Send to

Choose Destination

See 1 citation:

J Mol Cell Cardiol. 1994 Jul;26(7):831-40.

Contribution of leukocyte infiltration to lipoperoxidation occurring in the non-ischemic region of the rat heart submitted to permanent left coronary artery occlusion.

Author information

Physiopathologie Cellulaire Cardiaque, URA CNRS 1287, Université Joseph Fourier, Grenoble, France.


Previous studies have shown that during regional myocardial ischemia, the non-ischemic zone may be submitted to metabolic and structural alterations. In the present study, we have examined whether an inflammatory process could be responsible for increased lipoperoxidation in the non-ischemic zone of the rat heart subjected to permanent coronary artery ligation. Forty-eight hours after coronary artery ligation, tissue levels of malondialdehyde (MDA), taken as an index of lipoperoxidation, measured in the non-ischemic zone was increased by 25% when compared to sham operated hearts. Furthermore, an infiltration of polymorphonuclears was observed by immunofluorescence in the non-ischemic zone, while the activity of the neutrophil-specific myeloperoxidase enzyme (MPO) was significantly increased in that same zone (ligated 1.26 +/- 0.17 U/100 mg wet wt. v sham 0.33 +/- 0.01 U/100 mg wet wt.; P < 0.01). Examination of the temporal changes in MDA content and of MPO activity showed a significant linear decrease in both parameters of 6 to 48 h post-ligation. When compared to placebo, treatment with indomethacin (1 mg/kg, 5 min prior to ligation, then at 12 h intervals up to the harvesting of the hearts) led to a significant reduction in MDA content measured 6, 24 or 48 h after ligation. The treatment had no effect on infarct size measured 48 h after ligation. These results suggest that in the rat heart, permanent regional ischemia is associated with the rapid development of an inflammatory process in the non-ischemic zone which could in part account for the accumulation of lipoperoxidation products in that region.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center