- and afterload. Signs of subendocardial perfusion mismatch were not encountered. Presumed that the coronary vascular system is intact ANH to hct 20% does not provoque changes of LV diastolic function. Moreover neither myocardial perfusion and oxygenation nor myocardial function are endangered by this degree of dilutional anemia.
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PMID:[Acute normovolemic hemodilutin (ANH). Effects of ANH on the diastolic function of the left ventricle]. 1159 80

We describe the case of a 72-year-old woman who displayed massive multiple intramural gas collections of the bladder wall as an incidental finding on CT. The patient presented with critical ischemia of the left leg caused by paradoxical arterial embolism, raised corpuscular sedimentation rate, anemia by gastrointestinal blood loss, hypoproteinemia, diarrhea, malabsorption, and exudative enteropathia caused by mycobacterial ileocolitis. The patient had no dysuria and there was no evidence of diabetes. The intramural gas collections of the bladder wall, as shown by CT, were compatible with emphysematous cystitis. Urine samples proved infection by a multi-resistant strain of E. coli. Emphysematous cystitis is a rare form of bladder infection that can be diagnosed by plain-film radiograms or CT.
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PMID:Emphysematous cystitis in a patient presenting with paradoxical arterial embolism and intestinal mycobacteriosis without evidence of diabetes. 1121 22

Different tissues display distinct sensitivities to defective mitochondrial oxidative phosphorylation (OXPHOS). Tissues highly dependent on oxygen such as the cardiac muscle, skeletal and smooth muscle, the central and peripheral nervous system, the kidney, and the insulin-producing pancreatic beta-cell are especially susceptible to defective OXPHOS. There is evidence that defective OXPHOS plays an important role in atherogenesis, in the pathogenesis of Alzheimer's disease, Parkinson's disease, diabetes, and aging. Defective OXPHOS may be caused by abnormal mitochondrial biosynthesis due to inherited or acquired mutations in the nuclear (n) or mitochondrial (mt) deoxyribonucleic acid (DNA). For instance, the presence of a mutation of the mtDNA in the pancreatic beta-cell impairs adenosine triphosphate (ATP) generation and insulin synthesis. The nuclear genome controls mitochondrial biosynthesis, but mtDNA has a much higher mutation rate than nDNA because it lacks histones and is exposed to the radical oxygen species (ROS) generated by the electron transport chain, and the mtDNA repair system is limited. Defective OXPHOS may be caused by insufficient fuel supply, by defective electron transport chain enzymes (Complexes I - IV), lack of the electron carrier coenzyme Q10, lack of oxygen due to ischemia or anemia, or excessive membrane leakage, resulting in insufficient mitochondrial inner membrane potential for ATP synthesis by the F0F1-ATPase. Human tissues can counteract OXPHOS defects by stimulating mitochondrial biosynthesis; however, above a certain threshold the lack of ATP causes cell death. Many agents affect OXPHOS. Several nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit or uncouple OXPHOS and induce the 'topical' phase of gastrointestinal ulcer formation. Uncoupled mitochondria reduce cell viability. The Helicobacter pylori induces uncoupling. The uncoupling that opens the membrane pores can activate apoptosis. Cholic acid in experimental atherogenic diets inhibits Complex IV, cocaine inhibits Complex I, the poliovirus inhibits Complex II, ceramide inhibits Complex III, azide, cyanide, chloroform, and methamphetamine inhibit Complex IV. Ethanol abuse and antiviral nucleoside analogue therapy inhibit mtDNA replication. By contrast, melatonin stimulates Complexes I and IV and Gingko biloba stimulates Complexes I and III. Oral Q10 supplementation is effective in treating cardiomyopathies and in restoring plasma levels reduced by the statin type of cholesterol-lowering drugs.
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PMID:Mitochondrial medicine--molecular pathology of defective oxidative phosphorylation. 1131 62

People over 65 years account for more than 80% of heart failure hospitalizations, with almost half in patients morer than 75. Heart failure hospitalizations accounted for 21% of the annual health care budget for a representative senior program. Heart failure with preserved ejection fraction accounts for over half of heart failure hospitalizations in the elderly. Current therapy for the elderly is directed to relieve congestion by reducing volume overload and hypertension, while addressing exacerbating factors such as ischemia and anemia. Heart rate reduction is critical when sinus rhythm cannot be maintained but can also improve diastolic filling during sinus rhythm. While cardiac transplantation is rarely indicated, other interventions should be actively considered. Most elderly patients admitted with heart failure wish resuscitation. As heart failure progresses, decisions regarding implantable defibrillators or dialysis require careful consideration, and the risk/benefit balance may shift toward therapies to improve quality of life. (c)1999 by CVRR, Inc.
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PMID:Hospitalization for Heart Failure in the Elderly. 1141 23

Sickle cell anemia (SCA) is a disease caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within the red blood cell to cause rigid deformation of the cell. This deformation impairs the ability of the cell to pass through small vascular channels; sludging and congestion of vascular beds may result, followed by tissue ischemia and infarction. Infarction is common throughout the body in the patient with SCA, and it is responsible for the earliest clinical manifestation, the acute pain crisis, which is thought to result from marrow infarction. Over time, such insults result in medullary bone infarcts and epiphyseal osteonecrosis. In the brain, white matter and gray matter infarcts are seen, causing cognitive impairment and functional neurologic deficits. The lungs are also commonly affected, with infarcts, emboli (from marrow infarcts and fat necrosis), and a markedly increased propensity for pneumonia. The liver, spleen, and kidney may experience infarction as well. An unusual but life-threatening complication of SCA is sequestration syndrome, wherein a considerable amount of the intravascular volume is sequestered in an organ (usually the spleen), causing vascular collapse; its pathogenesis is unknown. Finally, because the red blood cells are abnormal, they are removed from the circulation, resulting in a hemolytic anemia. For the patient with SCA, however, the ischemic complications of the disease far outweigh the anemia in clinical importance.
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PMID:Sickle cell anemia. 1145 73

A 39 year old male comes to the emergency room because of rapidly increasing pain in his left leg one hour after the injection of Flunitrazepam into a groin vessel. There is a history of drug abuse for more than 15 years. The left leg is cool and shows intense patchy cyanosis. The same skin discoloration is seen at the left lower abdomen and parts of the thigh. The leg is paretic but foot-pulses are detectable. Color-coded duplex-sonography of the left leg shows normal shaped arteries with regular flow. Regarding the veins there are post-thrombotic changes but no signs of actual thrombosis. The ECG shows sinus rythme. No source of emboli can be found by echocardiography. The laboratory tests reveal normal results except of anemia (Hb 9.6 g/dl, normocytic, normochromic). As an accidental intraarterial injection with a toxic/allergic insult to the vessel-walls has to be supposed the patient is treated besides of analgesics with systemic anticoagulation, high doses of cortisone and calcium channel-blockers. With this therapeutic regimen the leg and the left lower abdomen improve gradually except for some toes which remain cyanotic. During the first days the patient develops signs of moderate rhabdomyolysis with swelling of the leg and an increase of creatininase concentration in blood. After 12 days the left leg has normalised but the toes show further demarcation. They have to be amputated six weeks later. The accidental injection of drugs into the femoral artery may result in the clinical picture of acute limb ischemia without occlusion of the big vessels of the leg. This obviously occurs most often with benzodiazepines, especially when crushed tablets soluted in water are injected. Color-coded duplex sonography is able to show open vessels within minutes and prevents ineffective surgical interventions.
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PMID:[Acute ischemia of the leg in a drug addict]. 1195

Gastric mucosal damage occurs in critically ill patients in intensive care units and develops in the setting of severe physiologic stress. Within 24 hrs of admission to the intensive care unit, 75% to 100% of critically ill patients demonstrate evidence of stress-related mucosal disease. Stress ulcers present a risk of clinically important bleeding, which is associated with alterations in physiology, such as hypotension or tachycardia, or results in anemia or the need for transfusion. Clinically important bleeding occurs in approximately 1% to 4% of critically ill patients. The pathophysiology of stress-related mucosal disease is complex. Major factors responsible for stress ulcer are decreased blood flow, mucosal ischemia, and hypoperfusion and reperfusion injury. Acid-suppressive regimens that elevate the intragastric pH and maintain the pH over time have the potential to prevent stress-related mucosal disease. Intragastric pH studies have demonstrated that, whereas a pH of >4 may be adequate to prevent stress ulceration, a pH of >6 may be necessary to maintain clotting in patients at risk of rebleeding from peptic ulcer. Studies comparing the ability of intravenous administrations of histamine-2-receptor antagonists and proton pump inhibitors to raise and maintain intragastric pH suggest that, although both can raise the pH to >4, proton pump inhibitors are much more likely to maintain this pH. Unlike histamine-2-receptor antagonists, proton pump inhibitors can elevate and maintain the intragastric pH at >6. This is relevant for patients in the intensive care unit at risk for rebleeding from peptic ulcers after hemostasis.
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PMID:Pathophysiology of the upper gastrointestinal tract in the critically ill patient: rationale for the therapeutic benefits of acid suppression. 1207 60

Allogenic blood transfusion may be required for the treatment of anemia due to a hematologic disease, the consequences of chemotherapy or other circumstances, such as haemorrage and/or surgery. Transfusion becomes indispensable to prevent the side effects of anemia, such as hypoxia, palpitations, tachycardia, cardiac ischemia and fatigue. However, frequent transfusions can cause several acute problems such as hemolysis, anaphylactic shock and septic shock but also chronic problems such as iron overload (hemochromatosis), alloimmunisation and metabolic disturbances. Each of these complications can produce serious consequences and could even be sometimes fatal. Therefore we should recognise, prevent and if necessary treat all these hazards. Our article emphasises the potential chronic problems. For hemochromatosis, an iron chelator (deferoxamine) should be administered. In the presence of allo-immunisation the more compatible ABO blood group must be chosen and blood products be eliminated by filtration, when there has been blood reaction. When an allo-graft of hematopoitic tissues is considered an irradiation of blood products is necessary. Research is being carried out to develop substitute products for transfusion (haemoglobine solutions) or molecules acting on the syntheses of haemoglobine (butyrate arginine). The efficacy of erythropoitine, (EPO) is well recognised for stimulation of haemoglobine syntheses in renal failure and oncology.
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PMID:[Surveillance and side-effects of transfusions]. 1218 32

Myocardial injury has been shown to be the most critical factor influencing quality of life and mortality in patients with chronic renal failure. Oxidative stress has been postulated to be an important risk factor for cardiovascular disorders. One reason for oxidative stress in patients with renal failure is the underlying disease itself. Renal toxicity, ischemia/reperfusion and immunological disorders of the kidney result in an elevated formation of reactive oxygen species active in the pathogenesis of kidney disease. However, treatment procedures were also shown to induce oxidative stress. Increased formation of free radicals leads to an accelerated lipid peroxidation (LPO). Furthermore, secondary aldehydic LPO products, e.g. malondialdehyde (MDA) and 4-hydroxynonenal (HNE), are formed which were shown to deplete antioxidants, inhibit protein syntheses, mitochondrial respiration, and enzyme functions. F2-isoprostanes, also metabolites of polyunsaturated fatty acids, represent an additional in vivo marker of oxidative stress. Both isoprostanes and aldehydic LPO products can be removed by hemodialysis, however, this suggests only in part their binding to other molecules which cause tissue damage. Protein carbonyls are end-products of such interventions. Oxysterols, another form of free-radical initiated oxidation products, were shown to initiate atherosclerosis and plaque formation increasing dramatically the risk of coronary heart disease. Today there is no doubt that the correction of the oxidant/antioxidant imbalance in patients with chronic renal failure is an important approach for the reduction of the risk of those patients to develop cardiovascular disorders. The complete correction of renal anemia represents an effective means of strengthening antioxidant capacity and, therefore, of reducting cardiovascular risk potential.
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PMID:Oxidative stress in chronic renal failure as a cardiovascular risk factor. 1222 20


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