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

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

Fifty-five ischemic attacks at rest with ST segment elevation were recorded by two-dimensional echocardiography (2DE) in 20 patients with Prinzmetal angina. Eighteen ischemic attacks were recorded starting from intravenous injection of ergonovine maleate while 37 spontaneous ischemic attacks were recorded from onset of either anginal pain or ECG changes or from the basal state. In each ischemic attack at least one of the following transient alterations was observed by 2DE during ST elevation: (1) Regional hypokinesia, akinesia, or dyskinesia; (2) "step sign," that is, a sharp demarcation between an akinetic or dyskinetic area and an adjacent normal or hypercontracting region; and (3) geometric changes in left ventricular shape, that is, globular appearance in diastole and hourglass silhouette in systole. Regional myocardial asynergy was detected earlier than onset of pain (which was not present in 21 [38%] ischemic episodes) or ST segment elevation on ECG, as documented in 40 ischemic episodes (16 induced and 24 spontaneous) in which echocardiographic monitoring was performed from basal state and carried on up to the appearance of ischemia. All described mechanical changes were fully reversible after pain subsided and ST segment was back to isoelectric, either spontaneously or with nitrates; furthermore, a contractile "rebound phenomenon" of the previously ischemic wall was observed in some episodes. In conclusion, these results outline a role for 2DE in detecting cardiac mechanical impairment due to transient myocardial ischemia with ST segment elevation in humans.
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PMID:Transient changes in left ventricular mechanics during attacks of Prinzmetal angina: a two-dimensional echocardiographic study. 623 83

The present study was undertaken to establish the time limit until the beginning of reperfusion that would permit restoration of contractility in acute myocardial infarction, and to confirm the delayed recovery of dyskinesis in ischemic area followed by reperfusion. Studies were carried out in 31 dogs of which 29 had temporary (20 min to 5 hours) occlusion of the left anterior descending coronary artery with short or long term reperfusion, and 2 had permanent occlusion. Dyskinesis was detected with tension curve obtained using a strain gauge arch. In the short term reperfusion study, dyskinesis disappeared if reperfusion was begun within 20 min of ischemia. However, dyskinesis remained after one hour of reperfusion, if reperfusion was done after 40 min of ischemia. Reperfusion for 10 days after 3 and 4 hours of occlusion resulted in recovery of regional myocardial contractility. However in 2 of 5 animals with 5 hours of coronary occlusion, the reperfused area remained dyskinetic even after 10 days of reperfusion. It is concluded that revascularization of myocardium that had been kept ischemic for less than 4 hours may lead to disappearance of dyskinesis. These findings also indicate that early coronary revascularization doses not always provide an immediate recovery of dyskinesis of the revascularized area.
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PMID:Time limit for early coronary artery revascularization. Restoration of contractility in reperfused myocardium in dogs. 697 46

The effects of 1 hour, 3 hours and 10 days coronary artery reperfusion after 20 minutes, 40 minutes, 3 hours, 4 hours and 5 hours coronary artery occlusion on the contractility of myocardium was studied by the strain gauge arch, and the myocardial changes was also studied histologically. Results obtained were follows. In the short term reperfusion study: 1) Dyskinesis disappeared in all cases if reperfusion was begun after 20 minutes of ischemia. 2) Dyskinesis remained in all cases if reperfusion was begun after 40 minutes of ischemia. In the long term reperfusion study: 3) Dyskinesis disappeared in all cases after 10 days reperfusion with 3 and 4 hours ischemia groups, and the recovery of myocardial contractility was good. 4) Dyskinesis remained in 2 of 5 dogs with 5 hours coronary occulusion even after 10 days of reperfusion, and the recovery of myocardial contractility in 3 of 5 dogs with this group was poor. It is concluded that revascularization of myocardium that has been kept ischemia for less than 4 hours may lead to disappearance of dyskinesis and recovery of myocardial contractility. These findings also indicate that early coronary revascularization does not always provide an immediate recovery of dyskinesis of the revascularized area.
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PMID:[Evaluation of early coronary artery reconstruction in acute myocardial infarction--time limit in the therapeutic effectiveness in relation to restoration of localized myocardial contraction]. 715 67

Thallium-201 scintigraphy was performed in 20 normals and 60 patients (pts) with angiographically proven coronary artery disease (CAD) at rest after maximal exercise for evaluation of severity and location of CAD. The Tl-scintigrams were quantified by a Tl-score. The results of the Tl-score were compared with invasive and non-invasive parameters. Sensitivity asnd specificity of the Tl-score in evaluation of CAD was 90%. In normals, there were no significant differences from rest to exercise (Tl-score less than or equal to 1.2). Twenty-six of the pts with CAD, who had no evidence of myocardial infarction, showed a significant increase of Tl-score from 5.0 +/- 1.7 to 8.7 +/- 2.6 after exercise (p < 0.001). In 34 pts with CAD and a history of MI, Tl-score increased from 24.9 +/- 3.1 to 33.3 +/- 3.8 (p < 0.001). Exercised-induced ischemia was assessed by exercise electrocardiography in 48%, by Tl-score in 62% and by angina pectoris in 77%. In 37 pts, the Tl-score was compared with the coronary score, ejection fraction (EF) and local wall motion derived from biplane cineventriculograms. There was a significant correlation between the Tl-score and the EF: y = 79.13 - 1.11 x, n = 74, r = 0.688 (p < 0.001). No correlation was found between the coronary score and the Tl-score. Hypokinetic wall motion disturbances were assessed by Tl-score in 34% only, whereas akinesia and dyskinesia were detected in 86% (p < 0.001). The data suggest that Tl-scintigraphy even with a quantitative Tl-score is not sufficient for exact assessment of extent and severity of CAD.
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PMID:[Quantitative Tl-201 scintigraphy in diagnosis of severity and location of coronary artery disease. Comparison of a Tl-score to invasive and non-invasive parameters (author's transl)]. 744 54

Inhibition of mechanical activity during ischemia could improve recovery of stunned myocardium. In this study, the effect of 2,3-butanedione-2-monoxime (BDM), an agent that disrupts excitation-contraction coupling, on the time course of recovery of contractile function of postischemic reperfused myocardium was studied in open-chest anesthetized dogs. Ischemia was produced by occluding the left anterior descending coronary artery (LAD) for 15 mins. In separate experimental groups, during the occlusion period, 6 ml of either 100 mM BDM or drug vehicle (0.9% normal saline) was infused into the distal perfusion bed subjected to occlusion. Regional myocardial function (percentages of segment shortening % SS) was assessed by sonomicrometry. LAD occlusion resulted in similar degrees of dyskinesia in both experimental groups. Subsequent recovery of contractile function during reperfusion was evaluated for 3 h. In control experiments, segment shortening remained significantly (p < 0.05) decreased throughout the reperfusion period, returning to only 36.1 +/- 9.2% of the preocclusion value at 3 h postreperfusion. In BDM experiments, regional contractile function returned to 72.4 +/- 11.3% of the preocclusion value at 1 h of reperfusion. Rapid recovery was sustained throughout reperfusion. Regional stroke work area (RSWA) also demonstrated rapid sustained recovery of function after treatment with BDM. RSWA was significantly greater in BDM experiments as compared with control experiments at all times during the reperfusion period. These results demonstrate that selective intracoronary (i.c.) administration of BDM during ischemia markedly enhances postischemic recovery of contractile function. The underlying mechanism for this action may involve modulation of several aspects of impaired cellular function in postischemic tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery of contractile function of postischemic, reperfused myocardium: influence of 2,3-butanedione-2-monoxime. 768 37

No definitive evidence for the participation of the immune system in progressive brain damage has been previously reported. However, glial cells continue to accumulate after degeneration of neurons appears to be completed, and a recent study showed that microglia and leukocytes also accumulate after brain damage. Thus, it seemed possible that immune responses might play a role in the delayed effects. Cyclosporin A (CsA) is a cyclic undecapeptide of fungal origin with a strong immunosuppressive action but low myelotoxicity. We examined the effect of CsA administration on three different kinds of animal models for neurological deficits. Late onset reduction of muscarinic receptors after transient forebrain ischemia in gerbils was prevented by daily post-ischemic administration of CsA. This indicates that an immune mechanism may be involved in the progressive brain damage occurring after transient ischemia. On the other hand, CsA exacerbated iminodipropionitrile-induced dyskinesia both behaviorally and biochemically. CsA also mimicked pentylenetetrazol-induced seizures. These findings suggest that immune mechanisms may play important roles in the progression of brain damage and possibly that immunosuppressants might open a new chapter in the pathophysiology and treatment of chronic progressive neurodegenerative diseases. Further investigations on the immune response in the progressive brain damage are needed.
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PMID:[Involvement of immune mechanism in the progressive brain damage]. 785 34

CDP-choline, supplied exogenously as citicoline, has beneficial physiological actions on cellular function that have been extensively studied and characterized in numerous model systems. As the product of the rate-limiting step in the synthesis of phosphatidylcholine from choline, CDP-choline and its hydrolysis products (cytidine and choline) play important roles in generation of phospholipids involved in membrane formation and repair. They also contribute to such critical metabolic functions as formation of nucleic acids, proteins, and acetylcholine. Orally-administered citicoline is hydrolyzed in the intestine, absorbed rapidly as choline and cytidine, resynthesized in liver and other tissues, and subsequently mobilized in CDP-choline synthetic pathways. Citicoline is efficiently utilized in brain cells for membrane lipid synthesis where it not only increases phospholipid synthesis but also inhibits phospholipid degradation. Exogenously administered citicoline prevents, reduces, or reverses effects of ischemia and/or hypoxia in most animal and cellular models studied, and acts in head trauma models to decrease and limit nerve cell membrane damage, restore intracellular regulatory enzyme sensitivity and function, and limit edema. Thus, considerable accumulated evidence supports use of citicoline to enhance membrane maintenance, membrane repair, and neuronal function in conditions such as ischemic and traumatic injuries. Beneficial effects of exogenous citicoline also have been postulated and/or reported in experimental models for dyskinesia, Parkinson's disease, cardiovascular disease, aging, Alzheimer's disease, learning and memory, and cholinergic stimulation.
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PMID:Metabolism and actions of CDP-choline as an endogenous compound and administered exogenously as citicoline. 786 46

Oxidized glutathione (GSSG) but not its reduced form (GSH) is taken up by intact myocardial cells, and is rapidly converted into GSH. Reduced glutathione is an important intracellular defense against oxygen-derived free radicals and has been found to enhance calcium sensitivity in skinned cardiac fibers. We have investigated the effects of intravenous GSSG on left ventricular systolic pressure, maximal rate of rise of pressure and regional segment-shortening in dogs subjected to occlusion of the left anterior descending artery for 30 minutes, followed by 45 minutes reperfusion. Starting 10 minutes before reperfusion, the dogs were randomly treated with either GSSG (100 mM, 5 ml/min, n = 5) or Ringer's solution (5 ml/min, n = 5) until 30 minutes of reperfusion. Myocardial blood flow was measured by radioactive microspheres. Infusion of GSSG increased total glutathione content in both ischemic (47 +/- 16 mumol/g protein) and nonischemic myocardium (71 +/- 17 mumol/g protein) as compared to controls (23 +/- 2 mumol/g protein, p < 0.05). In both groups paradoxical wall motion occurred in the ischemic region during occlusion. On reperfusion, regional dyskinesia persisted in controls; while, in glutathione-treated dogs, systolic segment-shortening reached half the baseline values (p < 0.05, treated vs controls, at 15, 30, 45 minutes reperfusion). During ischemia the area of pressure-length loops, obtained from simultaneous recordings of left ventricular pressure and regional segment length, decreased to 30 +/- 7% of baseline in controls and to 40 +/- 18% of baseline in GSSG-treated animals. After 45 minutes reperfusion it was restored to 78 +/- 22% baseline in treated hearts but was still 36 +/- 16 of baseline in controls (p < 0.05). We conclude that infusion of GSSG increases the intracellular stores of glutathione and improves the contractile state of postischemic myocardium.
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PMID:Infusion of oxidized glutathione enhances postischemic segment-shortening in dog hearts. 791 48

From a population of 2,698 patients (579 evaluated early after an uncomplicated acute myocardial infarction) who underwent dipyridamole echocardiography testing (DET) and subsequent coronary angiography, left main (LM) stenosis > or = 50% was present in 73 (61 men and 12 women, mean age 62 +/- 8 years). These 73 patients were compared with a control group comprising 100 consecutive coronary patients without LM disease. Both groups were similar regarding mean age, sex, incidence of previous myocardial infarction, left ventricular function at rest, and severity of coronary artery disease by the number of diseased vessels excluding the LM. The proportion of patients receiving antianginal therapy during DET was higher in the LM than in the non-LM group (32 vs 14%; p < 0.01). No major complication (severe hypotension, sustained arrhythmia, myocardial infarction or death) occurred during DET. Of 73 patients with LM disease, 68 had positive DET (sensitivity 93%), dipyridamole time was 7.1 +/- 3.8 minutes, and the rest-peak stress variation in dipyridamole wall motion score index (1 = normal to 4 = dyskinesia, in an 11-segment model) was 0.37 +/- 0.23; 14 patients (19%) were resistant to aminophylline and needed nitrates to resolve ischemia. In the non-LM group, DET was positive in 72% (p < 0.001 vs LM), with a longer dipyridamole time (9.6 +/- 5.2 minutes; p < 0.001 vs LM), lower rest-peak stress wall motion score index variation (0.29 +/- 0.25; p < 0.05 vs LM), and less frequent antidote resistance (1%; p < 0.001 vs LM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dipyridamole stress echocardiography in patients with severe left main coronary artery narrowing. Echo Persantine International Cooperative (EPIC) Study Group--Subproject "Left Main Detection". 814 Oct 85


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