Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography, a technique of assessing myocardial ischemia, was correlated with ischemia as identified by ST segment mapping and electron microscopy (EM) in 25 Langdneorff perfused rabbit hearts following coronary occlusion. Nicotinamide adenine dinucleotide (NAD), a component of the intramitochondrial electron transport chain, becomes reduced during periods of ischemia (NADH). NADH fluoresces when excited by ultraviolet light. NAD does not. All three techniques were compared to assess their resolution of the "border zone" between ischemia and nonischemic myocardium. The border zone defined by NADH fluorescence is 0.1 mm or less. Areas of high NADH fluorescence invariably revealed ST segment elevation, whereas minimally fluorescent areas did not. St segment mapping yields a border zone of approximately 7 mm. Areas of high NADH fluorescence following 1 hour of ischemia displayed severe damage on EM as compared to matched controls. A zone of intermediate ultrastructural damage is identified in a 1 mm biopsy taken between fluorescent and nonfluorescent myocardium. This evidence confirms epicardial NADH fluorescence photography as an assay of myocardial ischemia. This high resolution technique delineates a border zone of narrow dimensions as compared with ST segment mapping.
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PMID:Display of epicardial ischemia by reduced nicotamide adenine dinucleotide fluorescence photography, electron microscopy, and ST segment mapping. 20 64

Contractile dysfunction is characteristic of the acutely ischemic myocardium. This study was undertaken to assess the temporal relations between the onset of cell anoxia and ischemic contractile failure in isolated, isovolumetric contracting rabbit hearts. High speed epicardial fluorescence photography using reduced nicotinamide adenosine nucleotide (NADH) was used to identify areas of cell anoxia. The onset of ischemia was correlated with deterioration of pressure generation over the course of sequential 60 second coronary arterial occlusions. In the isovolumetric contracting rabbit heart, areas of ischemia were detected 2 seconds after coronary occlusion. Significant reduction in peak systolic pressure occurred at 6 seconds of ischemic time and pressure continued to decrease throughout the 60 second period of coronary occlusion. NADH accumulation indicates imbalance of myocardial oxygen supply and demand and the cessation of oxygen utilization by the mitochondria. The results of this study indicate that ischemia is detectable within 1 to 2 seconds after coronary occlusion and that ischemic ventricular dysfunction occurs several seconds thereafter. Myocardial oxygen reserve is negligible.
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PMID:Temporal relation between onset of cell anoxia and ischemic contractile failure. Myocardial ischemia and left ventricular failure in the isolated, perfused rabbit heart. 22 47

Laser fluorimetry of reduced nicotinamide adenine-dinucleotide (NADH) in situ is a new technique used for real-time studies of the degree of reduction of the first link in the mitochondrial respiration chain. We present here the first results obtained in animal experiments and in clinical exploration: In rats, coronary occlusion produces a substantial rise in mitochondrial NADH, followed by a fall below basal level during reperfusion. Tetanic contraction of slow-twitch muscles in rats results in a rise in NADH level higher than that produced by contraction of fast-twitch muscles. During coronary angiography, injection of the contrast medium induces a rise in NADH in patients with a significant degree of coronary stenosis. Intravenous nitroglycerin reduces both left ventricular end-diastolic pressure and NADH fluorescence concomitantly, due to preferential distribution of the coronary blood flow to sub-endocardial layers. Exercise-induced ischaemia results in a decrease of muscular NADH concentration in Mc Ardle syndrome, due to phosphorylase deficiency.
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PMID:[Laser fluorimetry of NADH]. 314 25

As one of the cause of acute myocardial ischemia, coronary vasospasm has attracted attention increasingly in clinical cardiology. We developed animal model of coronary vasospasm associated with transient myocardial ischemia by administration of histamine or serotonin in atherosclerotic miniature swine. Early systolic dysfunction as well as subendocardial NADH production of the ischemic region occurred within 10 sec after coronary occlusion, but ST segment started to elevate around 30 sec after occlusion in the isolated rat heart. As the important determinant factors of myocardial infarct size, the preocclusive perfusion area as well as collateral flow area could be measured quantitatively by use of double isotopes autoradiograms, and the close correlation was found between the salvaged area and collateral flow area in dogs. An importance of advancement in basic cardiology and development of new research techniques have been emphasized.
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PMID:Myocardial ischemia. 396 58

The distribution of coronary flow during high-flow hypoxia and ischemia has been assessed in the perfused rat heart. Surface and cross-section NADH fluorescence photography defined the pattern of oxygen delivery because regions of high NADH fluorescence denote areas of anoxia. Thioflavin S, a fluorescent dye that stains vascular endothelium, was added to the perfusate to label perfused vessels. The results indicate 1) that relatively large anoxic zones develop during high-flow hypoxia or ischemia, 2) that the pattern of oxygen delivery under hypoxic conditions is reproducible, and 3) that flow into these anaerobic areas is significantly decreased relative to control. The border zone between aerobic and anoxic tissue is shown to be sharply defined, indicating the absence of an appreciable volume of tissue that is partially anaerobic. The data may be relevant to human coronary artery disease, where coronary occlusion is usuallly not complete. They suggest that with reduced, but not insignificant, oxygen delivery into the domain of a coronary artery, the distribution of flow would be heterogeneous, making small areas of tissue severely ischemic while preserving flow and oxygen supply in the adjacent tissue.
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PMID:Heterogeneous coronary perfusion during myocardial hypoxia. 615 51

The effect of nifedipine on the myocardial energy demand--supply imbalance caused by vasopressin-induced vasoconstriction, coronary occlusion, and their combined action was studied in isolated perfused rabbit hearts using the method of NADH fluorometry. Nifedipine (0.015 microgram/ml) completely prevented the development of NAD/NADH imbalance caused by coronary vasospasm. The role of vasoconstriction as an addition to coronary occlusion was very small in the development of regional energy imbalance and the vasopressin-induced detrimental effect was prevented by nifedipine. Energy imbalance caused by the occlusion alone was only partially improved by the drug. There was a delay in the development of energy imbalance and reduction in the final degree of NADH fluorescence response to the occlusion (97 +/- 8% vs. 66 +/- 9%, p less than 0.05).
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PMID:Effects of nifedipine on myocardial energy balance in experimental coronary vasoconstriction and occlusion. 617 85

In this report we describe a new technique for the measurement of region at risk after coronary artery ligation in the rabbit by NADH fluorophotography. We also describe the application of this technique to a study of nifedipine combined with reperfusion in experimental myocardial infarction. In 16 untreated rabbits the epicardial surface area of NADH fluorescence immediately after coronary ligation correlated with infarct size at 24 hr after coronary occlusion, as measured by nitro blue tetrazolium staining (r = .84, p less than .001). In 24 rabbits we studied the effect of nifedipine administered immediately after coronary ligation and combined with reperfusion at 1 hr after occlusion. Nifedipine had no significant effect on region at risk or infarct size.
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PMID:Failure of nifedipine and reperfusion to reduce infarct size relative to region at risk as measured by NADH fluorophotography. 674 54

Catecholamines play a major role during initiation and propagation of myocardial ischemia (MI). Therefore their influence on the size of an acute regional MI was investigated in isolated, coronary ligated rabbit hearts during electrical pacing at different rates (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l). MI was quantified from NADH-surface-fluorescence-photography. After coronary occlusion the stimulation-rate was increased stepwise from 180 beats/min to 300/min. Experiments were performed in hearts of control and reserpinized rabbits (reserpine 7.0 mg/kg i.p. 24 h before preparation). Hearts of control animals were submitted to beta-blockade by propranolol (10(-8) mol/l) or the partial agonists pindolol (10(-6) mol/l) or carteolol (10(-6) mol/l). In untreated control hearts MI was significantly enlarged with increasing heart-rate (p < 0.05). At 300/min MI was doubled as compared to that observed at 180/min. In hearts of reserpinized animals this effect was absent (p > 0.05). Moreover, in control hearts the growth of MI could be prevented by beta-blockade with propranolol, pindolol or carteolol (p > 0.05), however, these hearts became insufficient as indicated by an increase in left ventricular enddiastolic pressure. Therefore we conclude that the pacing-rate dependent growth of MI seems not to be primarily related to myocardial left ventricular pressure nor to the heart rate. Nevertheless the growth of MI is strictly related to the release of catecholamines and might be caused by oxygen free radicals generated from noradrenaline by autoxidation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of propranolol, pindolol and carteolol on acute regional myocardial ischemia in isolated rabbit hearts. 810 27

Oxygen-derived free radicals may contribute to tissue injury in myocardial ischemia although the mechanism is unclear. Catecholamines possibly could be involved in the genesis of free radicals because it has been demonstrated that oxygen free radicals may be generated by autooxidation of noradrenaline. Superoxide dismutase (SOD) protects the myocardium against injury by superoxide anion radicals. We, therefore, examined whether the cardioprotective effect of superoxide dismutase still could be demonstrated after depletion of catecholamine stores by reserpine (7 mg/kg intraperitoneally 24 h premortem). We used electrically paced isolated hearts perfused according to Langendorff (Tyrode's solution, Ca2+ 1.8 mmol/L, constant perfusion pressure: 70 cm H2O, 3 Hz). Myocardial ischemia was induced by occlusion of a left coronary artery branch. Epicardial NADH-fluorescence was used for quantitation of the myocardial ischemia. SOD (48 U/mL) did not influence global coronary flow or left ventricular pressure significantly (P > 0.05). In control hearts, SOD significantly diminished both size and intensity of epicardial NADH-fluorescence after repetitive coronary ligatures (-45%) (P < 0.05). In hearts with depleted catecholamine stores, this cardioprotection by SOD was no longer observed (P > 0.05). Stimulation of noradrenaline overflow by increasing the pacing rate of control hearts from 180/min up to 300/min after coronary occlusion also significantly enlarged myocardial ischemia (P < 0.05). This pacing rate-dependent growth of myocardial ischemia could be prevented completely by either prior depletion of catecholamine stores with reserpine or SOD. Therefore, noradrenaline seems to be the most important source for the generation of oxygen free radicals during myocardial ischemia in isolated saline-perfused rabbit hearts.
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PMID:Cardioprotection by superoxide dismutase: a catecholamine-dependent process? 842 98

The effects of exogenous superoxide dismutase (SOD) on acute myocardial ischemia (MI) was investigated in isolated electrically-driven rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37 degrees C). Acute regional ischemia (MI) was induced by occlusion of a coronary artery branch (CAO) and quantitated from epicardial NADH-fluorescence photography. SOD (48 U/ml) was applied either 30 min after CAO in a single coronary occlusion model (treatment) or 30 min before the 2nd CAO in a repetitive coronary occlusion model (pre-treatment). SOD had no significant influence on the left ventricular pressure or the global coronary flow (p > 0.05). MI was significantly diminished in hearts pre-treated with SOD before CAO (-25%)(p < 0.05), but remained unaffected when SOD was applied after CAO (p > 0.05). The results suggest that superoxide anion radicals contribute to ischemic tissue injury. SOD shows cardioprotective properties only if present in the ischemic zone, requiring the application of SOD before CAO in poorly collateralised rabbit hearts.
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PMID:Comparison of the cardioprotective efficacy of superoxide dismutase in a single and a repetitive coronary occlusion model in rabbit hearts. 859 59


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