[Effect of sustained inflation on inflammatory response of extra pulmonary organs in acute respiratory distress syndrome in rabbit].
OBJECTIVE
To evaluate the influence of sustained inflation (SI) on inflammatory response of extra pulmonary organs in acute respiratory distress syndrome (ARDS) in rabbit.


METHODS
The ARDS rabbit model were replicated by saline alveoli-lavage. The rabbits were randomly divided into four groups: 1. normal group; 2. ARDS group; 3. low-volume(V(T)) + best end-expiratory pressure group (LVBP): V(T) 6 ml/kg, PEEP 2 cm H(2)O(1 cm H(2)O=0.098 kPa) greater than the pressure of lower inflection point in pressure-volume curve (Pinf); 4. SI group: same settings as LVBP group plus SI performed every hour. After 4 hours of ventilation, liver and intestine homogenates were prepared to assay tumor necrosis factor (TNF)-alpha and interleukin(IL)-10 levels by enzyme-linked immunoadsorbent assay and their mRNA expression by reverse transcription-polymerase chain reaction. Myeloperoxidase (MPO) and malondialdehyde (MDA) were assessed at the same time.


RESULTS
In SI group, TNF-alpha mRNA expression in the liver and intestine tissues (24.82+/-7.88 and 25.06+/-10.57) were decreased significantly compared with ARDS (36.88+/-6.83 and 36.48+/-8.23) and LVBP groups (42.34+/-8.55 and 37.59+/-10.63, all P<0.05). The expression of IL-10 mRNA in the liver and intestine of rabbits in SI group (17.31+/-5.72 and 10.90+/-3.30) was lower than that of ARDS (24.64+/-3.85 and 24.31+/-7.69) and LVBP group (25.03+/-9.38 and 21.83+/-7.34, all P<0.05) significantly. In SI group, the levels of TNF-alpha and IL-10 in liver and intestine tissue were similar to that of the other groups. The contents of MPO and MDA had no difference compared with the other groups too.


CONCLUSIONS
SI can down-regulate inflammatory mediator expression of extra-pulmonary organs in rabbits with ARDS, and it may inhibit the inflammatory response in extra pulmonary organs.
Department of Critical Care Medicine, Zhong-da Hospital and School of Clinical Medicines, Southeast University, Nanjing 210009, Jiangsu, China. yiyiyang@hotmail.com
Yi
Y
Yang
Hai-Bo
HB
Qiu
Yan-Li
YL
Yan
Hong-Yang
HY
Xu
Li
L
Wang
Shao-Xia
SX
Zhou
Rui-Qiang
RQ
Zheng
D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D011897:Random Allocation; D012121:Respiration, Artificial / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000378:metabolism* / Q000628:therapy; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D018836:Inflammation Mediators; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10