title: Neutrophil function in peripheral arterial occlusive disease: the effects of prostaglandin E1.
abstract: The role of polymorph nuclear neutrophils (PMN) in limb ischemia and reperfusion has been recognized only in recent years. The present study aimed to investigate the systemic and local (in femoral venous blood) effects of intra-arterially or intravenously applied prostaglandin E1 (PGE1) on systemic and ischemia-induced local changes in neutrophil function. Thirty patients with intermittent claudication were randomly assigned to intra-arterial or intravenous infusion of prostaglandin E1 (10 microg i.a. or 15 microg i.v. over 30 min). Prior to infusion femoral arterial and venous blood samples were obtained from the predominantly affected leg under resting conditions and immediately after a 3-min period of ischemia induced by suprasystolic thigh compression. After 24 h additional blood samples were obtained at baseline, following infusion of prostaglandin E1, and again after another 3-min period of ischemia following the prostaglandin E1 infusion. Intra-arterially administered prostaglandin E1 caused an increase in the PMN count by 3.5 +/- 2% (p<0.05) and a decrease in free oxygen radical production by 13 +/- 8% (p<0.05) measured by whole blood chemiluminescence. Additionally, a trend for lower PMN filterabilities (9 +/- 12%, NS) was observed. Intra-arterially infused prostaglandin E1 significantly reduced the ischemia-induced decrease in neutrophil filterability (arterial and venous blood difference after ischemia -- control: 22 +/- 17% (p<0.05); IA PGE1: 8 +/- 11% (NS), each compared to baseline). Intravenously administered prostaglandin E1 showed similar systemic effects as the intra-arterial application, but did not affect the ischemia-induced changes in neutrophil filterability. In conclusion, prostaglandin E1 reduces PMN activation in patients with peripheral arterial occlusive disease.
authors.affiliation: Department of Cardiology/Angiology, University of Heidelberg, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Weiss
authors.forename: H
authors.initials: H
authors.lastname: Eckstein
authors.forename: C
authors.initials: C
authors.lastname: Weiss
authors.forename: C
authors.initials: C
authors.lastname: Diehm
mesh_terms: D000368:Aged; D000527:Alprostadil / Q000008:administration & dosage / Q000627:therapeutic use*; D002469:Cell Separation; D005260:Female; D005263:Femoral Artery; D005268:Femoral Vein; D018056:Hemorheology; D006801:Humans; D007261:Infusions, Intra-Arterial; D007262:Infusions, Intravenous; D007383:Intermittent Claudication / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D007958:Leukocyte Count; D008163:Luminescent Measurements; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation / Q000187:drug effects*; D009504:Neutrophils / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D017382:Reactive Oxygen Species; D014665:Vasodilator Agents; D000527:Alprostadil