Preservation of myofilament calcium responsiveness underlies protection against myocardial stunning by ischemic preconditioning

Néstor Gustavo Pérez, Eduardo Marbán, Horacio E. Cingolani

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: Whereas diminution of infarct size by ischemic preconditioning (IP) is well-accepted, protection against stunning is controversial. Since stunning is characterized by decreased myofilament Ca2+ responsiveness, we investigated whether IP would preserve myofilament responsiveness in a model of stunning. Methods: Rat hearts were retrogradely perfused with Krebs-Henseleit (K-H) solution for 20 min and then subjected to 20 min of no-flow global ischemia, followed by 20 min of reperfusion in the absence (stunning) or in the presence (IP) of a previous 5-min period of ischemia followed by 15 min of reperfusion. A group of hearts perfused under non-ischemic conditions served as control. Thin ventricular trabeculae were dissected from each of the experimental groups and loaded with fura-2 to measure intracellular calcium concentration ([Ca2+](i)) and developed force. Results: After 20 min of reperfusion, left ventricular developed pressure decreased in stunned hearts to 61±5% of control (P<0.01), whereas recovery was complete in the IP hearts (97±4%). Steady-state [Ca2+](i)- force relationships revealed a decreased maximal Ca2+-activated force in stunned hearts relative to control, but no change in the IP group. The Ca2+ required for 50% activation increased in stunning but not in IP. Conclusions: These results show that the decrease in myofilament responsiveness that characterizes stunning is prevented by ischemic preconditioning.

Original languageEnglish (US)
Pages (from-to)636-643
Number of pages8
JournalCardiovascular research
Volume42
Issue number3
DOIs
StatePublished - Jun 1999

Keywords

  • Calcium (cellular)
  • Ischemia
  • Preconditioning
  • Reperfusion
  • Stunning

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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