Airway Humidification Reduces the Inflammatory Response During Mechanical Ventilation.
BACKGROUND
Currently, no clinical or animal studies have been performed to establish the relationship between airway humidification and mechanical ventilation-induced lung inflammatory responses. Therefore, an animal model was established to better define this relationship.


METHODS
Rabbits (n = 40) were randomly divided into 6 groups: control animals, sacrificed immediately after anesthesia (n = 2); dry gas group animals, subjected to mechanical ventilation for 8 h without humidification (n = 6); and experimental animals, subjected to mechanical ventilation for 8 h under humidification at 30, 35, 40, and 45°C, respectively (n = 8). Inflammatory cytokines in the bronchi alveolar lavage fluid (BALF) were measured. The integrity of the airway cilia and the tracheal epithelium was examined by scanning and transmission electron microscopy, respectively. Peripheral blood white blood cell counts and the wet to dry ratio and lung pathology were determined.


RESULTS
Dry gas group animals showed increased tumor necrosis factor alpha levels in BALF compared with control animals (P < .05). The tumor necrosis factor alpha and interleukin-8 levels in the BALF reached baseline levels when the humidification temperature was increased to 40°C. Scanning and transmission electron microscopy analysis revealed that cilia integrity was maintained in the 40°C groups. Peripheral white blood cell counts were not different among those groups. Compared with control animals, the wet to dry ratio was significantly elevated in the dry gas group (P < .05). Moreover, humidification at 40°C resulted in reduced pathologic injury compared with the other groups based on the histologic score.


CONCLUSIONS
Pathology and reduced inflammation observed in animals treated at 40°C was similar to that observed in the control animals, suggesting that appropriate humidification reduced inflammatory responses elicited as a consequence of mechanical ventilation, in addition to reducing damage to the cilia and reducing water loss in the airway.
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China.
Min
M
Jiang
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China.
Jun-Jie
JJ
Song
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China.
Xiao-Li
XL
Guo
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China.
Yong-Lin
YL
Tang
Department of ICU-D, Second Affiliated Hospital of Harbin Medical University, Anesthesiology and Critical Medicine Major Laboratory of Heilongjiang Province, Harbin, Heilongjiang, China. mzkicu@126.com.
Hai-Bo
HB
Li
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D006813:Humidity; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D008168:Lung / Q000737:chemistry / Q000473:pathology; D008297:Male; D053717:Pneumonia, Ventilator-Associated / Q000517:prevention & control; D011817:Rabbits; D011897:Random Allocation; D012121:Respiration, Artificial / Q000009:adverse effects / Q000379:methods*; D013696:Temperature; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D055397:Ventilator-Induced Lung Injury / Q000517:prevention & control*
D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha
cilia integrity; humidification; inflammatory cytokines; mechanical ventilation; temperature