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)

In order to evaluate the role of underlying disease in the high mortality observed in acute renal failure (ARF) and risk factors related to the development of oliguric ARF in renal allograft recipients, two groups were selected: 34 patients with native kidneys, aged 16 and 57 years, and presenting ischemic ARF caused by cardiovascular collapse, with no signs of infection at the time of diagnosis; and 34 renal allograft recipients who developed ARF immediately after transplantation, without rejection. ARF was defined either as 30% increase of basal plasmatic creatinine in patients with native kidneys or nonnormalization of plasmatic creatinine at day 5 after transplantation in renal allograft recipients; oliguria as diuresis < or = 400 mL/24 h. There were no differences in age, male frequency, oliguria presence and duration, need for dialysis, and infection episodes for renal allograft recipients and patients with native kidneys. The development of sepsis (3% and 41%) and death rate (3% and 44%) were higher in patients with native kidneys (p < 0.01). The renal allograft recipients with both oliguric (n = 18) and nonoliguric (n = 16) ARF were evaluated and no difference was observed in the recipient's age, donor's age, cold ischemia time, time elapsed until plasmatic creatinine normalization, donor's plasmatic creatinine or urea, and mean arterial pressure. No differences were observed between the groups regarding frequency of infection episodes during ARF and frequency of death. In conclusion, renal allograft recipients presented a lower death rate and were less susceptible to sepsis. Cold ischemia time, age, and hemodynamic characteristics of the donor did not affect the development of oliguria.
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PMID:Acute renal failure in renal allograft recipients and patients with native kidneys. 910 1

Recently, attention has been focused on the degradation of cytoskeletal proteins in animal models of cerebral ischemia, as the collapse of cytoskeletal proteins may be closely related to cytoskeletal disintegration and ultimate neuronal cell death. Among these proteins, microtubule-associated protein 2 (MAP2) has been shown to be highly vulnerable to ischemic injuries. To determine the degree of anesthetic effect on the collapse of cytoskeletal proteins, we compared the effect of three inhalation anesthetics; isoflurane, halothane, and nitrous oxide (N2O), on MAP2 degradation during 20 min of forebrain ischemia in the rat. Under equipotent anesthesia, forebrain ischemia was induced by the occlusion of the bilateral common carotid artery (CCA) combined with a lowering of mean arterial pressure (mAP) to 50 mmHg. After 20 min of ischemia, three regions of the brain, the frontoparietal cortex, brainstem, and hippocampus, were removed and separately homogenized. Subsequently, MAP2 of each region was measured using an enzyme-linked immunosorbent assay (ELISA). In the frontoparietal cortex and hippocampus, MAP2 was significantly protected from degradation when isoflurane was used combined with nitrogen (N2). However, the protective effects of isoflurane were drastically reduced when N2O was given instead of N2. These results suggest that the use of N2O should be discontinued when severe cerebral ischemia is accidentally incurred during anesthetic management.
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PMID:Nitrous oxide attenuates the protective effect of isoflurane on microtubule-associated protein2 degradation during forebrain ischemia in the rat. 932 46

In this study, we determined whether the retina cell death observed in response to an ischemic-like insult is related to an overactivation of the ionotropic glutamate receptors and/or to a collapse of the energy levels. Cultured chick retina cells were submitted to 'chemical ischemia' by metabolic inhibition with sodium cyanide and iodoacetic acid, which block oxidative phosphorylation and glycolysis, respectively. The assessment of neuronal injury was made spectrophotometrically by quantification of cellularly reduced MTT, which gives information about mitochondrial function, or by staining with fluorescein diacetate (FDA), which correlates with changes in the plasma membrane permeability. 'Chemical ischemia' induced both an acute and a delayed time-dependent degeneration of chick retina cells. We observed that 2 min after the ischemic insult, the levels of ATP were reduced to a minimum. On the other hand, the metabolic inhibition induced the release of aspartate, glutamate and gamma-aminobutyric acid, and the activation of AMPA/kainate receptors during the period of metabolic arrest was partially responsible for the loss of mitochondrial function. However, the NMDA and non-NMDA receptor antagonists (MK-801 and CNQX) did not prevent the plasma membrane damage caused by sodium cyanide and iodoacetic acid. The results show that the collapse of the energy levels, rather than the increase in excitatory amino acids, appears to underlie the observed cell injury, suggesting an important relationship between ischemia-induced depletion of high-energy metabolites and retina cell degeneration.
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PMID:'Chemical ischemia' in cultured retina cells: the role of excitatory amino acid receptors and of energy levels on cell death. 936 12

Williams-Campbell syndrome is a rare disorder characterized by a deficiency of cartilage in subsegmental bronchi leading to distal airway collapse and bronchiectasis. We report the first case of lung transplantation in a patient with end-stage lung disease secondary to Williams-Campbell syndrome. Although the patient did not have proximal airway collapse prior to transplantation, his posttransplant course was complicated by the development of bronchomalacia of the right and left mainstem bronchi. The patient experienced recurrent pulmonary infections and died of bacterial pneumonia 1 year after transplantation. Autopsy revealed cartilage deficiency in both right and left mainstem bronchi. A hypothesis may be made that a combination of proximal cartilage deficiency and posttransplant airway ischemia led to the development of bronchomalacia after lung transplantation. Thus, in contrast to previous reports, the cartilage deficiency in Williams-Campbell syndrome can involve both proximal and distal airways. Consequently, bilateral sequential lung transplantation may not be an effective therapeutic option in patients with this syndrome.
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PMID:Lung transplantation for Williams-Campbell syndrome. 949 79

Frostbite represents a spectrum of injury ranging from irreversible cellular destruction to reversible changes seen after rewarming. These changes include increases in tissue edema, circulatory stasis, and progressive thrombosis leading to further tissue necrosis. For this reason, it is often difficult at the time of surgical debridement to determine the extent of frostbite injury. This delayed tissue injury is similar to that seen in muscle during ischemia/reperfusion injury. Muscle that initially appears viable on reperfusion may subsequently necrose due to collapse of the microcirculation. Adherent neutrophils have been specifically cited as important components in ischemia/reperfusion injury and have also been suggested to play a role in frostbite injury. We have used an intravital microscopic muscle preparation to study microcirculatory changes carefully in frostbite injury during rewarming. The right gracilis muscle of male Wistar rats is dissected free from its primary vascular pedicle and the rat is positioned on a specially constructed microsurgical stage. Temperature changes of the muscle are recorded. The prepared axial pattern flap is transilluminated with a microscope and projected on a video screen, allowing measurement of arteriolar diameters and changes in the numbers of stuck and rolling neutrophils before frostbite, during rewarming, and for several hours later. Cold silicone oil is used to freeze the muscle to -5+/-2 degrees C in 2 to 3 minutes and to hold this temperature for 5 minutes. The muscle is rewarmed with 42 degrees C normal saline placed directly on the muscle surface. Baseline vessel diameter and leukocyte counts in 100-mm segments of the microvasculature are recorded as well as at 5, 15, and 30 minutes, and at 1, 2, and 3 hours postrewarming of frozen muscle. Observations from our initial 11 animals show that reperfusion of the muscle following freezing is varied temporally and spatially, with circulation to most vascular segments restored 5 to 10 minutes after rewarming. In 9 of 11 animals we observed the shedding of "white clots" in small arterioles and venules occurring as soon as 5 minutes after thawing. In some instances shedding continued for as long as 1 hour after rewarming. Microvascular hemorrhage was widespread 1 hour following the thaw, but there was no significant increase in neutrophil adherence observed until 3 hours following rewarming. The exact nature of the vascular injury and the composition of the "white clots" are now being determined from ultrastructural studies. Blood flow in microcirculation stops during freezing, but small-vessel perfusion returns immediately on thawing. This suggests that the vascular architecture is maintained during the freezing and thawing. Unlike ischemia/reperfusion injury, neutrophil adhesion plays a smaller role in the early response to frostbite injury. The early microcirculatory observations seen after rewarming suggest progressive and severe perturbations in platelet function and fibrin formation that are significantly different from ischemia/reperfusion injury.
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PMID:Microcirculatory studies of frostbite injury. 952 7

Heat stroke is a syndrome which reduces systemic vascular resistance and cardiac collapse. The gut plays an important role in shock. In hyperthermia, many of the same symptoms as heat stroke may be present, including inhibition of splanchnic vasoconstriction and endotoxemia. Furthermore, both conditions result in shock, in which the gut plays an important role. Detection of insufficient oxygenation of gut tissue, which sustains an earlier and more severe hypoxia, can warn of impending shock and can be performed by monitoring intramucosal pH (pHim). This index is very sensitive to tissue hypoxia and ischemia. In the present study both pHim, using tonometry, and gut blood flow during whole body heating (WBH) in pigs were measured. WBH was achieved by circulating warm water through a vinyl sheet covering the animal. Central venous pressure was maintained by fluid infusion. Body temperature was measured using a thermometer probe inserted into the right jugular vein. Mean arterial pressure, cardiac output and gut blood flow were also measured. pHim was evaluated using a tonometer placed into the midileum lumen. During WBH, cardiac index and mean arterial pressure increased, however systemic vascular resistance decreased. Gut blood flow was either maintained at the normal rate or increased. Intraarterial pH did not change significantly, however pHim significantly decreased from 7.30 at the beginning of WBH to approximately 7.05 after the body temperature reached 42.5 degrees C. These findings suggest that there was reduced oxygen delivery to the tips of the small intestinal villi during regional ischemia following WBH. In conclusion, insufficient tissue oxygen delivery as detected by a reduction in inramucosal pH is an important index in whole body heating.
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PMID:Changes in intramucosal pH and gut blood flow during whole body heating in a porcine model. 967 8

The mechanism responsible for the abrupt fall in myocardial contractile function following coronary artery obstruction is unknown. The "vascular collapse theory" hypothesizes that the fall in coronary perfusion pressure after coronary artery obstruction is responsible for contractile failure during early ischemia. To test the role of vascular collapse in downregulating myocardial contractile force at the onset of ischemia, coronary flow of isolated rat hearts was abruptly decreased by 50, 70, 85, and 100% of baseline, and subsequent changes in coronary perfusion pressure and ventricular function were recorded at 0.5-s intervals. At 1.5 s after flow reductions ranging from 50 to 100%, decreases in contractile function did not differ, although perfusion pressure varied significantly from 45 +/- 1 to 20 +/- 2 mmHg. When function fell to 50% of baseline, perfusion pressures ranged from 35 +/- 0.5 to 2.5 +/- 1 mmHg for flow reductions ranging from 50 to 100%. Identical contractile function at widely differing coronary perfusion pressures is incompatible with the vascular collapse theory.
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PMID:Downregulation of ventricular contractile function during early ischemia is flow but not pressure dependent. 981 56

Ischemic osteonecrosis is a complication of certain traumatic and a number of idiopathic conditions. The course of the disease may result in collapse of the convex member of a joint and osteoarthritis, often requiring arthroplasty. Increasing incidence in young adults poses a challenge for development of long-term joint prostheses. Current status of research into the disease is discussed and three new models using intravital microscopy described. The first, an arterial occlusion (AO) model, creates ischemia by occluding the common iliac artery exclusively, avoiding direct trauma on other tissues in the limb. The second, a total occlusion (TO) model utilizes classical tourniquet occlusion of the thigh vessels. The third, a venous occlusion (VO) model, is also a tourniquet procedure but it blocks occlusion of the femoral artery with a protective sheath. Preliminary results from AO and TO studies are reported which show that reperfusion injury is detectible after ischemia doses as short as 4 h. This complication was confirmed by observation of leukocyte adherence, secondary ischemia, and abnormal vessel leakage. Also, a new quantitation of osteonecrosis is introduced whereby fluorescently-tagged dead osteocytes and computer-based image processing provide values for an "osteonecrosis index." Viewing of all vascular events is made possible by intravital microscopy through a bone chamber window implanted in rabbit tibias. It is proposed that such chronic visual techniques allow quantitation of events leading to osteonecrosis as well as the revascularization, resorption and bone apposition of creeping substitution which characterizes postischemia recovery.
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PMID:Approaches to study of ischemia in bone. 985 99

The effects of long-term preoperative administration of low-dose erythromycin (EM) were experimentally examined in relation to the treatment of reperfusion disorders following pulmonary thermal ischemia. EM was administered at a dose of 100 mg/day for 1 month to adult mongrel dogs with an average weight of about 12 kg (EM group). A control group that did not receive EM was also enrolled. Using a pulmonary autograft model, collapse-thermal ischemia of the lungs was performed on each animal for 60 minutes. In the early stage of reperfusion, the following measurements were assessed: gas-exchange potency in the left lung, hemodynamics, water content, adhesion of neutrophils to vascular endothelium, and concentration of blood eicosanoids. The results for the 2 groups were then compared. In the control group, the blood level of leukotriene B4 (LTB4) increased shortly after reperfusion, neutrophils migrated toward the vascular endothelium and adhered to it, and pulmonary edema developed after 1 hour. However in the EM group, the blood level of thromboxane B2 was significantly suppressed before and after hilar stripping, and the increase in the blood LTB4 level and the migration of neutrophils shortly after reperfusion in thermal ischemia were suppressed. Eventually alleviation of pulmonary edema was indicated and significantly improved gas exchange was maintained. In conclusion, pulmonary injury during detachment of the hilum of the lung, as well as warm ischemia-reperfusion pulmonary injury, may be alleviated by preoperative administration of low-dose EM on a long-term basis.
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PMID:[Effects of long-term preoperative administration of low-dose erythromycin on warm ischemia-reperfusion pulmonary injury]. 991 77

Hypertrophic cardiomyopathy is the most common cause of sudden death in young individuals who are otherwise healthy. Risk of sudden death is highest in patients who are between 14 and 35 years old. Several mechanisms are involved in sudden death: ventricular arrhythmias, supraventricular arrhythmias leading to cardiac collapse, bradycardias and severe ischemia. Many studies have analyzed how to identify high risk patients. The factors that best identify high risk patients are: previous history of sudden death or syncope, induction in adults of sustained ventricular arrhythmias, the presence of non-sustained ventricular tachycardia in symptomatic patients, the presence of ischemia associated with hypotension in children, the presence of mutations in the beta-myosin heavy chain together with a family history of sudden death and a poor left ventricular ejection fraction. Risk stratification should be done on an individualized basis. In those patients in whom a high risk for sudden arrhythmic death is suspected, the only current effective treatment is the implantable defibrillator.
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PMID:[Sudden death in hypertrophic myocardiopathy]. 992 51


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