Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endomyocardial biopsies were taken from the apex of the left ventricle in 15 patients operated on for aortic valve disease or ischaemic heart disease and from papillary muscles in six patients operated on for mitral valve disease. Activities of cardiac phosphofructokinase (PFK), total lactate dehydrogenase (LD), its isoenzyme LD1, aspartate aminotransferase (ASAT), total creatine kinase (CK), its isoenzyme MB, citrate synthase (CS) and myoglobin content (MYO) were related to the angiographically determined left ventricular function. Activities of total LD, PFK and PFK/CS ratio were lower in patients with decreased, than in those with normal, left ventricular function. Myoglobin content and activities of CS and ASAT were not related to left ventricular function. It is suggested that depressed left ventricular contractility is associated with a decreased glycolytic capacity while the oxidative capacity is mainly unaltered.
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PMID:Key enzymes of myocardial energy metabolism in patients with valvular heart disease: relation to left ventricular function. 297 29

Myocardial ischemia was produced in 12 dogs by ligation of the anterior descending branch of the left coronary artery. The animals were sacrificed 0.5, 1, 3, 6, 12, and 24 hours later. The ischemic area was compared with control tissue from the posterior aspect of the left ventricle as to the glycogen content, myoglobin content, intracellular diffusion of IgG, diastase resistant-periodic acid-Schiff (PAS) (D-PAS) staining material and basic fuchsin-staining material. In the earliest time period studied, 0.5 hours, glycogen loss marked a large area of ischemic change. Myoglobin loss, intracellular diffusion of IgG, D-PAS-staining material and basic fuchsin-staining material were also found but involved only a small area within the glycogen-depleted zone. As the length of ischemic period increased, the area occupied by these changes approached the size of the area of glycogen loss. In all animals, the area of myoglobin loss, intracellular diffusion of IgG, D-PAS staining and basic fuchsin staining were in the area of glycogen loss. The IgG, D-PAS, and basic fuchsin parameters, in turn, were within the area of myoglobin loss but usually did not completely fill it. That is, some fibers showing myoglobin loss did not show the other changes. Can any of these changes serve as early markers for irreversible ischemic injury? Glycogen loss clearly does not. Additional data are needed to determine whether the extracellular diffusion of myoglobin and the intracellular diffusion of IgG are markers of irreversible injury.
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PMID:Diffusion of myoglobin in the diagnosis of early myocardial ischemia. 703 95

Myoglobin, myosin creatine kinase MM (CK-MM), creatine kinase BB(CK-BB) in cardiac muscle and H chain of myosin in atrial and ventricular muscle were studied in specimens from 8 patients who died of sudden nocturnal death syndrome (SNDS) by avidin-biotin complex (ABC) method to investigate the possible early or very early myocardial ischemia in the syndrome. Hematoxylin-eosin staining was conducted for comparison. The results showed evident loss of CK-MM, CK-BB, myoglobin and myosin from cardiac muscle cells, indicating that occurrence of SNDS is closely associated with acute myocardial ischemia.
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PMID:Changes of myocardial myoglobin, myosin and creatine kinase in cases of sudden nocturnal death syndrome. 818 70

The source(s) of reactive partially reduced oxygen species associated with myocardial ischemia/reperfusion injury remain unclear and controversial. Myoglobin has not been viewed as a participant but is present in relatively high concentrations in heart muscle and, even under normal conditions, undergoes reactions that generate met (Fe3+) species and also superoxide, hydrogen peroxide, and other oxidants, albeit slowly. The degree to which the decrease in pH and the freeing of copper ions, as well as the variations in pO2 associated with ischemia and reperfusion increase the rates of such myoglobin reactions has been investigated. Solutions of extensively purified myoglobin from bovine heart in 50 mM sodium phosphate buffer were examined at 37 degrees C. Sufficiently marked rate increases were observed to indicate that reactions of myoglobin can indeed contribute substantially to the oxidant stress associated with ischemia/reperfusion injury in myocardial tissues. These findings provide additional targets for therapeutic interventions.
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PMID:Potential roles of myoglobin autoxidation in myocardial ischemia-reperfusion injury. 1040 2

The objective was to test the hypothesis that a protocol using myoglobin and creatine kinase-MB (CK-MB) can rapidly and safely exclude myocardial infarction (MI). The study used a prospective, convenience cohort of ED patients with clinically suspected myocardial ischemia. Myoglobin was measured on presentation, 2 and 6 hours later; CK-MB was measured on presentation, 6, 12, and 18 hours later. Of 519 patients, 76 (15%) had MIs, all of whom "ruled in" within 12 hours using a combination of myoglobin and CK-MB, for a sensitivity of 100% (95% CI, 95% to 100%), specificity of 92% (95% CI, 89% to 94%), LR (+) of 12 (95% CI, 9 to 16), and an LR (-) of 0.03 (95% CI, 0.0 to 0.05). Of the 76 patients with MIs, 73 ruled in with a 6 hour protocol, also using a combination of CK-MB and myoglobin, for a sensitivity of 96% (95% CI, 89% to 99%), specificity of 92% (95% CI, 89% to 94%), LR (+) of 11 (95% CI, 8 to 16), and an LR (-) of 0.04 (95% CI, 0.01 to 0.12). Our results support the hypothesis that, using an abbreviated protocol with CK-MB and myoglobin, MI can be reliably ruled out in ED patients with suspected ischemia.
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PMID:Six-hour versus 12-hour protocols for AMI: CK-MB in conjunction with myoglobin. 1132 40

Hydrogen peroxide (H2O2) is implicated in cardiac myocyte (CM) damage during myocardial ischemia-reperfusion (IR) injury. Myoglobin (Mb) is present in CM at significant concentrations and reacts with H2O2 to yield one- and two-electron oxidants that may promote myocardial injury. Paradoxically, hearts from mice lacking Mb are more susceptible to H2O2-induced dysfunction than the corresponding controls [U. Flogel, A. Godecke, L.O. Klotz, J. Schrader, Role of myoglobin in the anti-oxidant defense of the heart, FASEB J. 18 (2004) 1156-1158]. We have overexpressed wild-type or Y103F variant of human Mb in cultured CMs to test whether Mb protects against H2O2 insult. Contrary to expectation, cells expressing WT or the Y103F Mb show increased mitochondrial dysfunction and apoptosis, and decreased ATP in response to H2O2 that follows the order native < Y103F Mb < WT human Mb consistent with the increasing pro-oxidant activity for these proteins. These data indicate that (i) Mb promotes oxidative damage to cultured CM and (ii) Mb may be a useful target for the design of inhibitors of myocardial IR injury.
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PMID:Expression of human myoglobin in H9c2 cells enhances toxicity to added hydrogen peroxide. 1688 98

The goal of this study was to assess whether early markers of myocardial ischemia, identified in a previous experimental work, can be applied in forensic pathology cases of sudden, ischemic cardiac death. These markers include desphosphorylated connexin 43 (Cx43), JunB, TUNEL assay, myoglobin, and troponin T. Fourteen cases of sudden cardiac death with gross and/or histological signs of myocardial infarction and 14 cases of sudden cardiac death with signs of early ischemia at histology and positive immunoreactions for fibronectin and C5b-9 were investigated. The control group was represented by 15 hanging (global hypoxia) cases. Immunohistochemical reactions were classified into four degrees and compared among groups. Cx43 and JunB were significantly more expressed in hanging than in ischemia/infarction, but they showed a different distribution in the tissue (sub-endocardial in ischemia/infarction, diffuse in hanging) and a different intensity of the signal. TUNEL assay was significantly more expressed in the group of early ischemia than in myocardial infarction. Myoglobin and troponin T did not show any significantly different expression among the three groups. Depletion markers have a limited application in forensic cases, and this is mostly because positive (depleted) areas are difficult to distinguish from artifactually paler areas. Nuclear markers (JunB and TUNEL), on the other hand, require a well-trained eye and a high magnification in order to be distinguished. Cx43, JunB, and TUNEL assays were confirmed to be early, sensitive markers for myocardial ischemia. Nonetheless, they are not specific, as they are expressed in global hypoxia as well, but with a different tissular distribution.
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PMID:Early markers of myocardial ischemia: from the experimental model to forensic pathology cases of sudden cardiac death. 2849 98