Int J Angiol 1997; 6(2): 142-145
DOI: 10.1007/BF01616686
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Effects of pentoxifylline on neutrophil function in patients with intermittent claudication

Thomas Weiss, Curt Diehm, Oliver Bartholomä, Franz-Josef Neumann, Wolfgang Kübler
  • Department of Cardiology/Angiology, University of Heidelberg, Heidelberg, Germany
Presented at the 36th Annual World Congress, International College of Angiology, New York, New York, July 1994.
Further Information

Publication History

Publication Date:
23 April 2011 (online)

Abstract

Short periods of ischemia, as in intermittent claudication, cause alterations in neutrophil activation and deformability, which may impair the microcirculation. The aim of this study was to evaluate the effect of pentoxifylline (PTX) on neutrophil function in patients with unilateral intermittent claudication. In 15 patients with predominantly unilateral peripheral arterial occlusive disease, lactate, proportion of activated neutrophils (by nitro blue tetrazolium test), neutrophil filterability (by St. George's filtrometer), and stimulated as well as unstimulated radical generation were assessed in the femoral venous blood of the diseased and healthy leg. The values were obtained at rest, immediately after claudication, and 15 minutes after claudication. After 14 days of treatment with PTX (3 × 400 mg/die p.o.) the measurements were repeated. Pentoxifylline reduced the effects of ischemia on neutrophil function, whereas the same exercise level before and after treatment was reached as measured by lactate production. Ischemia induced elevation in the proportion of activated neutrophils (+43%, p < 0.05) and in unstimulated radical generation (+10.7%, p < 0.05) was diminished by treatment with pentoxifylline (+2.4%, +1.9%, respectively). Decrease in filterability of neutrophils due to exercise was reduced from −17.5% to −12.4% (p < 0.05) and stimulated radical generation decreased from +19.8% to +6.4% (p < 0.05). In conclusion, PTX inhibits ischemia-induced alteration in neutrophil function in patients with intermittent claudication.

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