Effect of tumor necrosis factor on hypoxic pulmonary vasoconstriction

J Appl Physiol (1985). 1992 Mar;72(3):1044-9. doi: 10.1152/jappl.1992.72.3.1044.

Abstract

The effects of tumor necrosis factor (TNF) on hypoxic pulmonary vasoconstriction (HPV) and endothelium-dependent relaxation were examined in a blood-perfused rat lung preparation. Lungs from TNF-treated rats (0.26 mg/kg iv 12 h before experimentation) had a significantly greater HPV and a reduced vasorelaxant response to the endothelium-dependent vasodilator acetylcholine (ACh) but a similar vasorelaxant response to the endothelium-independent vasodilator nitroprusside compared with lungs from control rats (pretreated with 0.1 ml saline iv). Pentoxifylline (20 mg/kg iv and ip 20 min before administration of TNF) had no detectable effect on either HPV or ACh-induced relaxation but completely negated the augmentation on HPV and the inhibiting action on ACh-induced relaxation caused by TNF. The TNF effect on ACh relaxation was unaffected by pretreatment with L-arginine. These results indicate that TNF induces endothelial dysfunction and enhances HPV, effects that are inhibited by pentoxifylline.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Hypoxia / physiopathology*
  • In Vitro Techniques
  • Lung / drug effects
  • Lung / pathology
  • Lung / physiopathology
  • Pentoxifylline / pharmacology
  • Perfusion
  • Pulmonary Circulation / drug effects*
  • Pulmonary Circulation / physiology
  • Pulmonary Edema / physiopathology
  • Rats
  • Rats, Inbred Strains
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Tumor Necrosis Factor-alpha / physiology
  • Vasoconstriction / drug effects
  • Vasoconstriction / physiology

Substances

  • Tumor Necrosis Factor-alpha
  • Acetylcholine
  • Pentoxifylline