Middelveld R J M, Alving K
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Acta Physiol Scand. 2003 Oct;179(2):203-11. doi: 10.1046/j.1365-201X.2003.01141.x.
This study was carried out to study the prophylactic effects of inhalation of nitric oxide (NO) before and during the induction of endotoxic shock.
Eighteen anaesthetized pigs received an infusion of 10-20 microg kg(-1) endotoxin during 2 h after pre-treatment with the cortisol-synthesis inhibitor metyrapone. Three groups were tested (n = 6 each) and received 0, 0.2 or 20 ppm inhaled NO from 30 min before start of endotoxin infusion until 4 h after start of endotoxin. Both 0.2 and 20 ppm NO were able to improve blood gas values.
Area above curve values of arterial P2/FiO2 from 0 to 4 h were 0.83 +/- 0.09 kPa h (control), 0.78 +/- 0.22 (0.2 ppm NO, non-significant) and 0.31 +/- 0.06 (20 ppm NO, P < 0.01, Mann-Whitney U-test, compared to control). Area under curve values of PCO2 from 0 to 4 h were 3.96 +/- 0.66 kPa h (control), 1.20 +/- 0.46 (0.2 ppm NO, P < 0.05, Mann-Whitney U-test, compared to control) and 2.78 +/- 1.06 (20 ppm NO group, non-significant). The increase in pulmonary arterial pressure (PAP) was partly prevented by 20 ppm NO, but not by 0.2 ppm NO at 4 h. Inhaled NO did not affect the levels of BAL fluid total protein, tumour necrosis factor-alpha, interleukin-8 and neutrophil counts.
The addition of a high (20 ppm), but not a low (0.2 ppm), concentration of NO to the inhaled air during endotoxin shock improves arterial oxygen tension and reduces pulmonary artery pressure. Neither dose affects lung mechanics or inflammatory indices, in spite of being given prophylactically.
