Inhibition of p38 MAPK α/β reduces ischemic injury and does not block protective effects of preconditioning

Sharron Schneider, Weina Chen, Janet Hou, Charles Steenbergen, Elizabeth Murphy

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

We examined the effect of inhibition of p38 mitogen-activated protein kinase (MAPK) α/β during ischemia and preconditioning by using the inhibitor SB-202190. Isolated rat hearts were perfused with Krebs-Henseleit buffer, while left ventricular developed pressure (LVDP) and 31P nuclear magnetic resonance spectra were acquired continuously. After 20 min of ischemia and 25 min of reperfusion, recovery of LVDP in untreated hearts was 32 ± 4%, whereas hearts treated with SB-202190 5 min before ischemia recovered 59 ± 7% of their pretreatment LVDP. Preconditioning improved functional recovery to 65 ± 5%, which was unaffected by SB-202190 treatment, added either throughout the preconditioning protocol (56 ± 5% recovery) or during the final reperfusion period of preconditioning (71 ± 11% recovery). Necrosis was assessed after 40 min of ischemia and 2 h of reperfusion using 2,3,5-triphenyltetrazolium chloride (TTC) staining and creatine kinase release. The untreated group had 54 ± 8% necrotic myocardium, whereas the SB-202190-treated group had 32 ± 7% and the preconditioned group had 21 ± 4% necrotic tissue by TTC staining.

Original languageEnglish (US)
Pages (from-to)H499-H508
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number2 49-2
StatePublished - Feb 1 2001

Keywords

  • Intracellular pH
  • Left ventricular developed pressure
  • Necrosis
  • P nuclear magnetic resonance
  • SB-202190

ASJC Scopus subject areas

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

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