Myocardial ischemia

Pentosan polysulfate sodium was studied by Kilgore (2) and Tanhehco (3) for its potential to de-crease infarct size in an experimental model of myocardial ischemia/reperfusion injury. In an animal model it was shown that treatment with pentosan polysulfate sodium significantly reduced infarct size and, following tissue analysis, demonstrated decreased deposition of membrane-attack complex and neutrophile accumulation in the area at risk. Their results indicate that pentosan polysulfate sodium possesses the ability to decrease infarct size after an acute period of myocardial ischemia and reperfusion.

The observations are consistent with the suggestion that glycosaminoglycans (GAGs) such as pentosan polysulfate sodium protect the ischemic heart against reperfusion injury mediating its cytoprotective effect through modulation activation of the complement cascade (1). Studies provide evidence for the role of complement by demonstrating the deposition of the terminal complement complex, or the membrane attack complex, in irreversibly injured myocardial tissue. It is hypothesized therefore, that pharmacological inhibition of complement activation by pentosan polysulfate sodium may be beneficial in reducing tissue injury associated with ischemia and reperfusion.

References

1) DA. Lauver, EA. Booth, et. al. (2005), Sulodexide Attenuates Myocardial Ischemia/Reperfusion Injury and the Deposition of C-Reactive Protein in Areas of Infarction without Affecting Hemostasis. J Pharmacol Exp Ther 312:794-800.
2) Kilgore KS, Naylor KB, et al. (1998), The semisynthetic polysaccharide pentosan polysulfate prevents complement-mediated myocardial injury in the rabbit perfused heart. J Pharmacol Exp Ther 285:987-994.
3) Tanhehco EJ, Kilgore KS, et al. (1999), Reduction of myocardial infarct size after ischemia and reperfusion by the glycosaminoglycan pentosan polysulfate. J Cardiovasc Pharmacol 34:153-161.



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