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)

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

In our earlier experiments prolonged administration of the stable PgI2 analogue: 7-oxo-PgI2 ephedrine salt to dogs afforded a long-lasting protection against coronary occlusion induced ischemia as well as against postocclusion and reperfusion arrhythmias. In the present experiments we wanted to clear, whether this prolonged protective action is present in other types of arrhythmia, which are not due to ischemia. The ouabain-arrhythmia seemed to be suitable for elucidation of this question. Therefore guinea pigs were pretreated with 50 micrograms/kg i.p. 7-oxo-PgI2 and 24, 48, 72 and 96 hrs after treatment anesthetized with 35 mg/kg sodium pentobarbitone. To prevent ouabain bradycardia, 0.4 mg/kg atropine was administered i.p. Ouabain was applied by intermittent infusion technique i.e. an initial infusion for 5 minutes of a total dose of 60 micrograms/kg into the right jugular vein was followed after a 25 minutes interval by infusions of 30 micrograms/kg for 2.5 minutes every 10 minutes until cardiac arrest. The ouabain induced rhythm disturbances appeared in the following order: Anomalies in T wave morphology, ventricular or nodal extrasystoles, atrio-ventricular and intraventricular conduction disturbances, ventricular tachycardia, ventricular fibrillation and finally cardiac arrest. If 50 micrograms/kg i.p. 7-oxo-PgI2 was given to ouabain-intoxicated animals at the appearance of the first extrasystole a transient aggravation of this arrhythmia developed. In 7-oxo-PgI2 pretreated animals the total amount of ouabain necessary to induced rhythm disturbances was markedly elevated, the appearance of the various arrhythmias significantly delayed. Maximal protective effects were seen 48 hrs after the administration of 50 micrograms/kg 7-oxo-PgI2.
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PMID:On the 7-oxo-PgI2 induced lasting protection against ouabain arrhythmias in anesthetized guinea pigs. 247 Mar 57

The effects of digitalis (ouabain infusion, priming dose of 10 micrograms/kg/min followed by 2.0 micrograms/kg/min) on subepicardial and subendocardial ischemic dysfunction during partial occlusion (59.4% reduction in coronary flow) and total coronary occlusion were evaluated in 14 dogs using pairs of ultrasonic crystals implanted in the epicardial and endocardial layers. After 30 minutes of partial coronary occlusion, systolic shortening in the ischemic zone decreased from 12.4 +/- 2.9% to -0.4 +/- 0.9% (p less than 0.001) in the epicardium and from 18.9 +/- 3.1% to -1.0 +/- 1.1% (p less than 0.001) in the endocardium. Ouabain infusion increased the systolic shortening from -0.4 +/- 0.9% to 10.6 +/- 3.1% (p less than 0.001) in the epicardium and from -1.0 +/- 1.1% to 17.2 +/- 3.4% (p less than 0.001) in the endocardium. The end-diastolic length did not change. In contrast, after 30 minutes of total coronary occlusion, systolic shortening in both epicardial and endocardial layers was replaced by systolic lengthening and remained unaffected by ouabain infusion in both layers. Systolic shortening in the nonischemic epicardial and endocardial layers increased consistently. We conclude that ouabain improves the contractile function of both ischemic epicardial and endocardial layers layers after partial coronary occlusion and does not worsen subendocardial ischemic dysfunction. After total coronary occlusion, however, the contraction of the ischemic zone is unaffected by ouabain.
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PMID:Effects of digitalis on subendocardial and subepicardial dysfunction during acute ischemia. 707 93

The effect of ouabain (15 microgram/kg) on subepicardial and sub-endocardial blood flow, oxygenation, and small-vessel blood content was studied in anesthetized open chest rabbits with hearts subjected to acute coronary occlusion. 10 minutes after occlusion, blood flow was 48% lower than in the control region. Ouabain lowered blood flow significantly in the non-occluded region and insignificantly in the occluded area. Small-vessel blood content, a measure of open capillary density, was unaffected by occlusion or ouabain. After occlusion, relative tissue PO2 fell to a greater extent in the affected subendocardium than the affected subepicardium. Ouabain, therefore, appears to be well tolerated in both the control and ischemic regions in terms of oxygen supply and consumption.
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PMID:Effect of ouabain on O2 supply/demand in normal and ischemic heart. 718 34