Evaluation of multimeric tyrosine-O-sulfate as a cytoprotectant in an in vivo model of acute myocardial infarction in pigs

Cardiology. 2012;121(1):59-70. doi: 10.1159/000336485. Epub 2012 Mar 2.

Abstract

Objectives: Intracoronary administration of glycosaminoglycan analogs, including the complement inhibitor dextran sulfate, attenuates myocardial ischemia/reperfusion injury (I/R injury). However, dextran sulfate has a distinct anticoagulatory effect, possibly limiting its use in specific situations in vivo. We therefore developed multimeric tyrosine sulfate (sTyr-PAA), a novel, minimally anticoagulatory, fully synthetic non-carbohydrate-containing polyacrylamide conjugate, for in vivo testing in an acute closed-chest porcine model of acute myocardial infarction.

Methods: Following balloon occlusion of the left anterior descending artery just after the first diagonal branch (60-minute ischemia), sTyr-PAA (approx. 10 mg/kg bodyweight, fraction with strongest complement-inhibitory and minimal anticoagulatory properties, n = 11) or phosphate-buffered saline (controls, n = 9) was administered intracoronarily into ischemic myocardium prior to 120 min of reperfusion.

Results: sTyr-PAA significantly reduced infarct size (from 61.0 ± 12.0% of the ischemic area at risk to 39.4 ± 17.0%), plasma creatine kinase, local complement deposition and tissue factor upregulation, without affecting systemic coagulation. Protection was associated with significantly reduced myocardial neutrophil extravasation and translated into a significant improvement of ejection fraction and left ventricular enddiastolic pressure.

Conclusions: sTyr-PAA protected significantly against myocardial I/R injury without substantially affecting systemic coagulation. Local intravascular sTyr-PAA administration may prove advantageous in situations where bleeding complications are likely or are to be avoided at all costs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticoagulants / pharmacology*
  • Complement Inactivating Agents / pharmacology*
  • Complement Pathway, Classical / drug effects
  • Cytoprotection / drug effects
  • Dose-Response Relationship, Drug
  • Granulocytes / pathology
  • Hemodynamics / drug effects
  • Myocardial Infarction / complications*
  • Myocardial Infarction / immunology
  • Myocardial Reperfusion
  • Myocardial Reperfusion Injury / immunology
  • Myocardial Reperfusion Injury / pathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Neutrophils / pathology
  • Sus scrofa
  • Thromboplastin / metabolism
  • Tyrosine / analogs & derivatives*
  • Tyrosine / pharmacology
  • Ventricular Fibrillation / chemically induced

Substances

  • Anticoagulants
  • Complement Inactivating Agents
  • tyrosine O-sulfate
  • Tyrosine
  • Thromboplastin