The effects of inhaled carbon monoxide on lung injury in rats caused by lipopolysaccharide
Miyazaki, H.; Yamada, H.; Ohta, M.; Fujimoto, J.; Tazawa, T.; Kudoh, I.
Masui. Japanese Journal of Anesthesiology 52(4): 363-369
2003
ISSN/ISBN: 0021-4892 PMID: 12728485 Document Number: 553451
Background: Carbon monoxide (CO) has long been considered a toxic substance. Recent studies have revealed that CO may play an important role in intercellular signaling. We hypothesized that CO modulates the inflammatory mechanisms. Methods: SD rats (each study group consisting of 7 animals) inhaled 250 ppm of CO one hour prior to LPS challenges. These animals were incubated for a particular period of time (four different length of time; 1, 2, 4, and 8 hours). The control group (each study group consisting of 6 animals) had been left in the room air. Both groups were instilled with LPS (1 mg) into the lungs. At the end of each period, animals were exsanguinated, broncho-alveolar lavage (BAL) and blood sampling were performed, and a part of the small intestine was harvested. PMN numbers, protein, TNF, and IL-10 concentrations in BAL fluid were measured. Plasma TNF and IL-10 were also measured. The Wet/Dry ratio of a small intestine was calculated. Results: In the CO-inhalation group, the anti-inflammatory cytokine IL-10 concentration in the BAL fluid was higher at 8 hours after LPS challenge than the counterpart of room air group (37.6+-11.4 pg cntdot ml-1 vs. 92.8+-31.5 pg cntdot ml-1, P< 0.05). W/D ratio decreased (3.29+-0.2 vs. 2.94+- 0.06, P<0.05). Conclusion: These findings indicated that CO inhalation might modulate the inflammatory response to LPS. Further study is needed to prove the therapeutic role of CO inhalation without serious adverse effects.