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)

Sternothyroid muscle biopsy specimens, obtained during tracheostomies from 15 patients with acute stroke and respiratory failure, were examined immunohistochemically to immunoreactivity to myoglobin (Mb). A marked decrease or lack of Mb immunoreactivity in association with hyaline degeneration was observed in 0.8 to 44.4% of the muscle fibers on both the paretic and non-paretic sides of all patients. The percentages of negative staining for Mb were less than 3.1% in 5 patients with acute respiratory failure due to causes other than stroke. The pattern and incidence of attenuated Mb immunoreactivity in the muscle fibers was found to be distinctively different in the two patients groups. In one group of 5 patients, a large number of muscle fibers (24.8 +/- 15.6%) had no Mb staining and were clearly bordered and grouped. In another 10-patient group, only a limited number of muscle fibers (3.3 +/- 2.5%) had no staining for Mb and these fibers were scattered. Four patients in the former group had catastrophic outcomes, while all the patients in the latter group survived. Ischemia, produced by an increase in catecholamines, and the consequent vasoconstriction, rather than hypoxemia seemed to be the cause of the negative immunoreactivity for Mb in the group pattern. In contrast, hypoxemia may have caused the scattered pattern of negative Mb immunoreactivity. It was concluded that negative immunostaining for Mb in muscle fibers represents a common and characteristic complication in acute stroke patients.
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PMID:Lack of immunoreactivity for myoglobin in skeletal muscle of acute stroke patients. 902 93

Fluoride (F) is a widely distributed nephrotoxin with exposure potentially resulting from environmental pollution and from fluorinated anesthetic use (eg, isoflurane). This study sought to characterize some of the subcellular determinants of fluoride cytotoxicity and to determine whether subtoxic F exposure affects tubular cell vulnerability to superimposed ATP depletion and nephrotoxic attack. Human proximal tubular cells (HK-2) were cultured with differing amounts of NaF (0 to 20 mmol/L, overlapping with clinically relevant intrarenal/urinary levels after fluorinated anesthetic use). After completing 24-hour exposures, cell injury was determined (vital dye uptake). Fluoride effects on cell deacylation ([3]H-C20:4 release) and PLA2 activity were also assessed. To determine whether subtoxic F exposure alters tubular cell susceptibility to superimposed injury, cells were exposed to subtoxic NaF doses for 0 to 24 hours and then challenged with simulated ischemia (ATP depletion plus Ca2+ overload) or a clinically relevant nephrotoxic insult (myoglobin exposure). NaF induced dose-dependent cytotoxicity (up to approximately 90% vital dye uptake and increased [3H]C20:4 release). Extracellular Ca2+ chelation (EGTA) and PLA2 inhibitor therapy (aristolochic acid, dibucaine, or mepacrine) each conferred significant protective effects. When subtoxic NaF doses were applied, partial cytosolic PLA2 depletion rapidly developed (approximately 85% within 3 hours, determined on cell extracts). These partially PLA2-depleted cells were markedly resistant to ATP depletion/Ca2+ ionophore injury and to myoglobin-induced attack (approximately 50% decrease in cell death). We conclude that 1) F induces dose-dependent cytotoxicity in cultured human proximal tubular cells, 2) this occurs, in part, via Ca(2+)- and PLA2-dependent mechanism(s), 3) partial cytosolic PLA2 depletion subsequently results, and 4) subtoxic fluoride exposure can acutely increase cell resistance to further attack. Reductions in cytosolic PLA2 activity could potentially contribute to this result.
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PMID:Inorganic fluoride. Divergent effects on human proximal tubular cell viability. 903 86

The protective effects of carnosine and related compounds on isolated rat heart were studied under experimental ischemia. The ability of carnosine to suppress significantly the development of ischemic reperfusion contracture and to support the restoration of the contractile force during reperfusion were shown. At the same time, a decrease of myoglobin and nucleoside release from myocytes was observed, this indicating a membrane-protecting effect of carnosine. Methylation of carnosine at the N1 or N3 atom of the imidazole ring significantly decreased the protective effect; the substitution of beta-alanine with gamma-aminobutyric acid (resulting in formation of homocarnosine) actually augmented ischemic damage to the heart. Acetylation of carnosine at the beta-amino group amplified the membrane-protecting properties of the molecule, the acetylated derivative of carnosine also showing the ability to induce contractile activity of the ischemic heart. Histidine alone or in combination with beta-alanine and sodium acetate had no effect, while acetylhistidine showed a significant protective effect during reperfusion. The comparison of the effects of natural histidine-containing dipeptides versus synthetic antioxidants indicates that the anti-ischemic effect of carnosine and acetylcarnosine involves antiradical and membrane-protecting mechanisms; nevertheless, the effect cannot be reduced to these mechanisms alone. The observed phenomena of heart muscle protection by acetylated derivatives of carnosine and anserine under ischemia correlates with the preferential localization of these compounds in high quantities in the myocardium.
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PMID:Effect of histidine-containing dipeptides on isolated heart under ischemia/reperfusion. 911 34

The ischemia-reperfusion syndrome, first described by Haimovici in 1960, is a severe complication following surgery for acute ischemia. We evaluated the incidence of this complication in 264 patients operated on between 1972 and 1981 (1st group) and compared it with another of 392 patients operated on between 1982 and 1991 (2nd group), our aim being to assess the effects of pharmacological prophyiaxis based on preoperative overhydration followed by an intra-arterial bolus of 250 ml 14/1000 HCO3-, containing 1 g dexamethasone and 2500 I.U. sodium heparin, injected into the femoral artery before suturing the arteriotomy. This regimen was based on the measurement of myoglobin and glutathione levels respectively carried out in two subgroups of 25 patients. The results of experimental ischemia-reperfusion syndromes induced in animal using radical scavengers and membrane-protective compounds were also taken into consideration. Following experimental research on sheep, 5 patients in the second group with very severe ischemia due to aortic occlusion received local dialysis in the extracorporeal circulation using hemodialysis or hemofiltration techniques. Mortality was 6.3% in the first group and 5.4% in the second, while the amputation rate was 3% and 1.8% respectively. The overall incidence of the reperfusion syndrome was 3% in the 1st period and 1.8% in the second. Our findings confirm the protective effect of hyper-hydration, radical scavengers and dexamethasone in the ischemia reperfusion syndrome, and indicate that local hemodialysis is a useful adjunct in very severe ischemia.
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PMID:Ischemia: reperfusion syndrome of the lower limbs. 912 77

A growing body of evidence supports the trigger role of free radicals in the delayed functional and metabolic myocardial recovery following cardiopulmonary bypass (CPB) in humans, thus opening the field to specific therapies. This clinical study was designed to evaluate, in 15 patients undergoing aortic valve replacement, whether the extent of CPB- and reperfusion-induced lipid peroxidation, ascorbate depletion, tissue necrosis, and cardiac dysfunction is reduced by orally administered EGb 761, a Ginkgo biloba extract with potent in vitro antiradical properties. Patients received either EGb 761 (Tanakan, 320 mg/day, n = 8) or a matching placebo (n = 7) for 5 days before surgical intervention. Plasma samples were obtained from the peripheral circulation and the coronary sinus at crucial stages of the operation (i.e., before incision, during ischemia, and within the first 30 minutes post-unclamping), and up to 8 days postoperatively. Upon aortic unclamping, EGb 761 inhibited the transcardiac release of thiobarbituric acid-reactive species (p < 0.05), as assessed by high-performance liquid chromatography, and attenuated the early (5-10 minute) decrease in dimethylsulfoxide/ascorbyl free radical levels, an electron spin resonance index of the plasma ascorbate pool (p < 0.05). EGb 761 also significantly reduced the more delayed leakage of myoglobin (p = 0.007) and had an almost significant effect on ventricular myosin leakage (p = 0.053, 6 days postoperatively). The clinical outcome of recovery of treated patients was improved, but not significantly, compared with untreated patients. Our results demonstrate the usefulness of adjuvant EGb 761 therapy in limiting oxidative stress in cardiovascular surgery and suggest the possible role of highly bioavailable terpene constituents of the drug.
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PMID:Ginkgo biloba extract (EGb 761) pretreatment limits free radical-induced oxidative stress in patients undergoing coronary bypass surgery. 914 Jun 89

Variations in the levels of muscle hemoglobin and of myoglobin oxygen saturation can be detected non-invasively with near-infrared spectroscopy. This technique could be applied to the diagnosis of chronic compartment syndrome, in which invasive testing has shown increased intramuscular pressure associated with ischemia and pain during exercise. We simulated chronic compartment syndrome in ten healthy subjects (seven men and three women) by applying external compression, through a wide inflatable cuff, to increase the intramuscular pressure in the anterior compartment of the leg. The tissue oxygenation of the tibialis anterior muscle was measured with near-infrared spectroscopy during gradual inflation of the cuff to a pressure of forty millimeters of mercury (5.33 kilopascals) during fourteen minutes of cyclic isokinetic dorsiflexion and plantar flexion of the ankle. The subjects exercised with and without external compression. The data on tissue oxygenation for each subject then were normalized to a scale of 100 per cent (the baseline value, or the value at rest) to 0 per cent (the physiological minimum, or the level of oxygenation achieved by exercise to exhaustion during arterial occlusion of the lower extremity). With external compression, tissue oxygenation declined at a rate of 1.4 +/- 0.3 per cent per minute (mean and standard error) during exercise. After an initial decrease at the onset, tissue oxygenation did not decline during exercise without compression. The recovery of tissue oxygenation after exercise was twice as slow with compression (2.5 +/- 0.6 minutes) than it was without the use of compression (1.3 +/- 0.2 minutes).
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PMID:Near-infrared spectroscopy for monitoring of tissue oxygenation of exercising skeletal muscle in a chronic compartment syndrome model. 919 80

To evaluate the effect of reperfusion with hypertonic-hyperosmotic solution, cardiectomy was performed in 25 New Zealand white rabbits. Seven isolated hearts were submitted to 30 min of global ischemia and reperfused with oxygenated buffer for 60 min. Myoglobin and isoenzyme MB of creatine kinase concentrations were each measured in the effluent 15 min, and values were correlated (r = 0.5011, p = 0.015). After this procedure, 18 isolated hearts were randomized in two groups. Hearts of group I were reperfused with hypertonic-hyperosmotic solution (NaCl 7.5% dextran 60,000 MW) diluted in oxygenated buffer, and group II with oxygenated buffer. Myoglobin and coronary flow were measured in both groups, group I showed lower levels of myoglobin (p = 0.0069) and higher coronary flow (p = 0.028) than group II. In conclusion, changes in myoglobin concentration in the heart effluent are more sensitive than changes in isoenzyme MB of creatine kinase; thus, evaluation of this parameter may be useful in the detection of ischemia reperfusion injury. Additionally, hypertonic-hyperosmotic solution improves the coronary flow and has a protective effect against ischemia-reperfusion injury.
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PMID:Hypertonic-hyperosmotic solution modifies myoglobin levels in early reperfusion after ischemic cardiac arrest. Experimental model. 920 13

21-Aminosteroids (Lazaroids), acting as free radical scavengers and as membrane stabilizers, proved to have beneficial effects in various pathological conditions. In the present study we explored the effectiveness of one of these compounds, U 74389 G, in protecting pigs myocardium against the ischemia-reperfusion damage induced by transient coronary occlusion achieved by clampling the left anterior descending coronary artery. Animals were divided into three groups: control, untreated and treated. Control animals were operated but not subjected to ischemia-reperfusion; the untreated group underwent to ischemia-reperfusion without pharmacological treatment; while the treated group received the aminosteroid (4 mg/kg) before coronary occlusion and at the time of reperfusion. Specimens of myocardial tissue and blood samples were taken for morphological and biochemical studies. In the ischemic-reperfused myocardium of the untreated animals, the dominant morphological features were neutrophil infiltration, intercellular edema and severe swelling of mitochondria. All these alterations, notably neutrophil infiltration, were attenuated by aminosteroid treatment. As for the biochemical findings, the changes in adenine nucleotides and nucleosides levels, thus the reduction of energy charge, were reversed in the treated, but not in the untreated group. Myocardial concentration of malondialdehyde, which was undetectable in the control group, was raised in all the animals after reperfusion, but this effect was significantly less marked with aminosteroid treatment. In addition, the higher myocardial content of ascorbic acid and the reduced serum potential peroxidation exhibited by the treated animals compared with untreated group indicate an enhanced antioxidant protection induced by aminosteroid administration. On the other hand, the serum levels of myoglobin, cardiac troponin I and creatine kinase MB isoenzyme suggest the ability of the aminosteroid to attenuate the modifications of membrane permeability induced by ischemia-reperfusion injury. All these results lead to the conclusion that aminosteroid treatment, at least in the conditions of the present study, is effective in reducing the morphological and biochemical alterations occurring in ischemic-reperfused myocardium.
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PMID:Beneficial effects of the 21-aminosteroid U 74389G on the ischemia-reperfusion damage in pig hearts. 934 76

The acute coronary syndromes represent a continuum of myocardial ischemia ranging from angina, reversible tissue injury --> unstable angina, frequently associated with minor myocardial damage --> myocardial infarction and extensive tissue necrosis. Historically, coronary artery disease assessment has been mainly binary, using WHO criteria of symptoms, electrocardiography, and biochemical markers. The creatine kinase-MB isoenzyme (CK-MB) has been a benchmark for markers, but it is not specific for myocardium. Cardiac-specific isoforms of troponin T and I have emerged as sensitive myocardial infarction (MI) indicators and, importantly, for risk stratification of acute coronary syndrome patients. In addition to markers of myocardial cell necrosis, markers of plaque disruption (C-reactive protein and serum amyloid A), "angry" platelets (P-selectin), ischemia (glycogen phosphorylase-BB isoenzyme), and the procoagulant state and thrombosis (soluble fibrin) have potential use. Also, CK-MB and myoglobin have been combined with clinical indicators for monitoring reperfusion after thrombolytic therapy. Biochemical markers will continue to be an important clinical adjunct for MI diagnosis, risk assessment, and reperfusion monitoring in the future.
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PMID:Biochemical markers of the acute coronary syndromes. 970 95

Rhabdomyolysis results from muscular fibre lysis with release of cellular contents (myoglobin, enzymes, electrolytes) into the plasma. Traumatic (crush syndrome) and non-traumatic rhabdomyolysis have been mostly reported in adults. Traumatic rhabdomyolysis are mostly due to ischemic and reperfusion injuries. Non-traumatic rhabdomyolysis include several factors: muscular compression (comas), cytotoxic injury (infections and poisonings), ischemia (shock, cardiorespiratory arrest) or excessive muscular activity (seizures, strenuous exercise). The main etiologies reported in children are: anoxic-ischemic encephalopathy (including sudden infant death and life threatening events); electrolyte disorders; severe hyperthermia; poisonings; hereditary myopathies. Non-traumatic rhabdomyolysis must be suspected in these circumstances, requiring blood creatinine phosphokinase measurements. Indeed, clinical signs are inconstant and non-specific, and functional signs are difficult to appreciate in children. During the initial phase, the main risk is arrhythmias secondary to hyperkalemia. The two main complications are the compartmental syndrome leading to irreversible vasculo-nervous injuries and acute renal failure. Treatment of traumatic and non-traumatic rhabdomyolysis includes correction of hyperkalemia, active fluid loading in order to prevent acute renal failure and alkalinisation. Prognosis of rhabdomyolysis relates to the aetiology and the presence of acute renal failure.
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PMID:[Acute rhabdomyolysis in the child]. 975 96


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