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Research Article Free access | 10.1172/JCI114501
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224.
Find articles by Weiss, R. in: JCI | PubMed | Google Scholar
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224.
Find articles by Gerstenblith, G. in: JCI | PubMed | Google Scholar
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224.
Find articles by Lakatta, E. in: JCI | PubMed | Google Scholar
Published March 1, 1990 - More info
Delayed recovery of contractile function after myocardial ischemia may be due to prolonged recovery of high-energy phosphates, persistent acidosis, increased inorganic phosphate, and/or calcium loading. To examine these potential mechanisms, metabolic parameters measured by 31P nuclear magnetic resonance spectroscopy, and spontaneous diastolic myofilament motion caused by sarcoplasmic reticulum-myofilament calcium cycling indexed by the scattered light intensity fluctuations (SLIF) it produces in laser beam reflected from the heart, were studied in isolated atrioventricularly blocked rat hearts (n = 10) after 65 min of ischemia at 30 degrees C. All metabolic parameters recovered to their full extent 5 min after reperfusion. Developed pressure evidenced a small recovery but then fell abruptly. This was accompanied by an increase in end diastolic pressure to 37 +/- 5 mm Hg and a fourfold increase in SLIF, to 252 +/- 58% of baseline. In another series of hearts initial reperfusion with calcium of 0.08 mM prevented the SLIF rise and resulted in improved developed pressure (74 +/- 3% vs. 39 +/- 13% of control), and lower cell calcium (5.9 +/- 3 vs. 10.3 +/- 1.4 mumol/g dry wt). Thus, during reperfusion, delayed contractile recovery is not associated with delayed recovery of pH, inorganic phosphate, or high-energy phosphates and can be attributed, in part, to an adverse effect of calcium loading which can be indexed by increased SLIF occurring at that time.