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)

The quantitative relationship between abnormalities seen on technetium-99m pyrophosphate (99mTc-PYP) infarct scintigrams and the size of the myocardial infarction is unclear. We evaluated two possible determinants of 99mTc-PYP accumulation: myocardial perfusion measured with 7-10 mu microspheres and the extent of necrosis determined histologically. Hemodynamics and myocardial perfusion to small segments of the left ventricle were measured prior to, 5-10 min, and 44-48 hours following sudden occlusion of the left anterior descending coronary artery in ten awake dogs. 99mTc-PYP was injected i.v. following the third injection of microspheres and the animals were killed 2 hours later. The important findings were as follows: 1) there is a close relationship between the extent of myocardial necrosis observed and the perfusion of segments 5-10 min following coronary occlusion; and 2) that segmental myocardial perfusion is an important determinant of 99mTc-PYP accumulation by myocardial segments which contain areas of necrosis. Although the present data preclude statistical analysis of the relationship between the level of necrosis in a segment and the accumulation of 99mTc-PYP by that segment, the two do not appear to be related, a finding which would discourage use of intensity of 99mTc-PYP images for infarct size. The distribution of an abnormality on the scintigram may provide an estimate of infarct size. However, the geometry of the infarct and the resolving power of the scanning equipment will significantly limit this in many clinical situations.
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PMID:Relationships between myocardial perfusion, myocardial necrosis, and technetium--99m pyrophosphate uptake in dogs subjected to sudden coronary occlusion. 18 15

The relation between the accumulation of pyrophosphate and technetium-99m in myocardium with reversible and irreversible ischmic injury was studied in dogs subjected to transitory or persistent coronary arterial occlusion. Among four dogs with coronary occlusion maintained for less than 20 minutes, none had either increased MB creatine kinase (CK) (the "myocardial" CK isoenzyme) activity serum or a positive 99mTc stannous pyrophosphate image. Seven dogs with coronary occlusion maintained for 30 or more minutes had elevated serum MB CK activity, and five of the seven had positive (abnormal) images. Thus, although false negative images may occur occasionally despite myocardial damage, both increased serum MB CK and abnormal images generally accompanied prolonged coronary occlusion. In contrast, ischemia without infarction was not associated with abnormal images. Both 99mTc and 32P labeled pyrophosphate were accumulated extensively and proportionally in myocardium from zones of infarction, and uptake of both tracers was comparable although modest in isolated mitochondria. Similar results were obtained after myocardial infarction in animals with induced profound leukopenia. Thus, phagocytosis of the radiopharmaceutical agent by leukocytes migrating into the infarct is not an essential mechanism accounting for uptake. These results indicate that abnormal images reflect uptake of pyrophosphate, associated with 99mTc, by irreversibly injured myocardium rather than leukocytic infiltration involved in the inflammatory response in the heart.
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PMID:Mechanisms contributing to myocardial accumulation of technetium-99m stannous pyrophosphate after coronary arterial occlusion. 18 32

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.
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PMID:Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat. 20 67

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

To determine the effects of chronic exercise on the coronary collateral circulation of dogs with normal coronary arteries, 1-yr-old purebred beagles were divided into sedentary control and exercising groups. The latter were trained to run on a treadmill. A lower maximal heart rate during a standardized exercise test protocol after a 10- to 12-week training period and a higher gastrocnemius cytochrome oxidase activity in the runners attested to the presence of cardiovascular and skeletal muscle training effects. However, left ventricular weights, left ventricle/body weight ratios, myocardial myofibrillar and myosin ATPases, and hemodynamics were similar in sedentary and exercising dogs except for a significantly higher resting cardiac output in the runners. After occlusion of the left anterior descending coronary artery, both collateral conductance (retrograde flow/aortic pressure) and collateral flow measured with microspheres tended to be lower in the trained dogs, but differences were not significant. The endocardial/epicardial flow ratio in the ischemic area after coronary occlusion did not distinguish between exercisers and controls. Thus treadmill running in the dog with normal coronary arteries produced a training effect, but had no effect on coronary collateral vessels.
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PMID:Effect of exercise on collateral development in dogs with normal coronary arteries. 21 85

The interrelationships between coronary artery occlusion, alcohol consumption, and plasma levels of HDL cholesterol were investigated in 718 male patients undergoing coronary arteriography. A statistically significant inverse relationship was seen between the extent of coronary occlusion and alcohol intake and between coronary occlusion and plasma HDL cholesterol levels. A positive association was observed between the amounts of alcohol consumed and plasma HDL cholesterol levels, as well as between alcohol consumption and history of smoking. The findings of the present study suggest that the "retarding" effect of alcohol on coronary artery disease may be at least partially explained by the alcohol-induced rise of plasma HDL cholesterol.
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PMID:Interrelationship between coronary artery occlusion, high-density lipoprotein cholesterol, and alcohol intake. 22 53

In 27 closed chest dogs left ventricular wall motion abnormalities assessed quantitatively with two dimensional echocardiography were used as a measure of myocardial infarct size, and the change in extent of segmental wall motion abnormalities due to drug intervention early after infarction was evaluated. The extent of wall motion abnormalities was measured with echocardiography before and at 20 and 40 minutes and 5 1/2 hours after coronary occlusion. Three subgroups of dogs received, respectively, an infusion of nitroglycerin, phenylephrine or saline solution. Infarct size was measured with technetium pyrophosphate scintigraphy of the excised left ventricle. The infarct size correlated well with the extent of wall motion abnormalities before death. Wall motion was initially similar among the three groups but was significantly improved after treatment with nitroglycerin (P less than 0.025), remained stable with continued saline infusion and worsened significantly (P less than 0.05) after treatment with phenylephrine. Two dimensional echocardiography can be used to quantify experimental canine myocardial infarction and assess the effect of nitroglycerin.
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PMID:Two dimensional echocardiographic quantification of infarct size alteration by pharmacologic agents. 22 27

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

Alterations of hydrogen ion (H+) concentration in the myocardium of 60 cats were determined before release of coronary ligation of 30, 45, 60, 90 or 180 minutes' duration, or 5, 30 and 90 minutes after release of the occlusion, by pressing pH indicator paper on unfixed frozen heart sections. The H+ concentration had clearly increased (pH less than 6.0) in a transmural extension in the left ventricle before release of the coronary ligature. This elevated H+ concentration persisted some time in the subendocardial region despite release of the coronary occlusion, thus proving that the so-called no reflow phenomenon exists in involved myocardium after temporary coronary occlusion. A diminished H+ concentration (pH 7.4) was found in the border zone between the acid-reacting area and the normal muscle when the coronary occlusion lasted 180 minutes before release of the ligature or 30 minutes after release of the occlusion when the previous period of temporary occlusion had been longer than 30 minutes. Although areas manifesting an acid reaction vanished or diminished in size after release of coronary occlusion, the extent of alkaline-reacting zones showed no reduction in size, and muscle cell necrosis developed in these alkaline-reacting areas. It is assumed therefore that an alkaline reaction of the myocardium is an early sign of irreversible muscle cell damage.
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PMID:Alterations in myocardial hydrogen ion concentration after temporary coronary occlusion: a sign of irreversible cell damage. 23 88

Effects of nitroglycerin, dipyridamole, adenosine, reactive hyperemia, propranolol, norepinephrine and sympathetic nerve stimulation on retrograde coronary blood flow were investigated in dogs with experimental coronary occlusion. The retrograde blood flow (RF), pressure and conductance of the occluded left anterior descending coronary artery were measured and compared with the flow (CF), pressure and conductance of the non-occluded circumflex artery. The RF increased during sympathetic nerve stimulation and after the administration of nitroglycerin and norepinephrine, while it decreased during reactive hyperemia and following injection of dipyridamole, adenosine and propranolol. The RF/CF ratio was increased by nitroglycerin and propranolol, whereas it was lowered by dipyridamole and adenosine. The results suggest that nitroglycerin and propranolol may produce a redistribution of myocardial blood flow and that the collateral vessels are little influenced by sympathetic nerve stimulation.
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PMID:Effects of drugs and sympathetic nerve stimuation on retrograde coronary blood flow in dogs with experimental coronary occlusion. 23 50


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