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 tested whether recombinant human superoxide dismutase conjugated to polyethylene glycol (PEG-SOD) to prolong its plasma retention time could limit myocardial infarct size in an ischemia-reperfusion model in the rabbit. One group of animals received 1000 units/kg of PEG-SOD as an intravenous bolus 15 min before coronary occlusion. A second group received saline only and served as controls. Under pentobarbital anesthesia, a left coronary branch was occluded for 30 min and then reperfused. The surgical wounds were repaired and the animals were allowed to recover. Seventy-two hours after the coronary occlusion, the heart was excised and the size of the area at risk (ischemic vascular bed) was assessed with fluorescent particles and the infarct size was determined by histology (Hematoxylin-eosin, Azan stain). Infarct size as a percentage of the area at risk was similar between the groups, 46.5 + 2.7 in the PEG-SOD group (n = 8) and 48.9 + 3.1 in the control group (n = 8). There were no significant differences between the groups indicating that PEG-SOD did not limit infarct size in this model.
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PMID:Superoxide dismutase conjugated to polyethylene glycol fails to limit myocardial infarct size after 30 min ischemia followed by 72 h of reperfusion in the rabbit. 206 22

Increases in regional myocardial blood flow (Qm) developing soon after myocardial infarction may minimize myocardial necrosis. To test this hypothesis, Qm in the area surrounding an acutely occluded coronary artery was determined successively over 4 weeks in 11 dogs. Non-radioactive colored microspheres were injected into the left atrium 5 s (Qm at this time is referred to as Q1), 3 h (Q2), 12 h (Q3), and 4 weeks (Q4) after occlusion of the coronary artery. After termination of the experiment, the heart was removed, and Qm and three indices of myocardial necrosis i.e., myocardial creatine kinase activity (CK), infarct size determined by triphenyl tetrazolium chloride stain (TTC), and myocardial fibrosis visualized by Azan-Mallory stain, were determined. Each Qm was expressed as a percentage of normal: Qm (% of normal) = [Q/Qc] ischemic area/[Q'/Qc']non-ischemic area x 100, where Qc indicates Qm determined before coronary occlusion. In the ischemic area of the left ventricle, Q1, Q2, Q3, and Q4 were 25 +/- 3%, 30 +/- 3%, 31 +/- 3%, and 42 +/- 3% of normal, respectively, in the inner layer, and 31 +/- 3%, 52 +/- 4%, 52 +/- 4%, and 77 +/- 6% of normal, respectively, in the outer layers. During the 4-week period, the increase of Qm in the outer layer was greater than that in the inner layer. The inner layer showed a small increase of flow from Q3 to Q4 (9 +/- 2%), but in the outer layer there were greater flow increases from Q1 to Q2 (21 +/- 3%) and from Q3 to Q4 (24 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New collateral flow increasing early after coronary occlusion prevented myocardial necrosis in dogs. 853 Mar 20

It is not clear why late reperfusion therapy in patients with acute myocardial infarction is effective. An investigation was carried out as to whether or not reperfusion conducted 12 h after coronary occlusion causes myocardial salvage in dogs. Coronary arteries were occluded in 11 mongrel dogs and a portion of the occlusion (late reperfusion area; LR area) reperfused 12 h later; the other part was left occluded (permanent occlusion area; PO area). The dogs were maintained for 4 weeks after reperfusion. Regional myocardial blood flow (Qm) was measured by the non-radioactive colored microsphere method. In both areas, the transmurality of necrosis was measured by triphenyl tetrazolium chloride staining, and the amount of viable myocardium and the extent of fibrosis was determined by Azan-Mallory staining. Qm decreased markedly after coronary occlusion to similar levels in both areas until 12 h. Qm transiently increased in the LR area only following reperfusion after 12 h. The transmurality of necrosis in the PO area was 83.8+/-10.5%, but that in the LR area was 58.7+/-21.3%, a significant decrease (p<0.01). In the outer layer, the amount of viable myocardium was significantly greater, and the extent of myocardial fibrosis was significantly less in the LR area. Evaluation in the same heart of dogs confirmed the myocardial salvage effects of late reperfusion (12 h after coronary occlusion).
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PMID:Myocardial salvage by reperfusion 12 hours after coronary ligation in dogs. 958 65