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)

Resistance to O2 diffusion is reflected in the difference in pO2 between O2 reservoirs of hemoglobin (Hb) and myoglobin. The very low normal myocyte pO2 (less than one torr but adequate for optimal oxidative ATP synthesis) compared to venous pO2 indicates that blood does not achieve equilibrium with tissue during its passage through capillaries. In the lung, diffusion rate of O2 from alveolus to capillary is normally sufficient to achieve essential equilibrium. However, system-wide capillary pathology and reduced Hb saturation has been observed with distal local ischemia. In peripheral vascular disease (PVD) patients, we found a mean arterial pO2 of 77 torr (normal over 90 torr). Classical concepts based on "tissue pO2" values derived from venous blood or oxygen electrodes inserted into tissue need re-evaluation. Readings of O2 electrodes moved through tissue range widely from intracapillary levels down toward intracellular levels and do not reflect the pO2 of any particular site. Intravenous pO2 is the result of residual O2 after incomplete diffusion out of capillaries during transit through a tissue, and is not an equilibrium value with some tissue pool. The effect of HbO2 p50 on oxygen release during the passage of blood through a capillary bed, generally judged on the basis of percentage percent saturation at "tissue pO2", should be judged on the basis of the change in pO2 (the diffusion driving force) associated with a particular degree of HbO2 saturation at a particular p50. The thesis that O2 diffusion rate is a major determinant of oxygen delivery is supported by pO2 responses to treatment of PVD that does not alter blood flow or p50.
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PMID:Concepts of "tissue PO2" in relation to O2 delivery. 799 99

To assess the development of oxidative stress in cardiac ischemia/reperfusion, the resulting depletion of plasma ascorbate was monitored by electron spin resonance spectroscopic detection of ascorbyl free radical (AFR) in a homogeneous group of 12 patients undergoing aortic valve replacement. Dimethyl sulfoxide (DMSO) was used as an enhancer and stabilizer for AFR in plasma separated from blood samples collected 15 min before incision, 10 min before aortic declamping, and sequentially during the initial 30 min of reperfusion. Plasma DMSO/AFR levels of patients were found to be significantly lower than in healthy subjects (-25%), further decreased upon ischemia (-35%), dropped to their lowest values within the first 10 min of reperfusion (-46%), and did not recover their initial values within 30 min following reflow. Cardiac index measurements revealed a still depressed heart function 4 h postdeclamping and a more delayed tissue injury was evidenced by cardiac myosin and myoglobin release in plasma. DMSO/AFR levels at early reperfusion were slightly (+ 12%) higher in plasma obtained from coronary sinus samples than in plasma from peripheral blood, suggesting an extra ascorbate release from the injured heart tissue. The close analogy between these results and the reported measurements of other plasma markers of oxidative stress, including ascorbate, indicates that the present method could be of great value in clinical practice.
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PMID:Ascorbyl free radical: a noninvasive marker of oxidative stress in human open-heart surgery. 800 38

Evidence is presented that the radical observed upon reaction of myoglobin with hydrogen peroxide is a peroxyl radical. Simulation of this spectrum gives principal values for the g tensor of gx = 2.0357, gy = 2.0082, and gz = 2.0016, which are consistent with those of a peroxyl radical. Use of molecular oxygen isotopically labeled with 17O confirmed that the radical observed was a peroxyl radical. Removal of oxygen from the incubation by use of glucose and glucose oxidase revealed two radicals, one at giso = 2.0028 and the other at giso = 2.0073. Addition of various amounts of the spin trap 5,5-dimethyl-1-pyrroline N-oxide revealed that the spin trap and oxygen compete for the same radical site. Four model substrates, glutathione, styrene, arachidonic acid and linoleic acid, were individually added to both the aerobic and anoxic systems. Glutathione reacted with the peroxyl radical, reducing its intensity by 98%, and entirely eliminated the giso = 2.0028 line from the spectrum of the anoxic incubation. Styrene, arachidonic acid and linoleic acid reacted with the peroxyl radical, reducing its amplitude by 84, 57, and 35%, respectively, but did not decrease the amplitude of either radical species in the anoxic incubation. The giso = 2.0028 species detected in the anoxic incubation appears to be the original radical site to which molecular oxygen binds to form the peroxyl radical. This myoglobin-derived peroxyl radical species is responsible for the advent of lipid peroxidation as proposed in ischemia/reperfusion injury, as well as other reactions, as exemplified by the O2-dependent epoxidation of styrene.
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PMID:Reaction of myoglobin with hydrogen peroxide forms a peroxyl radical which oxidizes substrates. 812 65

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.
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PMID:Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations. 817 1

The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the high-frequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 +/- 0.9 uV above its nadir at 83 +/- 36 min after initiation of thrombolytic therapy) in 23 of 25 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High frequency QRS electrocardiography in the detection of reperfusion following thrombolytic therapy. 818 67

Acute myocardial infarction results from the cessation of myocardial blood flow caused by thrombotic occlusion of a coronary artery. Rapid restoration of blood flow to the ischemic myocardium minimizes cardiac damage and improves early and long-term morbidity and mortality. Chest pain is the first symptom of myocardial infarction, but in some patients with silent ischemia, the disease can be diagnosed only in retrospect. In symptomatic patients, myocardial infarction should be accurately and promptly diagnosed so that reperfusion therapy can begin immediately. Electrocardiography is the simplest diagnostic modality. Although regional ST-segment elevation is specific, it is not sensitive. In contrast, new computerized algorithms for electrocardiographic analysis and serial monitoring increase sensitivity without decreasing specificity. In the emergency room, echocardiography is used to diagnose patients with no prior history of coronary artery disease whose electrocardiograms proved nondiagnostic. Time-consuming perfusion nuclear studies are inferior to echocardiography but may nevertheless enable physicians to diagnose myocardial infarction in the emergency room. Although the presence of excess creatine kinase is a sign of myocardial necrosis, its increase is delayed for a few hours after coronary occlusion. Doctors can diagnose myocardial infarction as early as two hours after coronary occlusion with the help of simpler automatic assays of MB-creatine kinase mass that use monoclonal antibodies. Other investigational markers of myocardial necrosis include myoglobin and troponin. Elevation of a circulating protein marker also signifies established necrosis, but physicians hope to achieve reperfusion through therapy before irreversible damage occurs.
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PMID:The earliest diagnosis of acute myocardial infarction. 819 86

The role of polymorphonuclear neutrophils (PMN) in the injury of the heart following ischemia and reperfusion is still controversial. The aim of this study was to investigate whether small numbers of PMN may cause myocardial dysfunction in an isolated system, how the resulting loss of function can be characterized and whether the formation of hypochlorous acid (HOCl) can be responsible for the PMN-mediated effect. Isolated working guinea pig hearts were subjected to a 90% reduction of coronary flow for 30 min, with or without intracoronary infusion of homologous PMN (approximately 1-2 x 10(5) cells/min, i.e. about 5-10% of normal blood count). This ischemia was followed by a 15 min reflow period in a non-working ("Langendorff") mode before work was resumed. In hearts perfused only with buffer, post-hypoxic heart function recovered to 75-80% of the initial value. Inclusion of unstimulated PMN did not further attenuate cardiac function. However, cardiac output was decreased to 42% of the initial value, provided thrombin (0.3 U/ml) and H2O2 (10(-5) M) were also present, and the retained PMN (about 10% of those infused) were additionally stimulated during reflow by application of FMLP (10(-6) M for 1 min). In these instances, coronary flow at any time of the experiment and release of lactate or purines during ischemia and reflow did not differ significantly between hearts perfused with or without PMN. There was no substantial release of myoglobin in controls and in PMN-treated hearts. Inotropic stimulation of the hearts with noradrenaline or exogenous Ca2+ caused a sustained increase in contractile force. However, the response was significantly reduced in PMN-perfused hearts in comparison to control hearts. The myocardial contents of high-energy phosphates with and without inotropic stimulation proved to be identical irrespective of whether experiments had been performed in the absence or presence of PMN. A similar loss of myocardial function as mediated by PMN could be produced by infusing chemically generated hypochlorous acid (HOCl, 5 x 10(-7) M for 10 min). Strikingly, that portion of the infused HOCl which actually reacted with cardiac tissue was comparable to the amount shown to be generated by stimulating 10(6) PMN retained in the coronary system (about 7 nmoles). Supplementing the perfusate with the scavengers L-methionine (10(-4) M) or uric acid (5 x 10(-4) M) prevented the attenuation of heart function provoked by PMN. The results indicate that small numbers of PMN, sufficiently activated, can depress cardiac function after 30 min of ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Postischemic dysfunction of the heart induced by small numbers of neutrophils via formation of hypochlorous acid. 824 Feb 25

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early clinical, electrocardiographic and biological criteria of reperfusion after intravenous fibrinolysis during the acute phase of myocardial infarction]. 827 57

Bowel infarction can complicate acute aortic dissection (AAD); in that case early diagnosis, which decreases the high mortality, is often difficult. We report the case of one patient who underwent surgery for AAD and developed a colonic infarction, which was clinically manifest on the 4th postoperative day. However, bowel ischemia was suspected already 48 hours after surgery, on the basis of the suggestive CK pattern and the absence of myoglobin in plasma. Total CK activity reached the highest level only 48 hours after surgery (92,800 U/l); the peak was coincident with LDH, which increased proportionally less; CK-MM constituted 100% of total CK activity. The absence of myoglobin in plasma excluded the presence of rhabdomyolysis. We conclude that such laboratory findings suggest the occurrence of severe bowel ischemia.
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PMID:Creatine-kinase isoenzyme pattern in colonic infarction consequent to acute aortic dissection. A case report. 834 80

Stressful stimuli such as heat, oxidative stress, heavy metals, and tissue trauma induce the expression of a family of proteins commonly referred to as stress proteins or heat shock proteins. The functions of these proteins are varied but include glycolysis, antioxidant defense, and several postulated "chaperone" functions involving the folding, unfolding, and translocation of other proteins. Heme oxygenase, the enzyme that catalyzes the degradation of heme to biliverdin, is also heat inducible and is, therefore, a heat shock protein. In the kidney, ischemia has been observed by several investigators to induce expression of the more commonly studied heat shock proteins HSP 70 and HSP 72. In addition, exposure of the kidney to myoglobin after glycerol injection induced heme oxygenase. The purpose of this study was to determine whether heme oxygenase is expressed as a stress protein after renal ischemia. Renal ischemia was induced in rats after right nephrectomy by clamping the renal artery for 40 minutes. Gene expression was evaluated after 60 minutes to 96 hours of postischemic reperfusion. There was essentially no expression of heme oxygenase at any of the time points evaluated. The absence of heme oxygenase expression was in striking contrast to the prompt and dramatic expression of HSP 70. This finding is consistent with the concept that all "stress proteins" are not equivalent and that, although there is considerable overlap between heat-sensitive gene promoters and oxidant stress-sensitive gene promoters, there is specificity for the type of stimulus that is able to activate any given stress protein gene.
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PMID:Heme oxygenase is not expressed as a stress protein after renal ischemia. 840 10


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