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Am J Physiol Heart Circ Physiol 280: H802-H811, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H802-H811, February 2001

Effects of endotoxin on neutrophil-mediated I/R injury in isolated perfused rat hearts

Brian P. Lipton1, Abraham P. Bautista1, Joseph B. Delcarpio2, and Kathleen H. McDonough1

Departments of 1 Physiology and Cell Biology and 2 Anatomy, Louisiana State University Medical Center, New Orleans, Louisiana 70112

With the use of a syngeneic model, we demonstrate that rat polymorphonuclear neutrophils (PMNs) exacerbate ischemia-reperfusion injury in the isolated rat heart. However, PMNs (19 × 106 cells) from lipopolysaccharide (LPS)-treated rats (LPS-PMNs; 100 mg/kg administered 7 h before exsanguination) induce less reperfusion injury in the isolated heart. Average recovery of left ventricular developed pressure after 20 min of ischemia and 60 min of reperfusion was 51 ± 4% in hearts receiving PMNs from saline-treated control rats (saline-PMNs) versus 78 ± 2% in hearts receiving LPS-PMNs. Ischemic hearts reperfused with LPS-PMNs recovered to the same extent as did hearts reperfused with Krebs buffer only. LPS-PMNs and saline-PMNs showed no difference in basal or phorbol ester-induced superoxide production. Whereas twice the number of LPS-PMNs was positive for nitroblue tetrazolium, the percent positive for L-selectin, a receptor integral in PMN-adhesion to endothelium, was 50% less in LPS-PMNs than in controls. After reperfusion, three-fourths of the saline-PMNs remained within the hearts, whereas only one-fourth of LPS-PMNs were trapped. These data suggest that PMNs from LPS-treated rats do not exacerbate ischemia-reperfusion injury as do control PMNs, possibly, due to impaired PMN adhesion to endothelium as a result of decreased L-selectin receptors.

left ventricular function; neutrophils; endotoxin; ischemia-reperfusion


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