作者: Brian Herman , J. M. Bond , J. J. Lemasters
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摘要: Cardiac myocytes exposed to anoxia hypercontract into a blebbed, rounded mass. Such hypercontraction is usually considered manifestation of irreversible injury. Here, we studied functional recovery, long-term viability and ATP levels cultured neonatal rat cardiac after metabolic inhibition with cyanide 2-deoxyglucose, model 'chemical hypoxia' which mimics the depletion reductive stress hypoxia. After addition inhibitors, 5-day ceased spontaneous contractions within 1-2 min, blebbed hypercontracted 35 lost 100 min as assessed by nuclear labelling propidium iodide. 11-day exhibited similar progression When inhibitors were removed, resumed an average 11 in non-hypercontracted myocytes. In myocytes, weak regardless length time spent state, but restoration strong synchronous took hours. Recovering cells remained viable through 24 hours observation, whereas contractility never returned iodide-labelled cells. decreased rapidly chemical hypoxia partially restored upon washout inhibitors. recovery was Thus, contractile dysfunction during not due lack regeneration ATP. conclusion, hypercontracture Contractile following from observed here may represent 'in vitro stunning'.