The Protective Effects Of Hypercapnia In Lipopolysaccharide-induced Lung Injury

OBJECTIVE:We investigated whether hypercapnia -induced by adding CO₂ to inspired gas would be protective against lipoplyscaccharide-induced acute lung injury in an rabbit model.METHODS:Rabbits(n=24) were randomized to Control condition Group(CON Group),Therapetic hypercapnic Group(TH Group,i.e.induction of hypercapnia after achieving ALI) and Prophylactically hypercapnic Group(PH Group,i.e.induction of hypercapnia before LPS administration).Ventilated for 6 hours after achieving ALI induced by introvenouing LPS and measured mean arterial pressure,heart rate , PaO₂/FiO₂, PaO₂ , PaCO₂ and pH value during the course. Finishied ventilation ,lung histologic alternations ,percent of injuried alveolar ,lung wet-to-dry ratios,lung tissue myeloperoxidase content,IL-8 level and percent of apoptotic PMN in BALF was measured.RESULT: At the end of the experiment,the CON Group displayed lower mean artial pressure (P<0.05) ,heart rate (P<0.01) , PaO₂ (P<0.01), PaO₂/FiO₂ (P<0.01) and PaCO₂ (P<0.01) and showed higher pH value (P<0.05) comparied with the TH Group and PH Group .In the CON Group lung histologic alterations consistent with greater injury. Percent of injuried alveolar ( P<0.05 ) ,lung wet-to-dry ratios ( P<0.05 ) ,lung tissue myeloperoxidase content (P<0.01) ,IL-8 level in BALF (P<0.05) of the CON Group was higher than that of the TH Group and PH Group when percent of apoptotic PMN (P<0.01) in BALF of the CON Group was lower compaired with other two groups.There was no statistical significance between the TH Group and the PH Group. CONCLUSION: Therapetic hypercapnia and prophylactical hypercapnia induced by inhaled 0.12 CO₂ attenuated lipoplyscaccharide-induced acute lung injury and the mechanism was associate with the reduced of inflammation in ALI.