Hypercapnia via reduced rate and tidal volume contributes to lipopolysaccharide-induced lung injury

Lang J., Figueroa M., Sanders K., AYDIN ASLAN M., Liu Y., Chumley P., ...Daha Fazla

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, cilt.171, sa.2, ss.147-157, 2005 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 171 Sayı: 2
  • Basım Tarihi: 2005
  • Doi Numarası: 10.1164/rccm.200302-305oc
  • Dergi Adı: AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.147-157
  • Anahtar Kelimeler: carbon dioxide, low tidal volume ventilation, lung injury, RESPIRATORY-DISTRESS-SYNDROME, INHALED NITRIC-OXIDE, KAPPA-B ACTIVATION, PERMISSIVE HYPERCAPNIA, TYROSINE NITRATION, CARBON-DIOXIDE, MECHANICAL VENTILATION, INFLAMMATORY MEDIATORS, ALVEOLAR MACROPHAGES, OXYGEN RADICALS
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Hypercapnia via reduced rate and tidal volume contributes to lipopolysaccharide-induced lung injury.

Lang JD1, Figueroa M, Sanders KD, Aslan M, Liu Y, Chumley P, Freeman BA.

 

 

Abstract

Appreciating that CO2 modifies the chemical reactivity of nitric oxide (NO)-derived inflammatory oxidants, we investigated whether hypercapnia would modulate pulmonary inflammatory responses. Rabbits (n = 72) were ventilated with approximately 7-ml/kg tidal volume for 6 hours. Animals were randomized to one of the following conditions: eucapnia (Pa(CO2) at approximately 35-40 mm Hg), eucapnia + lipopolysaccharide (LPS), eucapnia + LPS + inhaled NO (iNO delivered at approximately 20 ppm), hypercapnia (Pa(CO2) at approximately 60 mm Hg), hypercapnia + LPS, and hypercapnia + LPS + iNO. The hypercapnia + LPS groups compared with groups exposed to eucapnia + LPS displayed significantly increased bronchoalveolar lavage fluid protein concentrations (p < 0.05), lung wet-to-dry ratios (p < 0.05), bronchoalveolar lavage fluid cell counts (p < 0.05), and lung histologic alterations consistent with greater injury. Furthermore, expression of inducible nitric oxide synthase (p < 0.05), tissue myeloperoxidase content (p < 0.05), and formation of lung protein 3-nitrotyrosine derivatives (p < 0.05) was greatest under conditions of hypercapnia + LPS. Groups exposed to hypercapnic conditions without LPS did not manifest these changes. The inhalation of iNO attenuated selected indices of lung injury. We conclude that hypercapnia induced by means of reduced rate and tidal volume amplifies pulmonary inflammatory responses.