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)

Reflectance spectroscopy was utilized to monitor the oxidation states of myoglobin (Mb) in isolated, buffer-perfused rat hearts. Hearts were subjected to 30 min global, no-flow ischemia, followed by reperfusion under anoxic conditions. The addition of Na2S to the buffer at reperfusion permitted the detection of ferryl myoglobin (MbIV) as its sulfmyoglobin derivative. The accumulation of MbIV was prevented by addition of ascorbic acid (1 mM), ergothioneine (2 mM), or desferal (1 mM) to the buffer prior to ischemia. Ascorbate and other agents have been previously shown to serve as one-electron reductants of MbIV. We propose that during the early phases of ischemia, deoxymyoglobin is oxidized to MbIV by residual H2O2. It also seems reasonable that the peroxidative activity of Mb(IV), during oxygenated reperfusion, might lead to cellular damage if this hypervalent form of Mb is not reduced.
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PMID:Detection of ferryl myoglobin in the isolated ischemic rat heart. 207 31

In cases of myocardial hypertrophy myocardial protection may be insufficient. In order to determine the factors responsible for myocardial injury we assessed myocardial injury in 54 patients undergoing isolated aortic valve replacement. In all cases hypothermic cardioplegic arrest was induced. At 13 different times we measured the serum level of creatine-kinase (CK), myocardial bound creatine-kinase (CKmb), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), glutamic oxaloacetic transferase (GOT) and myoglobin. The mean duration of ischemia was 52.6 +/- 16.2 minutes and the mean time of extracorporeal circulation was 85.85 +/- 20.25 minutes. By performance of a multiple regression analysis a significant correlation between ischemia and LDH and alpha-HBDH was found; CK, GOT, LDH and alpha-HBDH correlated with duration of extracorporeal circulation. In none of the patients was a low cardiac output syndrome observed. From our results we conclude that in our study myocardial protection was sufficient and therefore the detrimental effects of extracorporeal circulation were the determining factors of enzyme release.
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PMID:Perioperative myocardial injury in patients undergoing aortic valve replacement. 214 89

EIA was used to demonstrate that the development of acute ischemia of the heart muscle progressing to necrosis is accompanied by an increase of the concentration of cytochrome c and antibodies against cytochrome c in the blood serum. As regards its specificity and sensitivity, the alteration in the antibody concentration is comparable with that in the myoglobin concentration but it is marked 1 to 3 hours earlier. The high level of antibodies against cytochrome c remaining unchanged for 2 to 3 days in myocardial infarction patients attests to the possibility of a complicated, often relapsing course of the disease. The test for determining antibodies against cytochrome c may be recommended for the control over the patient's status and forecasting the course of myocardial infarction.
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PMID:[Determination of the concentration of cytochrome c and its antibodies in the blood serum for the diagnosis and prognosis of complications in myocardial infarct patients]. 216 94

Myocardial oxygenation may be altered markedly by changes in tissue blood flow. During brief ischemia and reperfusion produced by transient occlusion of the left anterior descending artery in 10 open-chest dogs, changes in the oxygenation of tissue hemoglobin (Hb) plus myoglobin (Mb) and the oxidation-reduction (redox) state of mitochondrial cytochrome aa3 were monitored continuously using near-infrared spectroscopy. The nondestructive optical technique indicated that coronary occlusion produced an abrupt drop in tissue oxygen stores (tHb02 + Mb02), tissue blood volume (tBV), and the oxidation level of cytochrome aa3. Changes in the cytochrome oxidation state were related inversely to transmural collateral blood flow within the ischemic region (r = 0.77) measured with radiolabeled microspheres. Furthermore, there was a direct relationship (r = 0.91) between collateral blood flow and the tissue level of desaturated Hb and Mb (tHb + Mb). Reperfusion after 2 min of ischemia led to a synchronous overshoot of baseline in coronary flow and tBV followed by supranormal increases in tHb + Mb02 and the oxidation level of cytochrome aa3. The tHb + Mb level increased transiently during reperfusion. This response correlated inversely with collateral flow during ischemia (r = 0.91). Accordingly, the time required to reach peak tHb + Mb levels was shortest in dogs with high collateral flows (r = 0.75). Thus collateral blood flow partially sustains myocardial oxygenation during coronary artery occlusion and influences tissue reoxygenation early during reperfusion.
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PMID:Dynamic mechanisms of cardiac oxygenation during brief ischemia and reperfusion. 217 24

In 10 patients undergoing aortic bypass grafting with peroperative aortic cross-clamping we measured the levels of myoglobin and creatine phosphokinase. The duration of peroperative lower limb arterial clamping ranged from 50 min to 95 min. No significant increase in either serum myoglobin or in serum creatine phosphokinase was found during lower limb arterial clamping or for the first two hours after release of ischemia. Both parameters reached a maximum value at 24 hours after release of ischemia, with a median serum myoglobin concentration of 565 micrograms/l (range: 132-2688 micrograms/l) and a median serum creatine phosphokinase activity of 457 U/l (range: 190-1602 U/l). The increase in serum myoglobin and creatine phosphokinase was not associated with the duration of lower limb arterial clamping. Renal impairment was not found in these patients, as evaluated by the serum concentration of beta 2-microglobulin.
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PMID:Myoglobin and creatine phosphokinase in serum during and after aortic bypass grafting. 243 46

The relationship between the progression of sarcolemmal damage and the appearance of amorphous matrix densities (AMDs) within myocardial mitochondria in the early phase of ischemia was studied in coronary-ligated rats by means of electron microscopy. The animals were divided into six groups according to the duration of ischemia (from 10 to 120 min). The severity of sarcolemmal damage was graded into four classes according to the ultrastructural ischemic changes, as follows: grade 0, normal cells; grade 1, slight ischemic changes in cellular organelles but intact sarcolemma; grade 2, formation of subsarcolemmal blebs, but overall sarcolemmal integrity; and grade 3, sarcolemmal disruption. In the experiment, grade 1 cells decreased and those of grade 3 increased with a longer period of ischemia. The appearance of grade 3 cells was distinct at 30 min of ischemia. This cellular damage proceeded from the subendocardial layer to the subepicardial layer indicating the "wavefront phenomenon." The number of AMDs within the mitochondria increased as the sarcolemmal damage became more severe. It was noteworthy that AMDs could be found in cells with an intact sarcolemma after subjection to 10 min of ischemia. Myoglobin staining of the myocardium obtained after 10 min of ischemia followed by 6 hr of reperfusion revealed no loss of myoglobin, indicating no irreversible cell damage. This finding suggests that the formation of AMDs may occur prior to the disruption of the sarcolemma or irreversible cell damage.
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PMID:Relationship between sarcolemmal damage and appearance of amorphous matrix densities in mitochondria following occlusion of coronary artery in rats. 259 63

Detailed review of the literature for chest discomfort evaluation in the Emergency Department leaves the clinician without a precise guideline as to whom to admit or send home. It is clear that the seasoned physician's instinct (the sum total of the history, physician examination, and ancillary laboratory tests) is as good an indicator as existing statistical decision models. Current decision rules appear most helpful as teaching aids for physicians-in-training and for providing reassurance to seasoned physicians. Although ancillary tests such as echocardiography and rapid myoglobin analysis may play more important roles in the future, emergency physicians must now rely primarily upon their clinical impression to guide admission decisions. Vigorous attempts to minimize the admission of patients without ischemia to the CCU will increase the incidence of infarction patients released from the Emergency Department. The liberal use of intermediate care unit beds may represent one future disposition alternative. Nonetheless, each physician must establish his or her own threshold for admission. Several studies have found a 5 per cent unintentional release of infarction patients from the Emergency Department. Decreasing the admission threshold may lower this rate substantially. Patients with chest discomfort who are released from the Emergency Department require close followup. At urban teaching hospitals, where private physician referral is often limited, the institution may need to establish a clinic specifically for this purpose. Unrecognized myocardial ischemia is one rationale for close followup; however, the pursuit of alternative diagnoses including gastrointestinal and psychiatric (e.g., panic disorders) etiologies may minimize subsequent morbidity in the released population.
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PMID:Detection of myocardial ischemia/infarction in the emergency department patient with chest discomfort. 328 Mar 3

The time course of the loss of myoglobin from the rat ventricular myocardium in the early phase of ischemia was studied with the use of an immunohistochemical technique and an image analyzer. The loss of myoglobin, as an index of myocardial injury, was evident in the left ventricular subendocardium as early as 0.5 hr after occlusion of the left main coronary artery. A clear-cut demarcation of the myoglobin-depleted area helped quantification of the injured areas with an image analyzer. The area with depleted myoglobin became transmural and reached maximum after 2 and 3 hr of occlusion, respectively. Electron microscopic observation of the myoglobin-depleted region revealed amorphous dense bodies in the mitochondria, indicating irreversible damage to the myocardial cells. On the other hand, no irreversible changes could be detected with hematoxylin-eosin stain until 6 hr after the start of the ischemia, and the distinction between the reversible and irreversible areas was unclear. We suggest that depletion of myoglobin from the myocardium serves as a marker for irreversible ischemic injury. Quantitative assessment of the injured areas by immunohistochemical staining for myoglobin together with an image analyzer could be of great value for the evaluation of early ischemic myocardial damage.
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PMID:Early loss of myocardial myoglobin detected immunohistochemically following occlusion of the coronary artery in rats. 331 39

Allopurinol has been shown to provide significant protection against ischemia/reperfusion-induced microvascular and parenchymal cell injury. It has been hypothesized that the protection seen with allopurinol after ischemia/reperfusion (I/R) is caused by inhibition of xanthine oxidase. However, recent reports suggest that the beneficial effects of allopurinol in I/R may be caused by direct free radical scavenging. The objective of this study was to determine whether the regimen of allopurinol administration used in most I/R studies leads to a significant modification of the free radical scavenging properties of extracellular fluid (ECF), i.e., plasma and lymph. Plasma and intestinal lymph samples obtained from both control and allopurinol-treated cats were used to assess the following: 1) allopurinol and oxypurinol concentrations, 2) xanthine oxidase inhibition, 3) myoglobin-catalyzed linolenic acid peroxidation, 4) hypochlorous acid scavenging, and 5) protein and nonprotein sulfhydryl content. ECF from allopurinol-treated animals contained approximately 10 microM each of allopurinol and oxypurinol. Ten percent ECF resulted in 80% inhibition of xanthine oxidase activity. Comparable volumes of control ECF did not inhibit xanthine oxidase. Furthermore, allopurinol treatment did not enhance the antioxidant properties of ECF. The results of this study do not support the contention that the beneficial effects of allopurinol in I/R injury are caused by the scavenging of oxidants produced in ECF by activated granulocytes.
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PMID:Allopurinol does not enhance antioxidant properties of extracellular fluid. 339 21

Serum myoglobin levels have been found to be elevated for a few hours after removal of a tourniquet. In the present study, levels of serum myoglobin were measured by radioimmunoassay from local blood samples in patients who were treated with surgery of the hand in a bloodless field. After removal of the tourniquet blood samples were obtained from the antecubital vein of each patient immediately after release, five minutes, one hour, and 24 hours later. In these samples the serum myoglobin levels were not influenced by the mode of anesthesia, tourniquet time, or specific type of surgery. When the upper extremity was cooled with ice water before application of the tourniquet, however, the increase of serum myoglobin was statistically significantly inhibited when compared with the normothermic condition. Muscle injury due to tourniquet ischemia may be decreased by cooling of the upper extremity prior to tourniquet application.
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PMID:Changes in serum myoglobin levels caused by tourniquet ischemia under normothermic and hypothermic conditions. 340 88


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