P. Dandona et al., Heparin inhibits reactive oxygen species generation by polymorphonuclear and mononuclear leucocytes, THROMB RES, 96(6), 1999, pp. 437-443
To examine the hypothesis that heparin may affect leukocyte function and th
at it may have antiinflammatory properties, we investigated the effect of h
eparin on reactive oxygen species (ROS) generation by leucocytes, Heparin w
as injected intravenously at a dose of 10000 units into eight normal subjec
ts. Blood samples were collected from the antecubital vein sequentially, pr
ior to and following heparin at 0, 0.5, 1.2, and 4 hours. ROS generation wa
s inhibited significantly by polymorphonuclear cells (PMNL) at 0.5, 1, and
2 hours and returned to baseline level at 4 hours. Similarly, ROS generatio
n was inhibited markedly by mononuclear cells (MNC) at 0.5 hours, with a pe
ak inhibition at 1 hour: it returned to baseline level by 4 hours. The maxi
mum inhibition of ROS generation by PMNL was 57.3+/-19% of the basal, while
that by MNC was 56.4+/-11% of the basal, Since ROS are proinflammatory and
cause tissue damage, it is possible that heparin may have an anti-inflamma
tory effect in vivo, apart from its antithrombotic effect. Since ROS also b
ind to nitric oxide (NO) and reduce the bioavailability of NO, heparin may
indirectly increase the bioavailability of NO and thus act as a vasodilator
. This effect of heparin may be of particular relevance to its use in unsta
ble angina and following thrombolysis in acute myocardial infarction in pre
venting reperfusion injury. (C) 1999 Elsevier Science Ltd. All rights reser
ved.