High-molecular-weight polyethylene glycol inhibits myocardial ischemia-reperfusion injury in vivo

J Thorac Cardiovasc Surg. 2015 Feb;149(2):588-93. doi: 10.1016/j.jtcvs.2014.10.074. Epub 2014 Oct 18.

Abstract

Objectives: Cardiac ischemia-reperfusion (I-R) injury remains a significant problem as there are no therapies available to minimize the cell death that can lead to impaired function and heart failure. We have shown that high-molecular-weight polyethylene glycol (PEG) (15-20 kD) can protect cardiac myocytes in vitro from hypoxia-reoxygenation injury. In this study, we investigated the potential protective effects of PEG in vivo.

Methods: Adult rats underwent left anterior descending artery occlusion for 60 minutes followed by 48 hours or 4 weeks of reperfusion. One milliliter of 10% PEG solution or phosphate-buffered saline (PBS) control (n = 10 per group) was administered intravenously (IV) immediately before reperfusion.

Results: Fluorescein-labeled PEG was robustly visualized in the myocardium 1 hour after IV delivery. The PEG group had significant recovery of left ventricular ejection fraction at 4 weeks versus a 25% decline in the PBS group (P < .01). There was 50% less LV fibrosis in the PEG group versus PBS with smaller peri-infarct and remote territory fibrosis (P < .01). Cell survival signaling was upregulated in the PEG group with increased Akt (3-fold, P < .01) and ERK (4-fold, P < .05) phosphorylation compared to PBS controls at 48 hours. PEG also inhibited apoptosis as measured by TUNEL-positive nuclei (56% decrease, P < .02) and caspase 3 activity (55% decrease, P < .05).

Conclusions: High-molecular-weight PEG appears to have a significant protective effect from I-R injury in the heart when administered IV immediately before reperfusion. This may have important clinical translation in the setting of acute coronary revascularization and myocardial protection in cardiac surgery.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Caspase 3 / metabolism
  • Cell Survival / drug effects
  • Glycogen Synthase Kinase 3 / metabolism
  • In Situ Nick-End Labeling
  • MAP Kinase Signaling System / drug effects
  • Male
  • Molecular Weight
  • Myocardial Reperfusion Injury / prevention & control*
  • Phosphorylation
  • Polyethylene Glycols / pharmacology*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Polyethylene Glycols
  • Proto-Oncogene Proteins c-akt
  • Glycogen Synthase Kinase 3
  • Caspase 3