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Alterations in the free radical generation and nitric oxide release from rat peripheral polymorphonuclear leukocytes

P Seth1, R Kumari, M Dikshit

  • 1Division of Pharmacology, Central Drug Research Institute, Lucknow, India.

Thrombosis Research
|August 1, 1997
PubMed

Insights

Thrombosis in rats reduced free radical generation but increased nitric oxide (NO) release from polymorphonuclear leukocytes (PMNLs). This suggests NO plays a protective role by suppressing PMNL free radical activity during thrombosis.

Area of Science:

  • Biomedical Science
  • Immunology
  • Cardiovascular Research

Background:

  • Polymorphonuclear leukocytes (PMNLs) play a critical role in thrombosis.
  • Alterations in PMNL function, including free radical generation and nitric oxide (NO) release, can impact thrombotic events.
  • Understanding these changes is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the changes in free radical generation and nitric oxide (NO) release from PMNLs after inducing thrombosis in a rat model.
  • To explore the functional consequences of these alterations on PMNL activity.

Main Methods:

  • Thrombosis was induced in rats using collagen and adrenaline.
  • PMNLs were isolated using dextran sedimentation and Ficoll-Hypaque.
  • Free radical generation was measured via luminol (LCL) and lucigenin (LUCDCL) chemiluminescence.
  • Nitric oxide synthase (NOS) activity and NO release were assessed using [14C] L-Arginine and oxy-hemoglobin assays.

Main Results:

  • Thrombosis significantly attenuated LCL and LUCDCL responses in rat PMNLs, indicating reduced free radical generation.
  • PMNLs showed increased NOS activity and NO release post-thrombosis.
  • Myeloperoxidase (MPO) release from PMNLs remained unchanged.
  • Pretreatment with L-NAME or sodium nitroprusside reduced AA-induced LCL response, suggesting NO's role in suppressing free radical generation.

Conclusions:

  • Induction of thrombosis leads to augmented nitric oxide (NO) release from PMNLs.
  • Simultaneously, free radical generation by PMNLs is attenuated following thrombosis.
  • These findings suggest a potential protective role for NO in modulating PMNL function during thrombotic events.

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