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)

Intramyocardial pressure and segment length were measured during control conditions, during 30 sec coronary artery occlusion, and during reperfusion in the subendocardial (ENDO) and in the subepicardial (EPI) layers of the left ventricular wall, in 9 open-chest dogs. Under control conditions systolic subendocardial pressure, 179 +/- 11 mmHg, exceeded subepicardial pressure, 97 +/- 9 mmHg (P less than .001); the maximal rate of change of pressure in the subendocardium, 2231 +/- 170 mmHg/sec, was greater than in the subepicardium, 960 +/- 125 mmHg/sec, (P less than .001). Subendocardial systolic shortening, 23 +/- 2% was greater than subepicardial systolic shortening 16 +/- 1% (P less than .001). The maximal rate of systolic shortening in the subendocardium, 32 +/- 5 mm/sec, was also higher than in the subepicardial, 14 +/- 1 mm/sec (P less than .001). When the left anterior descending coronary artery was closed, subendocardial and subepicardial systolic pressures decreased immediately; conversely, appreciable changes in segment length were delayed 10-12 heart beats. After 30 sec of coronary occlusion a 35% reduction was observed in subendocardial and subepicardial systolic pressures, and systolic lengthening occurred. During reperfusion systolic shortening showed a brief overshooting and was back to control after 10 +/- 2 sec in subepicardium and 13 +/- 2 sec in subendocardium. Systolic intramyocardial pressure recovered in 14 +/- 3 sec in EPI and 18 +/- 2 sec in ENDO and subsequently rose above control level. Peak rebound occurred after 50-75 sec of reperfusion and was 27% higher than control in subendocardium and 20% in subepicardium. In 5 dogs the effects of coronary occlusions lasting 5, 15, 30, 45 and 60 sec were investigated. A progressive increase in ischemic depression and reperfusion rebound in subendocardial and subepicardial pressures was observed. These data show that subendocardial and subepicardial are both functionally depressed by coronary occlusion and that subendocardial and subepicardial both contribute to reperfusion hyperkinesis. Systolic intramyocardial pressures persist when shortening is abolished. Ischemic depression and reperfusion rebound of systolic intramyocardial pressures are affected by duration of coronary occlusion.
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PMID:Regional myocardial systolic function. Effects of coronary occlusion and reperfusion. 653 84

The effect of phenoxybenzamine (2 mg/kg) on subepicardial (EPI) and subendocardial (ENDO) blood flow and oxygenation was determined in ischemic and non-ischemic areas of hearts subjected to acute coronary occlusion in 24 pentobarbital-anesthetized open-chest New Zealand white rabbits. Ten minutes after occlusion, blood flow measure with radioactive microspheres was 57% lower in the occluded region compared to the non-occluded area. There were no EPI vs. ENDO differences at this time. Phenoxybenzamine was then administered and one hour after occlusion, flow in all areas was significantly reduced. Flow in the occluded area fell to a lesser extent than in the non-occluded area. ENDO flows were lower than EPI in both areas. After occlusion, relative tissue PO2 fell significantly in the affected areas. No other changes were significant. Phenoxybenzamine lowered relative tissue PO2 in the occluded ENDO but had no other effect. This indicates that the relationship of O2 supply to consumption is preserved in the heart after phenoxybenzamine except in the occluded ENDO. In this region, the fall in relative tissue PO2 indicates that the reduction in flow is large compared to any change in metabolism. The reduction in this relationship may be due to reduced perfusion pressure for collateral flow and/or "coronary steal".
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PMID:Regional blood flow and oxygenation of the rabbit heart subjected to acute coronary occlusion - effect of phenoxybenzamine. 707 52