Calpain inhibition improves collateral-dependent perfusion in a hypercholesterolemic swine model of chronic myocardial ischemia

J Thorac Cardiovasc Surg. 2016 Jan;151(1):245-52. doi: 10.1016/j.jtcvs.2015.08.101. Epub 2015 Sep 3.

Abstract

Purpose: Calpain overexpression is implicated in aberrant angiogenesis. We hypothesized that calpain inhibition (MDL28170) would improve collateral perfusion in a swine model with hypercholesterolemia and chronic myocardial ischemia.

Methods: Yorkshire swine fed a high cholesterol diet for 4 weeks underwent surgical placement of an ameroid constrictor to their left circumflex coronary artery. Three weeks later, animals received no drug, high cholesterol control group (n = 8); low-dose calpain inhibition (0.12 mg/kg; n = 9); or high-dose calpain inhibition (0.25 mg/kg; n = 8). The heart was harvested after 5 weeks.

Results: Myocardial perfusion in ischemic myocardium significantly improved with high-dose calpain inhibition at rest and with demand pacing (P = .016 and .011). Endothelium-dependent microvessel relaxation was significantly improved with low-dose calpain inhibition (P = .001). There was a significant increase in capillary density, with low-dose calpain inhibition and high-dose calpain inhibition (P = .01 and .01), and arteriolar density with low-dose calpain inhibition (P = .001). Calpain inhibition significantly increased several proangiogenic proteins, including vascular endothelial growth factor (P = .02), vascular endothelial growth factor receptor 1 (P = .003), vascular endothelial growth factor receptor 2 (P = .003), and talin, a microvascular structural protein (P = .0002). There was a slight increase in proteins implicated in endothelial-dependent (nitric oxide mediated) relaxation, including extracellular signal-regulated kinase, phosphorylated extracellular signal-regulated kinase, and inducible nitric oxide synthase with calpain inhibition.

Conclusions: In the setting of hypercholesterolemia, calpain inhibition improved perfusion, with a trend toward increased collateralization on angiography and increased capillary and arteriolar densities in ischemic myocardium. Calpain inhibition also improved endothelium-dependent microvessel relaxation and increased expression of proteins implicated in angiogenesis and vasodilatation.

Keywords: angiogenesis; animal model surgery; calpain inhibition; collateral circulation; ischemic heart disease; myocardial revascularization; perfusion.

Publication types

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

MeSH terms

  • Angiogenic Proteins / metabolism
  • Animals
  • Calpain / antagonists & inhibitors*
  • Calpain / metabolism
  • Chronic Disease
  • Collateral Circulation / drug effects*
  • Coronary Angiography
  • Coronary Circulation / drug effects*
  • Coronary Vessels / drug effects*
  • Coronary Vessels / enzymology
  • Coronary Vessels / physiopathology
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Hypercholesterolemia / complications*
  • Male
  • Microcirculation / drug effects
  • Microvessels / drug effects*
  • Microvessels / enzymology
  • Microvessels / physiopathology
  • Myocardial Ischemia / drug therapy*
  • Myocardial Ischemia / enzymology
  • Myocardial Ischemia / etiology
  • Myocardial Ischemia / physiopathology
  • Myocardial Perfusion Imaging
  • Neovascularization, Physiologic / drug effects
  • Protease Inhibitors / pharmacology*
  • Time Factors
  • Vasodilation / drug effects

Substances

  • Angiogenic Proteins
  • Protease Inhibitors
  • Calpain