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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in stroke volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation MAP (8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.
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PMID:Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion. 47 39

Ventricular function curves relating stroke work and left ventricular end-diastolic pressure were generated in awake dogs during increases in preload produced by infusion of fluid and during increases in afterload produced by administration of phenylephrine. The ventricular function curves produced by preloading were steeply upsloping whereas those produced by afterloading were essentially horizontal. Coronary occlusion produced downward displacement of these horizontal curves, but no change in slope. This increases in afterload did not help to demonstrate the functional impairment produced by coronary occlusion.
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PMID:Effect of increases in afterload before and after coronary occlusion in awake dogs. 48 80

We studied the effects of coronary occlusion and of subsequent ouabain administration on regional myocardial function, flow, and electrograms in 14 conscious dogs. Coronary occlusion resulted in a graded loss of regional function as reflected by measurements of segment length (SL), velocity of SL shortening and myocardial "work" from the normal to severely ischemic zones, along with graded flow (radioactive microsphere technique) reductions and graded elevation of the regional S-T segment. Ouabain, 20 microgram/kg, improved function in the normal zone, in which stroke shortening rose by 0.23 +/- 0.07 mm (mean +/- SE) and "work" rose by 30.2 +/- 9.5 mm Hg-mm. In moderately ischemic segments, stroke shortening rose by 0.60 +/- 0.05 mm and "work" rose by 58.1 +/- 6.1 mm Hg-mm. In the majority of severely ischemic segments, stroke shortening and "work" also increased; the average effect in all severely ischemic segments was an increase in stroke shortening of 0.35 +/- 0.10 mm and in "work" of 31.5 +/- 9.9 mm Hg-mm. In addition, ouabain reduced S-T elevation by 0.90 +/- 0.20 mV in moderately ischemic zones and by 3.14 +/- 0.35 mV in severely ischemic zones, and increased flow by 28 +/- 6% and 46 +/- 9% in moderately and severely ischemic zones, respectively. All these changes were significant, P less than 0.01. Thus, ouabain caused an improvement in perfusion of ischemic tissue, which was associated with significant enhancement of stroke shortening and "work." Most strikingly, ouabain returned normal systolic shortening to 10 severely ischemic segments which previously were akinetic.
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PMID:Effects of a cardiac glycoside on regional function, blood flow, and electrograms in conscious dogs with myocardial ischemia. 67 24

The influence of an instantaneous increase in afterload on the hemodynamics and regional myocardial function was studied in five anesthetized dogs before and after occlusion of the left anterior descending coronary artery. By inflation of an intaaortic balloon during single ejections, an instantaneous increase in afterload was obtained. From biplane cineventriculograms, the following parameters were calculated: left ventricular volumes (EDV, ESV), stroke volume (SV), ejection fraction (EF). Mean circumferential fiber shortening (V CF) was calculated in three ventricular diameters in the RAO projection. Simultaneously PLV, PLVED, PAo, and LV dp/dt were obtained. In the control ventriculograms, an increased afterload (delta PLV 16.4 +/- 8 mm Hg) caused only a minor decrease of SV (2.6 +/- 2.5 ml), EF (4.2 +/- 2.4%), and V CF (0.20 circ . s -1). After coronary occlusion (delta PLV 14.5 +/- 6.7 mm Hg),the reduction of SV (5.9 +/- 2.7 ml) and EF (8.2 +/- 2.6%) was more pronounced. This was caused mainly by a significant reduction of V CF in the center of ischemia (delta V CF -93%). For the evaluation of regional myocardial function by ventriculography, the marked influence of afterload in ischemic areas must be taken into consideration. This is of special interest in comparative ventriculograms, such as those before and after coronary bypass surgery.
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PMID:[The influence of afterload on the normal and ischemic myocardium in the dog]. 71 34

An on-line, real-time histogram display of heterogeneity of oxygen delivery to perfused and in situ organs is afforded by a flying-spot fluorometer that provides excitation for either oxidized flavoprotein of the mitochondrial space or reduced pyridine nucleotide of mitochondrial and cytosolic spaces. Emission from the two fluorochromes is acquired at 10(4) to 10(5) data points/s and histograms of the fluorescence intensity versus the number of occurrences of that intensity are displayed at 1--10 times per second. The histograms show alterations of the intensity and of the degree of heterogeneity of the redox states of perfused heart with model coronary occlusion, of perfused and in situ rat liver, and of rat and gerbil models of stroke. The percentage change of oxygen delivery to the intracellular space can be calculated from the areas under the histogram.
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PMID:Heterogeneity of oxygen delivery in normoxic and hypoxic states: a fluorometer study. 73 69

The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.
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PMID:Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion. 81 89

The hemodynamic and metabolic changes, during coronary occlusion and during coronary perfusion with non-oxygenated solution, were studied in anesthetized dogs. Coronary perfusion with non-oxygenated Tyrode's solution was performed through a cannula inserted into the left circumflex coronary artery. Left ventricular peak systolic and end-diastolic pressure (LVSP and LVEDP) were measured, and peak LV-dp/dt/IIP calculated. Stroke volume was measured, and the changed of the local myocardial segment length were recorded by a strain gauge arch sutured on that portion of the myocardium perfused through the left circumflex coronary artery. The efflux of lactic acid into the venous blood from the myocardium perfused through the left circumflex coronary artery was calculated. After 10 sec of coronary occlusion, LVSP, SV, and peak LV-dp/dt/IIP declined; LVEDP elevated and a systolic bulge appeared on the local myocardial segment length curve. There was almost no change in these parameters during 3 min of perfusion with non-oxygenated solution. The efflux of lactic acid was more marked during the perfusion with non-oxygenated solution than during coronary occlusion. The delay of the depression of cardiac function during perfusion with the non-oxygenated solution could be related partly to the "wash-out" of metabolites, such as lactic acid, accumulated in the anoxic myocardium.
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PMID:Cardiac function under myocardial ischemia. 88 51

Effect of increased left atrial pressure and a positive inotropic agent upon asynergic left ventricle which was produced by acute occlusion of LAD were examined in 8 open-chest dogs. Systolic bulging in ischemic area was qualified by ESL/EDL in percentage. Left atrial pressure was controlled by the reservoir connected to left atrial appendage with a large bore tubing. Cardiac output and aortic pressure were decreased following coronary occlusion without change in isometric developed tension in nonischemic area of left ventricle. Increase of left atrial pressure from 5 mmHg to 14 mmHg produced rise in stroke volume to 191% and rise in aortic pressure to 156% in asynergic left ventricle respectively. These increases were not accompanied by change in ESL/EDL. Therefore, extracardiac factors were assumed to explain the prominent increase in left ventricular stroke work by elevation of left atrial pressure in asynergic left ventricle. Isoproterenol enhanced total cardiac performance by increasing the function of nonischemic area without deterious effect on the ischemic area.
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PMID:Behavior of asynergic ventricle. 92 17

The results of the present investigation indicate that ISDN infusion following experimental coronary occlusion in anesthetized dogs (1) lowers systemic, cardiac, and pulmonary blood pressures; (2) decreases systemic resistance; (3) has no significant effect on cardiac output, heart rate, and stroke volume; (4) decreases serum CPK levels; and (5) has little effect on blood biochemical parameters. These results suggest that ISDN may have a minimal effect on the ischemic heart by means of a slight decrease in peripheral vascular resistance and systemic blood pressure.
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PMID:The effect of isosorbide dinitrate following experimental coronary occlusion. 94 33

1. This study includes 1038 patients (325 men and 713 women) who consulted the medical out-patient clinic, Rigshospitalet, Copenhagen, during the years 1932-38. All these patients had a blood pressure of 160/100 mmHg or 180 mmHg or more. 2. The average age at the first examination was 54 years; 97% were followed at intervals of 10 years until 1975, when sixty patients were still alive. Treatment was minimal until 1970. 3. Sixty percent of the men and 76% of the women reached an age of 65 years or more. Nine percent of the total patients lived to 85 years or more. Excess mortality was far higher in men than in women. 4. Causes of death were stroke in 17%, heart failure in 24%, coronary occlusion in 16%, uraemia in 4% and other diseases in 39%. At the first examination, thirteen cases of malignant hypertension were registered, none at later sessions.
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PMID:A 40 years' follow-up study of 1000 untreated hypertensive patients. 107 6


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