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)

Recovery of mechanical function by ischemic myocardium is dependent on the restoration of nutritive blood flow and oxidative metabolism subsequent to reperfusion. To characterize the time course and extent of recovery of perfusion and metabolism, we used positron emission tomography with 15O-labeled water and 11C-labeled palmitate to sequentially study six dogs after 2 hr of ischemia followed by reperfusion for 4 wk. Myocardial blood flow in the ischemic region increased from 15 +/- 8% of normal during coronary occlusion to 82 +/- 25% 1 hr after reperfusion. Despite maintained coronary patency documented angiographically, flow was reduced after 24 hr to 37 +/- 16% of normal. This decrease was temporary, with flow returning to 66 +/- 11%, 62 +/- 7%, and 64 +/- 18% of normal after 1, 2, and 4 wk of reperfusion, respectively. Uptake of 11C-labeled palmitate paralleled alterations in perfusion during ischemia and early reperfusion, averaging 32 +/- 15% of normal during ischemia, and 67 +/- 22% and 36 +/- 10% after 1 and 24 hr of reperfusion. After that, palmitate uptake was more variable. Flow and fatty acid uptake after 4 wk of reperfusion were not related to collateral flow during ischemia or the extent of initial reperfusion. However, uptake of palmitate 1 hr after reperfusion was a strong predictor of the uptake of palmitate 4 wk after reperfusion (r = 0.86, p less than 0.03). The results indicate that positron emission tomography with 15O-labeled water and 11C-labeled palmitate may be useful for assessing the success of recanalization in restoring nutritive perfusion and fatty acid metabolism and that the uptake of [11C]palmitate early after reperfusion predicts the ultimate salvage of myocardium.
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PMID:The temporal pattern of recovery of myocardial perfusion and metabolism delineated by positron emission tomography after coronary thrombolysis. 311 76

In twenty-one anaesthetized open chest cats the left anterior descending coronary artery (LAD) was occluded for three hours. Seven cats were pretreated with a bolus injection of Verapamil, followed by a continuous infusion of Verapamil during the ischaemic period. Seven cats were pretreated with a bolus injection of Timolol to a heart rate reduction of 20 beats/min or more and seven cats were given saline. In the latter two groups the cats received a continuous infusion of saline during the period of coronary occlusion. Biopsies were taken from the mid-myocardium of the normal, border and ischaemic zones, as defined by fluorescein staining, and verified by blood flow measurements with radiolabelled microspheres. Standard point counting techniques were used for calculations of fractional volumes of mitochondria, cytoplasm and myofibrils as well as of mitochondrial surface density and surface to volume ratio. We observed a cytoplasmic oedema in the border and ischaemic zones, that was not altered by medical treatment. In the border zone of the control cats there is greater mitochondrial swelling than in the ischaemic zone. This particular swelling is not seen in the treatment groups. However, in the normal and border zones of the verapamil group the mitochondria are smaller when compared with the respective zones in the two other groups, but increases relatively more in size in the border and ischaemic zones. Furthermore, we measured the water content, sarcomere length and per cent heavily damaged cells. These variables were not altered by Verapamil or Timolol in any zone when compared with the respective zones in the control group.
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PMID:Effects of verapamil and timolol on cellular morphometric changes in cat hearts with regional ischaemia. 312 69

Functional recovery with surgical revascularization of acutely ischemic myocardium has not been compared with its nonsurgical counterpart in experimental preparations of coronary occlusion. This study compares the functional and metabolic recovery of ischemic (1 hr coronary occlusion) segments revascularized either by restoration of coronary patency (simulating nonsurgical recanalization, e.g., angioplasty) or by surgical revascularization with multidose hypothermic potassium blood cardioplegic solution. Twenty-two anesthetized open-chest dogs were instrumented with Millar micromanometer-tip catheters to measure left ventricular and aortic pressures. Piezoelectric ultrasonic dimension gauges were implanted in the subendocardium supplied by the left anterior descending coronary artery to measure segmental contractile function. In five dogs, only biopsy samples were obtained for control measurements of ATP, creatine phosphate, and tissue water content. In the remaining 17 dogs, the left anterior descending artery and collaterals were ligated for 1 hr. The ligatures were removed in eight dogs and coronary perfusion continued for 2 hr, simulating nonsurgical reperfusion. The remaining nine dogs were placed on cardiopulmonary bypass and the hearts were arrested for 1 hr with multidose (every 20 min) blood cardioplegic solution enhanced with glutamate and aspartate, simulating surgical revascularization (coronary artery bypass grafting). The coronary ligatures were not released until the second cardioplegic infusion, simulating graft placement. One hour of coronary occlusion placed 39.4 +/- 2.5% of the left ventricle at risk, and converted active systolic shortening to persistent paradoxical bulging (25.2 +/- 2.2% to -5.8 +/- 1.2% systolic shortening).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immediate functional recovery and avoidance of reperfusion injury with surgical revascularization of short-term coronary occlusion. 315 12

It has been suggested that coronary ischemia increases extravascular lung water. To determine whether pulmonary microvascular permeability is increased by coronary ischemia, we measured pulmonary hemodynamics, lung lymph flow (QL), and lymph-to-plasma protein concentration ratio (L/P) in 12 sheep with chronic lung lymph fistulas. Studies were done in 3 groups: in group 1 (n = 7) a marginal branch of the left circumflex artery (Lcx) was occluded, in group 2 (n = 5) left atrial pressure (Pla) was mechanically raised by 10 mmHg, and in group 3 (n = 5) Lcx was occluded and Pla was raised by 10 mmHg. In group 1, coronary occlusion increased QL (4.6 +/- 0.4 to 8.3 +/- 2.6 ml/h) without changes in L/P. In group 2, elevated Pla increased QL (5.1 +/- 1.2 to 10.1 +/- 3.0 ml/h) with decreases in L/P (0.71 +/- 0.02 to 0.61 +/- 0.02). In group 3, coronary occlusion with elevated Pla caused a further increase in QL (5.0 +/- 1.5 to 16.9 +/- 4.6 ml/h) without significant decreases in L/P (0.71 +/- 0.01 to 0.65 +/- 0.06). Lung lymph concentrations of 6-keto-prostaglandin F1 alpha (a degradation product of prostacyclin) increased transiently after coronary occlusion. These results indicate that coronary occlusion can increase transcapillary protein transport in lungs of conscious sheep and simultaneously increase prostacyclin production in the lung.
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PMID:Effects of coronary ischemia on lung fluid balance in conscious sheep. 317 Apr 13

In 24 anesthetized open-chest dogs, we examined the time course of changes in contractile function, diastolic muscle stiffness (sonomicrometry), tissue water content, and ultrastructure after 1 hour of occlusion of the left anterior descending coronary artery and after 2 hours of unmodified reperfusion. One hour of occlusion of the left anterior descending artery replaced active shortening with passive bulging (21.4% +/- 2.9% versus -5.9% +/- 0.9%, p less than 0.05) in the involved segment. There was no increase in either subendocardial water content (78.6% +/- 0.1% versus 79.7% +/- 0.7%) or operative muscle stiffness (2.80 +/- 0.72 versus 2.36 +/- 0.42 mm Hg/mm) after the occlusion period. There were only mild to moderate ultrastructural alterations suggestive of reversible injury. In sharp contrast, reperfusion was associated with a 2.48% increase in subendocardial water content (p less than 0.05), a 42% increase in diastolic muscle stiffness (3.34 +/- 0.42 mm Hg/mm, p less than 0.05), and greater ultrastructural damage. We conclude that myocardial injury is significantly extended with unmodified blood reperfusion after temporary coronary occlusion.
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PMID:Reperfusion injury after temporary coronary occlusion. 337 61

Concomitant use of pharmacologic agents may be required for maximal salvage of ischemic myocardium by reperfusion. Accordingly, in dogs with induced thrombotic coronary occlusion, the effects of intravenous diltiazem given 30 minutes before administration of streptokinase on myocardial blood flow and myocardial salvage were evaluated. Two independent types of end points were employed. Positron emission tomography was utilized for noninvasive assessment of myocardial perfusion and infarct extent. Direct measurements included quantification of myocardial infarction by assay of creatine kinase activity in myocardial homogenates. Infarct extent averaged 27.9 +/- 11.4% of left ventricular weight in 10 control dogs in which coronary occlusion was maintained for 24 hours. In eight dogs given streptokinase alone, the infarct extent averaged 16.7 +/- 10.0% of left ventricular mass (p less than 0.05 versus control). In nine other dogs given diltiazem (15 micrograms/kg per min continuously until death was induced) beginning 30 minutes before streptokinase, infarct extent averaged 9.4 +/- 6.7% of left ventricular mass (p less than 0.05 compared with reperfusion alone). At the dose administered, diltiazem did not alter blood flow, heart rate or mean arterial pressure after coronary occlusion or thrombolysis. The region at risk, determined in 16 dogs from perfusion images obtained with positron tomography and oxygen-15-labeled water after coronary occlusion, was similar in the three groups (30.6 +/- 7.3% of the left ventricle in six control dogs, 31.8 +/- 4.5% in five dogs with reperfusion alone and 30.5 +/- 11.6% in five dogs with reperfusion plus diltiazem). Infarct size quantified in terms of the extent of myocardium exhibiting less than 50% of peak carbon-11-labeled palmitate uptake 24 hours after occlusion and expressed as the percent of the region at risk averaged 89.6 +/- 11.4% in control dogs, was significantly reduced to 45.1 +/- 29.8% in dogs with reperfusion alone and was reduced further to 22.3 +/- 16.4% in dogs given diltiazem and reperfusion. Thus, concomitant treatment with diltiazem markedly enhances salvage of reperfused myocardium after coronary thrombolysis.
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PMID:Enhancement of salvage of reperfused ischemic myocardium by diltiazem. 348 47

This study determines the additional protection provided by multidose hypothermic potassium blood cardioplegia over cardiopulmonary bypass alone following one hour of coronary occlusion. In 19 anesthetized dogs having an open-chest procedure, the left anterior descending coronary artery (LAD) was occluded for one hour, and this resulted in loss of active shortening in the affected zone (sonomicrometry). Cardiopulmonary bypass was established, and the dogs were divided into two groups based on the mode of reperfusion. In 10 dogs, hearts were arrested for one hour with amino acid-enhanced multi-dose blood cardioplegia; the ligatures were removed prior to the second infusion. In the 9 remaining dogs, the ligatures were removed and reperfusion was initiated with unmodified blood on total vented bypass. Both groups were reperfused for one additional hour. Postischemic levels of adenosine triphosphate (ATP) were comparable in the blood cardioplegia and bypass groups, and subendocardial levels averaged 42.8% and 45.8% of controls, respectively. Levels of creatine phosphate returned to control values. Subendocardial water content was significantly less in the blood cardioplegia hearts than the bypass hearts (79.4 +/- 0.5% vs. 81.5 +/- 0.5%; p less than .05); subendocardial water content in the blood cardioplegia group was not different from controls (78.6 +/- 0.1%). Blood cardioplegia restored significantly more fractional shortening than total vented bypass alone (39.3 +/- 9.8% vs. 6.3 +/- 9.1% of control), despite similarities in postischemic levels of ATP. We conclude that blood cardioplegia allows better myocardial salvage in the setting of evolving infarction. Therefore, attention must be directed to both the conditions (bypass, delivery pressure) and composition (cardioplegia) of reperfusion.
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PMID:Surgical revascularization of acute evolving myocardial infarction without blood cardioplegia fails to restore postischemic function in the involved segment. 360 61

Extracellular and intracellular longitudinal resistances (ro and ri), transmembrane potentials, and conduction velocity were determined in arterially blood-perfused rabbit papillary muscles. Cable analysis was made possible by placing the muscle in a H2O-saturated gaseous environment, which acted as an electrical insulator. Ischemia was produced by exchanging the O2 in the atmosphere by N2 (94% N2-6% CO2) in addition to arresting coronary flow. The first 10-15 minutes of ischemia were characterized by an increase in ro, while ri remained constant. The early part of the increase in ro coincided with the drop in perfusion pressure and was probably due to the diminution of intravascular volume. Rapid electrical uncoupling, reflected by an increase in ri (threefold within 5 minutes), occurred thereafter. The dissociation between the early increase in ro and the delayed increase in ri produced an initial increase in the ratio ro:ri, which subsequently decreased. The decrease in conduction velocity was less than observed in intact hearts with ischemia. This difference is explained by the relatively small changes in resting membrane potential and action potential amplitude in the preparation used. Our results suggest that in the early, reversible phase of ischemia, the increase in ro contributes to a small but significant extent to the slowing of conduction. After 15-20 minutes, the rapid cellular uncoupling, which was most likely coincident with breakdown of cellular homeostasis, may contribute to the occurrence of arrhythmias during this phase of ischemia. Moreover, the early change in the ratio ro:ri will influence the amplitude of the extracellular electrograms following coronary occlusion (TQ-segment and ST-segment shifts).
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PMID:Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. 362 91

The effects of repeated brief episodes of ischemia on myocardial cell volume, electrolytes and ultrastructure were studied in dogs. Seventeen animals were divided into five groups. Group 1 underwent a single 10 minute occlusion of the circumflex coronary artery, with no subsequent reperfusion. Group 2 was similarly subjected to a 10 minute coronary occlusion, but was allowed a 20 minute reperfusion period. Group 3 underwent two 10 minute occlusions separated by 20 minutes of reperfusion and Group 4 underwent four 10 minute occlusions, each separated from the next by 20 minutes of reperfusion. Group 5 was subjected to a single, uninterrupted 40 minute occlusion. The anterior and posterior papillary muscles in each heart were sampled to compare nonischemic versus ischemic myocardium. No changes in myocardial water or electrolytes occurred during ischemia. However, reperfusion was associated with slight increases in tissue water and potassium, loss of magnesium and minimal changes in sodium or calcium ions. Electron microscopic analysis revealed signs of mild ischemic injury (absence of normal intramitochondrial granules, partial loss of glycogen and slight clumping of the nuclear chromatin) in posterior papillary muscle from Groups 1, 3 and 4. Group 2 showed complete recovery with 20 minutes of reperfusion, whereas Group 5 showed evidence of irreversible injury. There was no difference in the appearance of myocardium that had been subjected to one, two or four 10 minute occlusions. It is concluded that intermittent periods of reperfusion between brief episodes of coronary ischemia have a protective effect and prevent a cumulative deterioration of myocardial ultrastructure.
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PMID:Effect of repetitive brief episodes of ischemia on cell volume, electrolytes and ultrastructure. 371 42

This study tests the hypothesis that improved myocardial salvage following regional ischemia occurs when attention is directed toward the duration of blood cardioplegic reperfusion rather than the reperfusate "dose". Pilot studies after global ischemia established the postischemic oxygen use pattern consistent with normal and impaired recovery; the best recovery occurred when postischemic muscle consumed oxygen in excess of basal demands. Experimental studies were then performed on 22 dogs undergoing 2 hours of left anterior descending coronary occlusion. Nine dogs received normal blood reperfusion, with the heart allowed to remain in the beating, working state. In 13 dogs, cardiac O2 demands were kept low during reperfusion by delivering a dose of 150 to 250 mumol/L Ca2++ aspartate-glutamate-enriched blood cardioplegic solution containing 250 to 350 micrograms/kg body weight diltiazem during total vented bypass. This same reperfusate dose with diltiazem was given over 10 minutes in five dogs and over 20 minutes in eight others. Persistent systolic bulging (ultrasonic crystals) of -27% (p less than 0.05) of systolic shortening followed normal blood reperfusion without bypass. During blood cardioplegic reperfusion, regional O2 uptake exceeded basal demands by 24 ml/100 gm/min at 10 minutes (p less than 0.05) and did not return to baseline until 20 minutes had elapsed. Hearts reperfused with blood cardioplegia for 20 minutes had better recovery of systolic shortening (58% versus 30%, p less than 0.05), less edema (79.8% versus 80.9% water content, p less than 0.05), and less triphenyltetrazolium chloride nonstaining (12% versus 21%, p less than 0.05) than those reperfused for 10 minutes with the same solution containing the same diltiazem dose. Continuing blood cardioplegic reperfusion until myocardial oxygen uptake reaches control levels enhances regional functional recovery after acute coronary occlusion. These results indicate that attention should be directed toward the duration of reperfusion, as well as the "dose" of cardioplegic reperfusate.
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PMID:Effects of "duration" of reperfusate administration versus reperfusate "dose" on regional functional, biochemical, and histochemical recovery. 374 87


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