Alleviation of myocardial stunning by leukocyte and platelet depletion.

摘要: Neutrophils accumulate in myocardium rendered ischemic and reperfused. Activated neutrophils release mediators such as metabolites of oxygen that can compromise myocellular integrity provoke cardiac dysfunction. Although it is established leukopenia reduces infarct size, the role leukocytes source free radicals postischemic contractile dysfunction unresolved. A carotid left anterior descending coronary-artery extracorporeal circuit without (n = 8) or with a Leukopak filter 6) to deplete platelets from blood entering artery was anesthetized, open-chest dog 30 minutes before ischemia. Subendocardial segmental function monitored by sonomicrometry, ischemia produced stopping flow for 15 followed 3 hours reperfusion. Depleting 90 +/- 3.2% 100% improved (from 30.5 7% 74.1 12.7% control versus leukocyte-depleted dogs, respectively) at In leukopenic group, however, there progressive decline contractility 32.5 13.8% reperfusion associated return and, lesser extent, 70.2 21.9% 15.5 4.3% systemic values, respectively. Removal perfusing coronary vascular bed only 67.7 6.9% 54.7 12.1% 6). Scanning electron microscopy revealed adherent epicardial arteries animals after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)