Neutrophil-independent myocardial dysfunction during an early stage of global ischemia and reperfusion of isolated hearts

Immunopharmacology. 1995 Apr;29(3):261-71. doi: 10.1016/0162-3109(95)00065-2.

Abstract

The effect of global ischemia and reperfusion on the expression of cytokine genes and cell adhesion molecules by myocardial tissues and neutrophils was studied by using the Langendorff model. Although cardiac function deteriorated after reperfusion of ischemic hearts, there was no evidence of inflammation and myocardial degeneration, which is in contrast to previous findings that neutrophil-mediated inflammation is a critical step in post-ischemic reperfusion injury in regional ischemia. Flow cytometry analysis demonstrated that the global ischemia and reperfusion did not affect the expression of adhesion molecules on neutrophils. We also examined the expression of various cytokines which are involved in inflammatory responses. Only interleukin 1 alpha was induced after the reperfusion of the ischemic hearts. These results suggest that neutrophils barely contribute to the myocardial dysfunction and IL-1 alpha may play a role in post-ischemic myocardial dysfunction during the early stage of reperfusion.

MeSH terms

  • Animals
  • Base Sequence
  • Cell Adhesion Molecules / biosynthesis
  • Cell Adhesion Molecules / blood
  • Cytokines / biosynthesis
  • Cytokines / blood
  • Cytokines / genetics
  • Flow Cytometry
  • Heart / physiopathology
  • Heart Function Tests
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / blood
  • Interleukin-1 / genetics
  • Macrophages / physiology
  • Male
  • Molecular Sequence Data
  • Myocardial Ischemia / genetics
  • Myocardial Ischemia / immunology*
  • Myocardial Ischemia / physiopathology
  • Myocardial Reperfusion Injury / genetics
  • Myocardial Reperfusion Injury / immunology*
  • Myocardium / pathology
  • Neutrophils / immunology*
  • Polymerase Chain Reaction
  • Rats
  • Rats, Wistar
  • Up-Regulation

Substances

  • Cell Adhesion Molecules
  • Cytokines
  • Interleukin-1