UMLS:C0151814 - FACTA Search

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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the relationship between regional myocardial perfusion and segmental dyskinesis, 22 open chest dogs were studied using ultrasound to register cardiac wall motion and radioactive labeled microspheres to determine myocardial perfusion. In six dogs, motion and perfusion were correlated at two levels of partial circumflex coronary artery occlusion followed by complete occlusion. A good correlation between declining myocardial perfusion of all the ischemic segments and development of aneurysmal bulging (during isometric contraction) was seen: r = minus 0.80. A similar correlation between myocardial perfusion and endocardial wall velocity (during systolic ejection) was observed: r = 0.92. In nine dogs, the effect of 45 minutes of complete coronary occlusion followed by 30 minutes of reperfusion was evaluated with respect to perfusion and motion. After coronary reperfusion myocardial perfusion of the ischemic area returned to control levels (from 32.6 +/- 3.5 to 130.3 +/- 13.3 ml/100 g/min), but aneurysmal bulging during isometric contraction persisted. Endocardial wall velocity during systolic ejection showed a variable response to reperfusion, achieving values ranging from 32% to 162% of the preocclusion levels. In seven dogs the ultrasound beam was reflected off nonischemic myocardium adjacent to areas of ischemia resulting from coronary occlusion. Despite preservation of normal myocardial perfusion in these nonischemic areas wall motion abnormalities were evident: endocardial wall velocity declined from 25.8 +/- 5.8 to 14.0 +/- 4.9 mm/sec (P less than 0.01), and aneurysmal bulging in three animals. These changes may be due to transient undetected ischemia in the segments struck by the ultrasound beam, or to passive alteration of the motion of the normally perfused areas by the severe dyskinesis of the adjacent ischemic myocardium.
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PMID:Correlation between echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion. 118 55

The effect of 40- or 90-min periods of temporary myocarardial ischemia on the distribution of coronary flow and capillary structure were assessed in groups of mongrel dogs. Thioflavin S. a fluorescent dye which stains vascular endothelium when injected intravenously, was used to demonstrate the distribution of microvascular perfusion at 10 sec, 5 min, or 20 min following release of a 40-or 90min circumflex coronary artery occlusion. Hearts which demonstrated perfusion defects were sampled for electron microscopy. Following 40 min of occlusion, thioflavin S was distributed uniformly throughout the myocardium. In contrast, following 90-min periods of coronary occlusion, perfusion defects always were present in the subendocardial half of the posterolateral left ventricular wall. Several morphological features in these areas of no reflow were observed by electron microscopy, including decreased endothelial pinocytotic vesicles, endothelial gaps and bleb formation, capillaries packed with erythrocytes, occasional intraluminal thrombi, and extravascular erythrocytes and fibrin. Myocardial cells showing severe injury always were seen within but also extended beyond the areas of poor perfusion. These results demonstrate that areas of no reflow occur following 90-min periods of ischemic injury in the dog, but that primary myocardial cell injury occurs during the ischemic period and not as a function of the "no-reflow" phenomenon.
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PMID:Demonstration of the "no-reflow" phenomenon in the dog heart after temporary ischemia. 120 94

Acute occlusion of the circumflex branch of the left coronary artery was produced in chronically instrumented conscious dogs. Tracer microspheres were used to measure during an established time period, the distribution of collateral flow within the infarcting myocardium. For up to 2 hours after coronary occlusion the amount and distribution of the collateral flow remained unchanged. Two to 4 hours after coronary occlusion the subendocardial flow fell to almost zero and the subepicardial flow rose. Between 6 and 48 hours subepicardial and total collateral flow rose markedly. A no-reflow phenomenon is responsible for the decline of collateral flow in the subendocardium. Evidence for this hypothesis was provided by releasing the artery 1,2, 4 and 6 hours after occlusion. The amount of subendocardium that could not be reperfused was small after 1 hour and large after 6 hours of occlusion. When the total collateral flow was very low, the subepicardium was not able to be reperfused and a transmural myocardial infarction developed. We conclude that the time delay between onset of ischemia and the appearance of a no-reflow phenomenon depends upon the amount of collateral flow. The occurrence of a no-reflow phenomenon in the subendocardium increases the amount of flow to the subepicardium which increases its chances of survival. Beyond the sixth hour after occlusion the total amount of collateral flow increases which is interpreted as a reduction of collateral resistance by passive caliber changes of the collateral vessels. DNA-synthesis that signal active caliber changes through cellular proliferation were always detected 24 hours after complete occlusion of a coronary artery regardless whether the time between onset of stenosis until complete occlusion was varied between 36 hours and 5 days. When the time to complete occlusion was 4 days, myocardial infarction was prevented due to growth-transformation of pre-existing collaterals. Four phases of collateral reactions in acute coronary occlusion were observed: redistribution of available collateral flow in favor of the subepicardium (t = 1 to 4 hours after occlusion), 2) increase of total collateral flow due to passive "stretch" of collateral vessels (t = 4 to 24 hours after occlusion), 3) radial growth of collateral vessels due to active cellular proliferation, (t = 24 hours to 5 days) 4) cellular proliferation to ensure a normal wall thickness in growth'transformed collaterals (t = 5 days to 20 days after coronary occlusion). In subacute coronary occlusion the first phase does, of course, not apply.
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PMID:Influence of collateral flow on the ischemic tolerance of the heart following acute and subacute coronary occlusion. 125 70

Disorders of contractile function constitute one of the earliest events to follow acute coronary occlusion, and occur in the central ischemic region within approximately 10 seconds. Measurements of regional myocardial dimensions and function in the central, border, and normal zones around an area of ischemia allow assessment of such changes, and when these disorders are persistent after permanent coronary occlusion they may offer an indirect means for assessing the severity and extent of myocardial ischemia and infarction. Recent experimental studies that used pairs of miniature ultrasonic crystals implanted within the subendocardium of open-chested and chronically instrumented, unanesthetized dogs indicate that functional function may be studied simultaneously in these regions; a holosystolic bulge rapidly develops in the central zone of ischemia while hypokinesis is apparent in marginal zones bordering the central region. It has been shown that function in the marginal zone reflects the balance between oxygen supply and demand and may be favorably or unfavorably influenced by acute therapeutic interventions. This finding suggests that the extent of an ischemic region may be altered by such therapy.Our studies further indicate that regional changes in dynamic wall thickness closely parallel the characteristics of shortening of nearby subendocardial segments, indicating that measurement of wall thickness alone may be useful for characterizing regional function. Studies in chronically instrumented animals also have established that the miniature crystals are useful for measuring regional dimensions and function over prolonged periods of time; for example, reduction in end-diastolic dimensions that reflex tissue loss over a 3- to 4-week period after coronary occlusion is substantially greater in the central ischemic regions than in the marginal zones. It is proposed that persistent changes in myocardial function and progressive alterations changes in dimensions over time offer indirect measures of the extent and severity of ischemic damage and infarction. With the development of improved echocardiographic or other clinically applible methods, such measurements may be a useful tool for assessing the effects of therapy on myocardial infarct size.
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PMID:Analysis of regional myocardial function, dimensions, and wall thickness in the characterization of myocardial ischemia and infarction. 125 75

The effect of coronary reperfusion on the uptake of cardiac glycosides by ischemic myocardium was studied in 17 open chested dogs undergoing anterior wall infarction produced by snaring confluent branches of the left coronary system. Epicardial electrograms delineated ischemic zones of S-T elevation, border, and nonischemic zones. Animals were reperfused by snare release 1, 2, and 6 hr after occlusion. After 15 min of reperfusion, 1.0 mg of [3H] digoxin was given intravenously, and 2 hr later the hearts were excised and endocardial (endo) and epicardial (epi) samples from each zone were analyzed for [3H] digoxin concentration. In five dogs occluded for 1 hr and reperfused, [3H] digoxin uptake was comparable in endo and epi layers of all three zones. In six dogs reperfused after 2 hr of occlusion, mean (+/-S.E.) [3H] digoxin concentrations (nanograms per gm) were significantly reduced by 54 percent in endo (111 +/-18) and 35 percent in epi (151 +/- 23) layers of the ischemic zone as compared with the mean nonischemic concentration (endo249 +/- 34; epi 239 +/- 34). Border zone endo and epi [3H] digoxin uptake was reduced by 21 and 17 percent, respectively. In six dogs reperfused after 6 hr of occlusion, [3H] digoxin uptake in the ischemic zone was markedly reduced by 85 percent in endo (34 +/- 4) and 60 percent in epi (86 +/- 12) layers as compared with the nonischemic concentration (endo 232 +/- 19; epi 217 +/- 15). Border zone uptake was decreased by 54 percent in endo and 38 percent in epi regions. We conclude that coronary reperfusion between 2 and 6 hr of coronary occlusion is associated with markedly reduced myocardial digoxin uptake, more pronounced in subendocardial regions of ischemic tissue. This alteration in digoxin binding by reperfused ischemic myocardium is consistent with ischemia-induced structural or functional alterations in the putative digitalis receptor, (Na++K+)-ATPase.
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PMID:Effects of ischemia and reperfusion on myocardial uptake of tritiated digoxin. 125 85

To test the hypothesis that prior steroid administration may enhance the mechanical and metabolic response to myocardial reperfusion, regional myocardial function (Hg-in-silastic length gauges), transmyocardial lactate balance and K+ difference were measured in 12 control and 13 treated (30 mg/kg methyl-prednisolone, 30 to 60 min postocclusion) dogs. At three hours of ischemia, systolic shortening in the ischemic segment was greater in treated dogs (40.6% vs. 12%, P less than 0.05), while both lactate balance and K+ arteriovenous difference became positive. Lactate balance and K+ difference remained negative in the untreated animals. After three hours of occlusion and one hour of reperfusion, recovery of shortening was significantly greater in the treated animals (75.9 vs. 31.6%, P less than 0.05). In addition, while lactate balance remained negative among the control dogs, it further improved in the treated dogs. Thus, steroid administration during experimental coronary occlusion impedes the progression of ischemia and is additive to reperfusion in reversing ischemic dysfunction.
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PMID:Myocardial reperfusion in acute experimental ischemia. Beneficial effects of prior treatment with steroids. 126 Sep 88

The effect of intra-aortic balloon counterpulsation (IABC) on the motion and perfusion of ischemic left ventricular posterior myocardium was studied in 30 open-chest dogs, using ultrasound to register motion and 7-10 mu radioactive microspheres to determine perfusion. Circumflex coronary artery ligation produced acute aneurysmal bulging during isovolumetric contraction and diminished ischemic wall velocity during systolic ejection. Myocardial perfusion was determined in five dogs; perfusion of the area supplied by the ligated coronary artery fell from a control value of 72.9 +/- 13.8 (SE) to 30.0 +/- 2.3 cc/100 g/min (P less than 0.05) at 5 minutes after coronary occlusion. IABC was then administered for one hour, with a fall in aortic systolic pressure (112 +/- 6 to 105 +/- 7 mm Hg, P less than 0.05) and rise in peak aortic diastolic pressure (94 +/- 6 to 102 +/- 7 mm Hg, P less than 0.05). Despite this the ischemic area showed no change in perfusion (measured at the same time): 30.0 +/- 2.3 to 28.0 +/- 2.4 cc/100 g/min. Little change in wall motion occurred: aneurysmal bulging decreased modestly (4.5 +/- 0.3 to 3.6 +/- 0.3 mm, P less than 0.05), but ischemic wall velocity did not increase. After cessation of counterpulsation and one hour of coronary reperfusion aneurysmal bulging disappeared and wall velocity improved. The addition of norepinephrine (eight dogs) or nitroprusside (seven dogs) to intraaortic balloon counterpulsation did not cause a significant further improvement in the response of the dyskinesis during the period of ischemia. We conclude that IABC has little effect on ischemic dyskinesis, probably due to its failure to improve perfusion of the acutely ischemic myocardium.
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PMID:Effect of intra-aortic balloon counterpulsation on the motion and perfusion of acutely ischemic myocardium. An experimental echocardiographic study. 126 Sep 89

This study was designed to examine local effects of acute cellular injury on regional myocardial blood flow. Studies were carried out in awake dogs chronically prepared with indwelling catheters in the aorta and left atrium and an occluder on the left circumflex coronary artery. Regional myocardial blood flow was measured by using 7-10-mum radioisotope-labeled microspheres after reestablishing inflow to a region subjected to a 2-h complete coronary occlusion. Microspheres were injected 15 s, 15 min, 4 h, and 3 days after reperfusion to assess effects of cell injury at varying intervals after reperfusion. Effects of acute cellular injury on blood flow were assessed by determining the relationship between regional blood flow and the extent of subsequent cellular necrosis measured in multiple tissue samples, weight 1-2 g, from the entire ischemic zone. The extent of cellular necrosis was determined from histological sections of each tissue sample. Prolonged ischemia effected local tissue responses which altered perfusion as a function of the interval after reperfusion and the subsequent extent of myocardial necrosis. Although the net response in each region immediately after reperfusion was vasodilation, the hyperemia in regions which subsequently suffered cellular necrosis was attenuated in direct proportion to the extent of subsequent infarction. Blood flow to acutely injured regions remained equal to, or in excess of, flow to nonischemic regions 15 min after reperfusion, but at 4 h and 3 days after reperfusion, flow was significantly decreased in regions with greater than 50% infarction. Thus, these data indicate that prolonged ischemia initiates tissue responses which progressively reduce myocardial perfusion after reperfusion. These effects on tissue perfusion may result from normal responses to irreversible injury and (or) abnormal responses to reversible and thus, potentially alterable, ischemic injury.
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PMID:Local effects of acute cellular injury on regional myocardial blood flow. 126 76

The mechanical behavior of ischemic myocardium was studied in anesthetized open chest dogs. In each animal, a small well localized myocardial infarction was produced by ligation of a single ventricular branch of the left circumflex coronary artery. Serial in situ measurements of segment length were made by mercury-in-Silastic gauges sutured directly to the left ventricular surface. After coronary ligation, systolic aneurysmal bulging of the ischemic segment was uniformly noted. This was quantified as follows: normalized segment length change in this region, expressed in muscle lengths (where muscle lengths = phasic segment length amplitude/end-diastolic segment length), immediately increased from 0.06 +/- 0.01 (standard error of the mean) to 0.10 +/- 0.02 muscle lengths (+67 percent, P less than 0.02). Over a 6 hour period, muscle lengths progressively declined to near control values, but retained an aneurysmal contour. End-diastolic segment length increased 5 percent above control values after coronary occlusion and remained fixed at this level for 6 hours. In contrast, noninfarcted myocardium exhibited no significant changes in muscle length or end-diastolic segment length. These studies demonstrate that the degree of systolic aneurysmal bulging in infarcted myocardium, although initially great, resolves within 6 hours but retains an aneurysmal contour. These findings are consistent with either partial return of contractility or diminished local compliance, but persistence of an aneurysmal shape favors the latter mechanism. The fixed increase in end-diastolic segment length suggests that "stress-relaxation" takes place in the infarcted region. It is possible that diminished compliance in zones of infarction, previously noted after several days, begins within a few hours after the onset of ischemia.
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PMID:Experimental myocardial infarction: XII. Dynamic changes in segmental mechanical behavior of infarcted and non-infarcted myocardium. 126 50

Changes in both the structure and function of mitochondria occur in the dog heart as a consequence of severe ischemia produced by acute coronary occlusion. Brief periods of severe ischemia (reversible injury) produced no significant change in mitochondrial ultrastructure and no defects in pyruvate or succinate metabolism. However, periods of ischemia of 40-60 minutes' duration (irreversible injury) produced striking structural changes including swelling, an increase in matrix space, disorganization of cristae, and the appearance of amorphous matrix densities. After 60 minutes of severe ischemia, one or more amorphous densities were present in each mitochondrial profile. These osmiophilic structures contained lipid but have not been characterized further. Their presence was typical of the irreversible state. Mitochondria of irreversibly injured cells were fragile, and consequently were more difficult to isolate than mitochondria of control tissue. Furthermore, after isolation from tissue injured by 60 minutes of ischemia, they showed markedly defective function.
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PMID:Mitochondrial structure and function in acute myocardial ischemic injury. 126 93

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