Inhaled nitric oxide induces cerebrovascular effects in anesthetized pigs

Neurosci Lett. 2003 Sep 11;348(2):85-8. doi: 10.1016/s0304-3940(03)00722-5.


Although inhaled nitric oxide (NO(i)) is considered to act selectively on pulmonary vessels, EEG abnormalities and even occasional neurotoxic effects of NO(i) have been proposed. Here, we investigated cerebrovascular effects of increasing concentrations of 5, 10 and 50 ppm NO(i) in seven anesthetized pigs. Cerebral hemodynamics were assessed non-invasively by use of near-infared spectroscopy and indicator dilution techniques. NO(i) increased cerebral blood volume significantly and reversibly. This effect was not attributable to changes of macrohemodynamic parameters or arterial blood gases. Simultaneously, cerebral transit time increased while cerebral blood flow remained unchanged. These data demonstrate a vasodilatory action of NO(i) in the cerebral vasculature, which may occur preferentially in the venous compartment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anesthetics / pharmacology
  • Animals
  • Cerebral Arteries / drug effects*
  • Cerebral Arteries / physiology
  • Cerebrovascular Circulation / drug effects*
  • Cerebrovascular Circulation / physiology
  • Drug Administration Routes
  • Female
  • Hemodynamics
  • Male
  • Nitric Oxide / pharmacology*
  • Reaction Time / drug effects
  • Reaction Time / physiology
  • Sus scrofa
  • Vasodilation / drug effects*
  • Vasodilation / physiology


  • Anesthetics
  • Nitric Oxide