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

We produced myocardial ischemia in 18 mongrel dogs by ligating the left anterior descending coronary artery. The animals were killed 0.5 to 24 hours after the onset of ischemia to study the intracellular diffusion of myoglobin by immunofluorescence and electron microscopy employing colloidal gold particles coated with antibody to myoglobin. In areas that showed early ischemia (0.5, 1, and 2 hours), myoglobin had diffused into the nuclei and mitochondria of ischemic cells. This intranuclear diffusion of myoglobin was transient as it was not present in the 4-, 6-, 12-, and 24-hour areas of ischemia. This appearance and subsequent disappearance of intranuclear myoglobin may be useful in identifying early areas of myocardial ischemia that are not evident by histologic techniques. This pattern of diffusion may also be helpful in studying other types of cell injury.
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PMID:Intracellular diffusion of myoglobin. A manifestation of early cell injury in myocardial ischemia in dogs. 620 21

The myoglobin concentration, creatine kinase and creatine kinase sub-unit B activity were estimated in fourteen patients with ischaemic heart disease before and after exercise induced angina pectoris. No changes in these parameters were found.
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PMID:Myoglobin concentration, creatine kinase, and creatine kinase sub-unit B activity in serum after myocardial ischaemia. 652 13

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

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

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

A 22-year-old man developed transient unconsciousness during running. He developed fever, nausea, vomiting, diarrhea and general fatigue. Next day, he was admitted to National Hospital Nayoro because of high serum CK level of 13,610U/l. Biochemical analyses revealed elevated serum myoglobin, increased CK-MM isozyme, aldolase and lactate dehydrogenase, increased serum osmolality, increased uric acid, and decreased serum potassium levels. Therefore, he was diagnosed as having rhabdomyolysis. In addition, serum CK-MB isozyme, cardiac myosin light chain I and troponin T were increased, suggesting the damage of cardiac muscle. Electrocardiogram showed elevated ST segment and inverted T on V2-4, which were not observed previously. He had no preceding infectious disease, drug ingestion or an underlying metabolic disorder. The rhabdomyolysis may be precipitated by the superimposition of dehydration and loss of potassium due to diarrhea and vomiting. The myocardial injury, probably produced by transient myocardial ischemia, should be paid attention in case of rhabdomyolysis.
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PMID:[A case of rhabdomyolysis complicated with myocardial injury]. 856 47

Previous studies on cytoskeletal changes of in vitro and in vivo animal models of ischemic myocardium have suggested the possibility of using alterations in cytoskeleton proteins as an early marker for the post-mortem diagnosis of myocardial ischemia in cases of sudden death due to coronary artery disease (CAD). In the present study, using the technique of ABC-immunohistochemistry, we examine the changes of three cytoskeletal proteins: vinculin, desmin and alpha-actinin in human myocardial samples taken from 14 cases of CAD sudden death and 13 cases of non-CAD death. Results of these examinations are compared with immunohistochemical changes of myoglobin and histochemical staining of hematoxylin and eosin and phosphotungstic acid, and Masson trichrome. Patchy and extensive loss of the three cytoskeletal proteins was demonstrated in the myocardium of victims who died 1 h or later following the onset of symptoms of ischemic myocardium. The pattern of cytoskeleton change is equivocal in the cases of CAD who died less than 1 h after the onset of symptoms and of the cases of non-CAD. In these cases, no significant histological change was observed. With less non-specific background changes and stronger positive staining, immunohistochemical staining of the three cytoskeletal proteins is more reliable than myoglobin, which has attracted the attention of many pathologists searching for anatomic evidence of ischemic myocardium in coronary artery disease.
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PMID:Cytoskeleton immunohistochemical study of early ischemic myocardium. 868 23

Recently Dr. Rowe made a hypothesis according to which small areas of myocardial necrosis can be caused by microvascular spasm, related to high catecholamine concentrations and other mechanisms, following extraordinary unremitting endurance exercises or due to the cumulative effect of several endurance events. It was this last suggestion which prompted us to investigate 25 top cyclists, taking part in the 77th Giro d'Italia. Blood samples were obtained the day before the start of the competition and once a week thereafter until the end. We measured myoglobin, lactic dehydrogenase, total creatine kinase, creatine kinase isoenzyme MB and serum cardiac troponin T (Tn-T), a highly sensitive and specific method for the detection of myocardial injury. While at measuring time points which followed we found a significant increase in the serum indicators of muscle damage, compared with their values at the beginning of the race, creatine kinase isoenzyme MB did not rise significantly and cardiac Tn-T was found in the serum of only 5 athletes, repeatedly in some cases, but always below the cut off values considered as indicating myocardial ischemia. On the basis of the behaviour of creatine kinase isoenzyme MB and, above all, of cardiac Tn-T, we can conclude that heavy endurance exercises, repeated daily for 22 days, as was the case in our study, do not seem able to produce, in top athletes, permanent heart damage by means of acute myocardial injury.
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PMID:Serum cardiac troponin T after repeated endurance exercise events. 881 6

It has been shown by a number of authors that early myocardial infarction constitutes a dynamic process of cyclic oscillation between coronary occlusion and spontaneous coronary reopening. Infarct-markers, such as ST-segment elevation, serum-creatine kinase isoenzyme MB, the atrionatriuretic peptide (ANP) and serum-myoglobin (Mb) exhibit cyclic behaviour pattern during early AMI and thus reflect episodes of intermittent, spontaneous reperfusion. The latter have recently been verified by angiography. The mechanism underlying the phenomena seen in early myocardial infarction is likely to be based on a constant vasoconstrictive stimulus, deriving from aggregating platelets. The vasoconstriction subsequent to platelet aggregation produces an initial episode of myocardial ischemia. This episode is followed by a hypoxia of the artery wall. Reactive coronary dilation secondary to ischemia is than promoted by the release of vasoactive by-products of anaerobic glycolysis as well as changes in the open propability of certain transmembrane ion channels. Thereafter, the initial coronary occlusion is interrupted by transient vasodilation. A wave of reperfusion follows and leads to reoxygenation and wash-out of ischemia-induced vasodilative components as well as biochemical markers. The vasoconstrictive forces then take over again. This results in repeated waves of reperfusion. A number of arguments in favour of this concepts are discussed in this paper.
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PMID:Cyclic phenomena in early myocardial infarction. 883 24

A 54-year-old male experienced the Hanshin earthquake at 5:46 am on Jan. 17, 1995. He was rescued after being buried under his house for 20 h. After being treated at two hospitals, he was admitted to our hospital with acute renal failure caused by crush syndrome. The maximal serum creatinine kinase level was 35,000 IU/L (CK-MM: 100%), and the maximal myoglobin level was 12,600 ng/ml. An electrocardiogram showed inverted T waves in V5,6 which later became giant negative T waves, and a QS pattern in a VL and V1-6. Two-dimensional echocardiography showed a hypokinetic left ventricle. He was treated with hemodialysis 13 times. Cardiac contraction gradually improved to the normal level. Coronary angiography revealed normal coronary arteries and acetylcholine did not induce coronary spasm. Biopsy specimens from the right ventricular septum showed slight degeneration. 201Tl imaging showed hypoperfusion except in the anterior wall and 123I-MIBG imaging showed a perfusion defect except in the anterior wall. After about 1 month, only 201Tl imaging showed improvement. We believe that myocardial ischemia, cardiac sympathetic nerve damage and/or cardiac contusion caused giant negative T waves and left ventricular dysfunction. This is a rare case which showed significant myocardial damage with crush syndrome.
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PMID:A case of Crush syndrome with giant negative T waves and reversible left ventricular dysfunction. 893 45


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