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)

Experiments were performed to examine the response of cyt a,a3 to transient ischemic and hypoxic episodes in the empty, fibrillating canine heart in situ. Using a dual wavelength, differential spectrophotometer, reaction spectra show an absorption peak at approximately 605 nm consistent with that obtained from purified cyt a,a3. The characteristics of the averaged reaction spectrum in the interval 590 nm to 610 nm indicate that hemoglobin/myoglobin contribute no more than 23% to the signal measured at 605 nm. A regimen of one 30 sec global ischemia (GI) repeated once every 3 minutes over a 90 min period showed no appreciable signal deterioration. Therefore, five such interventions were subsequently used as the test perturbation. Studies of the effects of ischemic episodes of 30 and 60 min show that the response of cyt a,a3 to this test intervention was smaller (90 +/- 6% and 89 +/- 7%) than that observed prior to the ischemic episode. Changes in coronary perfusion pressure (+/- 10 Torr) produced an immediate oxidation/reduction of cyt a,a3. In the working heart, just prior to fibrillation, 6 sec to interrupted ventilation resulted in a continuous reduction of cyt a,a3. The data from these studies show: 1) The redox state of cyt a,a3 may be continuously monitored in the canine heart in situ. 2) Following ischemias of 30 and 60 min duration, respiratory chain function may be impaired; and 3) The well-perfused epicardium is extremely sensitive to small changes in oxygen delivery.
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PMID:Response of cyt a,a3 in the situ canine heart to transient ischemic episodes. 626 57

The relationships among isometric tension development, the oxidation-reduction states of pyridine nucleotides and cytochrome c, and the oxygenation state of myoglobin have been assessed using the arterially perfused rabbit interventricular septum under different conditions of contraction rate, perfusate [Ca2+] and pH, catecholamine stress, and hypoxia. Hypoxia was produced either by decreasing oxygen availability with maintained flow (high-flow hypoxia) or by decreasing the flow rate (ischemia). Under normoxic conditions, increased work caused a fall of the cytosolic adenine nucleotide phosphorylation potential, delta G(ATP)c, an oxidation of the pyridine nucleotides, and a reduction of cytochrome c; the opposite occurred with decreased work. Thus, the redox potential span from NADH to cytochrome c, delta Eh, varied with the energy demand such that delta Eh and delta G(ATP)c changed in the same direction. Under hypoxic conditions, all respiratory components became more reduced, and myoglobin was partially deoxygenated. The percentage change of developed tension under hypoxic conditions was approximately proportional to the percentage change of oxidized cytochrome c. When high-flow hypoxia and ischemia were compared at the same rates of oxygen delivery, the developed tension at any level of cytochrome c reduction was always lower with ischemia than with high-flow hypoxia. This difference was attributed to the low intracellular pH of ischemic tissue. Myoglobin deoxygenation was linearly related to cytochrome c reduction under all conditions of hypoxia, indicating steep oxygen gradients. The results support the concept of heterogeneous oxygenation of the tissue with mixed populations of aerobic and anaerobic mitochondria in the hypoxic state. In the full aerobic state, the control of mitochondrial respiration in situ appears similar to that of isolated mitochondria.
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PMID:Mitochondrial function in normal and hypoxic states of the myocardium. 630 29

To evaluate morphologic changes and myoglobin content in normal, ischemic and necrotic myocardium, the authors studied human (n = 13) and dog (n = 28) myocardium by triphenyltetrazolium chloride staining, light and electron microscopy, periodic acid-Schiff stain for glycogen loss, and by an immunoperoxidase technique. Myocardium from autopsied patients with infarction 10-24 hours old showed loss of myoglobin from necrotic fibers. Dogs with infarcts after 3 hours or more of coronary occlusion showed myoglobin loss in fibers shown to be necrotic. In 4 dogs with 50% reduction in left main coronary artery flow for 3 hours, which demonstrated ischemia without necrosis (glycogen loss with no triphenyl tetrazolium chloride evidence of necrosis), myoglobin staining in myocardial sections was similar to nonischemic and positive control tissues. By comparison of immunoperoxidase staining with concomitant study by light and electron microscopy and histochemistry, loss of myoglobin from necrotic myocardium was demonstrated, while ischemic but not necrotic fibers stained normally. These findings indicate that necrosis is necessary for myoglobin loss from myocardium to be detected by this immunoperoxidase technique.
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PMID:Myocardial myoglobin following coronary artery occlusion. An immunohistochemical study. 634 48

Myoglobinuria and acute renal failure were observed in two patients with vasopressin-treated gastrointestinal hemorrhage. Because there were no other obvious causes of renal failure in either patient, we propose that skeletal muscle ischemia developed during vasopressin infusion, followed by release of myoglobin and renal damage. This association should be considered in the period after vasopressin-treated gastrointestinal hemorrhage.
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PMID:Myoglobinuria and acute renal failure associated with intravenous vasopressin infusion. 661 Sep 43

Revascularization syndrome is one of the dangerous postoperative complications which results sometimes in loss of a limb, renal shutdown and death due to myoglobin-nephrosis and hyperkalemia. During the past 3 years, 2 cases of revascularization syndrome were experienced in 16 cases of thrombo-embolectomies for acute peripheral arterial occlusion. One patient died from hyperkalemia 100 minutes after revascularization. Another patient suffered from a renal shutdown, and was treated with hemodialysis and thigh amputation. It is sometimes very difficult to predict whether the revascularization syndrome will occur or not. When revascularization is performed within 12 hours after an onset of acute occlusion and when the amount of ischemic muscle is not large, the syndrome may not occur. When the time-interval between the onset of ischemia and revascularization is longer than 24 hours and when the mass of ischemic muscle is large, the syndrome will occur. Preoperative serum creatinine and urea nitrogen level are important parameters predicting the prognosis.
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PMID:[Pathogenesis and prevention of the revascularization syndrome]. 667 83

The myoglobin content of heart muscles was examined by the indirect immunoperoxidase method in eight autopsy cases where death was due to electricity. Seven cases showed a considerable release of myoglobin from the myocardial fibers. In experimental comparison, the heart muscles and skeletal muscles from nine cases where death was natural were exposed to electricity, and considerable deletion of myoglobin was also demonstrated. We believe that the findings of ischemia or thermal effects due to electricity were the cause of the release of myoglobin. Because the demonstration of myoglobin is preferable to estimation of the damaged areas of muscles by hematoxylin-eosin staining, this examination may be more advantageous in forensic examination of death by electricity.
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PMID:[The effect of electricity on the myoglobin content of the human heart and skeletal muscles]. 670 17

Rhabdomyolysis leading to acute renal failure necessitating hemodialysis is described in three chronic alcoholics. In each case an acute medical or surgical event, but not alcoholic intoxication, was implicated. Renal biopsies demonstrated acute tubular necrosis with intraluminal deposits consisting of Tamm-Horsfall protein and myoglobin. After recovery all three patients were demonstrated to have proximal muscle weakness with similar electromyographic abnormalities but nerve-conduction was impaired in only two. Muscle biopsies showed mixed, but predominantly type II fiber atrophy and reduced muscle phosphorylase levels. In the one patient tested the lactate response to forearm muscle ischemia was abnormal. It is postulated that chronic alcoholics may be predisposed to rhabdomyolysis and acute renal failure following acute medical and surgical stress as well as acute alcohol abuse. The muscle damage in these patients may be due to impaired intra cellular glycogen metabolism.
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PMID:Rhabdomyolysis and acute renal failure in chronic alcoholics with myopathy, unrelated to acute alcohol ingestion. 673 97

Regional changes in myocardial function and oxidative metabolism during acute coronary artery occlusion were recorded spectrophotometrically by incorporating fiber optics in the isolated rat heart perfused by Langendorff's procedure. Oxygen saturation of myoglobin, reduction of cytochrome aa3, and the dynamic wall thickness of the left ventricle were continuously and concurrently measured from absorbancy increments at 581-592 nm, 605-630 nm, and 568-592 nm, respectively. In contrast to a gradual decrease in the extent of systolic wall thickening in anoxia, observed decreases in both the extent and the duration of systolic wall thickening and the appearance of a late systolic bulge occurred within 5 s after the onset of regional ischemia. After 10 s of both anoxia and regional ischemia, oxygen saturation of myoglobin decreased by 50%, but fluorescence of nicotinamide adenine dinucleotide remained at aerobic level which indicated that mitochondrial oxidative energy production might still be maintained. Thus early and pronounced dysfunction of the ischemic region appeared to precede a substantial loss of ATP production.
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PMID:Regional myocardial function and metabolism during acute coronary artery occlusion. 709 58

The functional behaviour of membrane systems of the cardiac cell during oxygen deficiency was analyzed and the alterations were related to the metabolic state of the tissue as an index of injury. 1. The retention function of the cell membrane for proteins. With increasing energy deficiency the cardiac sarcolemma loses its ability to retain macromolecules (myoglobin, enzymes) within the cell. Close correlations exist between protein release and oxygen supply as well as ATP content of the tissue. 2. Function of isolated mitochondria after ischemia. In parallel with a strong impairment of oxidative phosphorylation (decrease of QO2, RCI values, phosphorylation rates) the Ca++-transporting activity of mitochondria is continuously depressed with decreasing myocardial ATP. 3. Function of isolated sarcoplasmic reticulum after ischemia. With breakdown of high energy phosphates during ischemia rate and extent of Ca++ binding with decrease markedly.
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PMID:Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell. 738 1

alpha-Lipoic acid, which plays an essential role in mitochondrial dehydrogenase reactions, has recently gained considerable attention as an antioxidant. Lipoate, or its reduced form, dihydrolipoate, reacts with reactive oxygen species such as superoxide radicals, hydroxyl radicals, hypochlorous acid, peroxyl radicals, and singlet oxygen. It also protects membranes by interacting with vitamin C and glutathione, which may in turn recycle vitamin E. In addition to its antioxidant activities, dihydrolipoate may exert prooxidant actions through reduction of iron. alpha-Lipoic acid administration has been shown to be beneficial in a number of oxidative stress models such as ischemia-reperfusion injury, diabetes (both alpha-lipoic acid and dihydrolipoic acid exhibit hydrophobic binding to proteins such as albumin, which can prevent glycation reactions), cataract formation, HIV activation, neurodegeneration, and radiation injury. Furthermore, lipoate can function as a redox regulator of proteins such as myoglobin, prolactin, thioredoxin and NF-kappa B transcription factor. We review the properties of lipoate in terms of (1) reactions with reactive oxygen species; (2) interactions with other antioxidants; (3) beneficial effects in oxidative stress models or clinical conditions.
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PMID:alpha-Lipoic acid as a biological antioxidant. 764 94


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