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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of myoglobin in plasma was assessed before and up to 68 hours after tourniquet release in 27 patients who underwent elective operations with no incision into skeletal muscle. The duration of ischemia was 1-3 hours. A control group underwent the same kind of surgery without the use of tourniquet. There was a minimal elevation in myoglobin values after 65 and 90 minutes of ischemia, and a marked elevation after more than 150 minutes of ischemia. Maximum values were reached 8 to 10 hours after tourniquet release, and preoperative values after 50 to 60 hours.
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PMID:Myoglobin release after tourniquet ischemia. 342 87

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.
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PMID:New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI. 354 66

The relative time courses of early changes in myocardial metabolism and function during anoxia, global ischemia, and regional ischemia were compared in isolated rat hearts. Transmural anoxic wave front was determined with NADH fluorescence photography, and oxygen saturation of myoglobin and dynamic systolic wall thickening were measured with spectrophotometry of light transmitted through the left ventricular free wall. In all three treatments, anoxic wave front first appeared in the subendocardium and reached the epicardial half of the myocardium in 10 s, when oxygen saturation of myoglobin decreased by 50% and tissue ATP and creatine phosphate remained at aerobic levels. During this period, systolic wall thickening decreased gradually in anoxia and global ischemia, whereas a marked decrease in systolic wall thickening and appearance of dyskinesia (wall thinning) occurred in regional ischemia. Thus the early extension of anoxic wave front and metabolic changes are similar with all three treatments, and dyskinesia, observed only in case of regional ischemia, occurs when the inner half is ischemic or anoxic.
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PMID:Transmural anoxic wave front and regional dysfunction during early ischemia. 361 98

The effect of an antioxidant dibunol and calcium antagonist verapamil on postperfusion release of myoglobin (Mb) and MB-creatine kinase (MB-CK) has been assessed in 30 dogs with experimental coronary occlusive myocardial infarction. It has been shown that reperfusion after 3-hour ischemia does not only accelerate the release of intracellular proteins, but also leads to pronounced myoglobinemia and blood enzymes. In postischemic blood flow recovery with combined dibunol and verapamil preliminary injections, an almost threefold decrease in MB-CK and Mb blood content, as compared to "reperfusion" indexes, was observed by the 10th minute of reperfusion.
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PMID:[Effect of dibunol and isoptin on the creatine kinase and myoglobin content of the blood serum in dogs undergoing postischemic coronary reperfusion]. 367 55

Possible enhancement of myocardial protection by oxygenation of a crystalloid cardioplegic solution was evaluated in a three-part study. In Part I, canine hearts underwent ischemia followed by heterogeneous cardioplegic arrest for 45 to 60 minutes. Oxygenation led to improved recovery in the left anterior descending region (47% versus 86% recovery, p less than 0.05) (15 minutes of ischemia) and in the circumflex region (9.5% versus 52% recovery, p less than 0.05) (30 minutes of ischemia). Part II was a blind prospective randomized study in 12 patients. It examined creatine kinase, myoglobin, and lactate as well as coronary sinus flow, oxygen consumption, and cardiac work 1 hour after aortic cross-clamping during atrial and during ventricular pacing. No significant difference was demonstrable between control and oxygenated solutions. In Part III, 57 coronary bypass patients were protected with a nonoxygenated solution while 94 patients received an identical oxygenated solution. Twelve-hour creatine kinase levels were similar in the nonoxygenated (9.5 +/- 16 IU, +/- standard deviation) and oxygenated (11 +/- 22 IU) groups if the cross-clamp interval was 28 minutes or less. In patients subjected to longer than 28 minutes of arrest, the 12 hour creatine kinase MB levels were more than twice as high in the nonoxygenated group (26.5 +/- 26 IU) compared to the oxygenated group (9.9 +/- 14 IU, p less than 0.05). In this canine model of heterogeneous cardioplegia and in the routine conduct of coronary bypass operations, oxygenated crystalloid cardioplegia is superior to an identical nonoxygenated solution.
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PMID:Improved myocardial recovery after cardioplegic arrest with an oxygenated crystalloid solution. 387 82

Recently, prostacyclin (PGI2) has been reported to have a role of potential importance in myocardial ischemia. The direct effects of PGI2 on ischemic myocardial injury (60 minutes ischemia at 30 degrees C) were examined, using a hemoglobin free isolated rat heart perfused by the Langendorff's technique. Dual-wavelength reflectance spectrophotometry was used to measure myoglobin oxygenation in cardiac tissue, from which the intracellular oxygen concentration was calculated. The effect of PGI2 on cardial function under normoxic perfusion condition was studied. PGI2 was infused for 10 minutes with the doses of 5ng/g X body weight per minute. PGI2 infusion increased heart rate, LV dp/dt and myocardial oxygen consumption. The average 9.7% increase in myoglobin oxygenation was noted during PGI2 infusion which indicated the improvement in tissue oxygen metabolism. The global ischemia was produced for 60 minutes at 30 degrees C, following to the pretreatment of 10 minutes infusion of PGI2, by the discontinuation of Langendorff's perfusion. Recovery of cardiac function such as double product and LV dp/dt at 15 minutes after reperfusion was significantly higher in the PGI2 treated group than in hearts receiving only the vehicle. Infusion of PGI2 inhibited the decrease in ATP level of the ischemic myocardium at 15 minutes after reperfusion (P less than 0.025, P less than 0.05). PGI2 prevented the increase in lactate release from the ischemic myocardium, observed in vehicle group at 1 minutes after reperfusion. In summary, prostacyclin seems to have a direct cytoprotective effect on ischemic myocardium.
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PMID:[Effects of prostacyclin on the cardiac functions and energy metabolism in the perfused rat heart]. 389 89

Perfusion of rat hearts according to the Langendorff technique with micromolar concentrations of palmitoylcarnitine or millimolar concentrations of phenylmethylsulfonyl fluoride protect the heart from deterioration by reperfusion after total-ischemia. This is based on the retention of the cytosolic enzymes determined (lactate dehydrogenase, glycogen phosphorylase and glycogen synthase) and of myoglobin, as well as on the resumption of contractile activity. Palmitoylcarnitine, like phenylmethylsulfonyl fluoride, could protect through plasma membrane stabilization, since more hydrophilic compounds had no effect.
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PMID:Protection by acyl-carnitines and phenylmethylsulfonyl fluoride of rat heart subjected to ischemia and reperfusion. 393 96

It has not previously been possible to study the in vitro effects of reperfusion on severely injured isolated perfused hearts because of the development of the no-reflow phenomenon, concomitant with the onset of irreversible myocardial cell injury. A new model of ischemic injury which utilizes an intraventricular balloon to allow uniform reperfusion of irreversibly damaged hearts is described. The effects of reperfusion were studied in Langendorff perfused rat hearts after no-flow ischemia for 60 and 150 minutes at 37 C. Uniform reflow was facilitated by maintaining the left ventricle at an isovolumic diastolic volume with a balloon during ischemia and removal of the balloon prior to reflow. Reperfusion was with 1) anoxic media, 2) oxygenated media, 3) oxygenated media in the presence of the mitochondrial inhibitor Amytal, or 4) an initial anoxic reperfusion followed by oxygenated media. Injury was monitored by the assay of released creatine kinase (CK) and myoglobin (Myo), by light-microscopic estimates of the percent of cells containing contraction bands, and by ultrastructural changes. CK and Myo were released with anoxic reperfusion, but larger releases occurred with oxygenated reperfusion. Amytal inhibited the oxygen but not the nitrogen component of release. Contraction bands occurred following oxygenated, but not anoxic, reperfusions and were inhibited by Amytal. Following an initial anoxic reperfusion, oxygen caused additional CK and Myo release and produced an increase in the percent of cells with contraction bands, compared with that with oxygen alone. The response of cells to injury was heterogeneous, and the hearts contained cells with a spectrum of ultrastructural changes. Anoxic reperfusion was associated with cellular swelling and oxygenated reperfusion with contraction band necrosis.
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PMID:Effects of anoxic or oxygenated reperfusion in globally ischemic, isovolumic, perfused rat hearts. 401 39

A 23-year-old male was admitted to hospital with severe dehydration and hypokalemic myopathy due to secondary aldosteronism. On admission serum sodium and chloride were markedly elevated to 198 mEq/l and 169 mEq/l, respectively, and serum potassium was down to 2.3 mEq/l. Serum electrolytes were normalized by transfusion therapy, but subsequently rhabdomyolysis grew worse due to metabolic abnormalities such as dehydration, hypothermia, oppressive ischemia and metabolic acidosis, at the same time transient polyuria and the elevation of serum myoglobin and enzymes originating in muscle tissue were observed. Serum CPK went up to 26,532 IU/l on the sixth day and other enzymes reached a peak following CPK. Dexamethasone was administered when the increase in enzyme levels caused the patient to fall into a stupor. He rapidly regained consciousness from the 15th day after admission, and he was able to stand up on the 29th day. Serum enzymes originating in muscle tissue decreased gradually to the normal range by the 30th day and no renal failure occurred.
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PMID:A case of severe dehydration with marked rhabdomyolysis. 402 Dec 12

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


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