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Effects of lidocaine on cytosolic pH regulation and stimulus-induced effector functions in alveolar macrophages

A Bidani1, T A Heming

  • 1Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-0876, USA.

Lung
|January 1, 1997
PubMed

Insights

Lidocaine disrupts pH regulation and reduces superoxide production in alveolar macrophages. However, it does not affect tumor necrosis factor-alpha release, indicating specific impacts on macrophage functions.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Leukocyte functions are modulated by local anesthetics.
  • Alveolar macrophages play a crucial role in immune responses.

Purpose of the Study:

  • To investigate the effects of lidocaine on intracellular pH (pHi) regulation, superoxide production, and tumor necrosis factor-alpha (TNF-alpha) release in rabbit alveolar macrophages.
  • To determine if lidocaine impacts macrophage effector functions.

Main Methods:

  • Alveolar macrophages were isolated from rabbits via bronchoalveolar lavage.
  • Cells underwent an acid load, and pHi recovery was measured with or without V-type H(+)-translocating ATPase (V-ATPase) inhibitors or amiloride.
  • Superoxide production and TNF-alpha release were assessed following stimulation.

Main Results:

  • Lidocaine dose-dependently inhibited pHi recovery by impairing Na+/H+ exchange and V-ATPase activity.
  • Lidocaine significantly reduced phorbol ester-induced superoxide production.
  • Lidocaine did not significantly affect endotoxin-induced TNF-alpha release.
  • Macrophage viability and ATP levels remained unaffected.

Conclusions:

  • Lidocaine inhibits key pHi regulatory mechanisms in alveolar macrophages.
  • Disruption of pHi regulation by lidocaine may contribute to its inhibitory effects on macrophage functions.
  • Lidocaine specifically impacts certain, but not all, alveolar macrophage effector functions.

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