Effects of hypothermia on lung inflammation in a rat model of meconium aspiration syndrome

Abstract

1 2-Experimental SurgeryActa Cir Bras. 2018;33(6):483-490 AbstractPurpose: To evaluate the effects of hypothermia treatment on meconium-induced inflammation. Methods: Fifteen rats were instilled with human meconium (MEC, 1.5 mL/kg, 65 mg/mL) intratracheally and ventilated for 3 hours. Eight rats that were ventilated and not instilled with meconium served as a sham group. In MEC-hypothermia group, the body temperature was lowered to 33±0.5°C. Analysis of the blood gases, interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in bronchoalveolar lavage (BAL) fluid samples, and histological analyses of the lungs were performed. Results: The BAL fluid TNF-α, IL-1β, IL-6 and IL-8 concentrations were significantly higher in the MEC-hypothermia group than in the MEC-normothermia (p < 0.001, p < 0.001, p = 0.001, p < 0.001, respectively) and sham-controlled groups (p < 0.001, p < 0.001, p < 0.001, p < 0.001, respectively). Conclusion: Meconium-induced inflammatory cytokine production is affected by the body temperature control.

Glycyrrhizic acid alleviates the meconium-induced acute lung injury in neonatal rats by inhibiting oxidative stress through mediating the Keap1/Nrf2/HO-1 signal pathway

“…In the present study, a MAS model was successfully established on rats, which was verified by the symptoms, such as increased W/D ratio, elevated production of inflammatory factors, and aggravated apoptotic state in the lung tissues, which was consistent with the pathological changes described previously [26,27]. In addition, according to the results of HE staining, significant infiltration of leukocytes and large amounts of alveolar exudates were observed in the lung tissues from MAS rats, which corresponded to the description by Turhan [7]. After the treatment of different dosages of GA, the elevated W/D ratio, severe inflammation and apoptotic state, significant infiltration of leukocytes, and the accumulated alveolar exudates were dramatically ameliorated, revealing a promising therapeutic property of GA on MAS rats.…”

“…In the clinic, after the inhalation of meconium, meconium will travel into the alveoli and the viscosity of the pulmonary surfactant will be reduced and the ultrastructure of the pulmonary surfactant will be changed by the liposoluble materials in the meconium, which result in the decreased level of surfactant proteins [ 5 , 6 ]. As a consequence, the plasma protein leakage will be induced and the local inflammation will be developed, including the excessive production of inflammatory factors [ 7 , 8 ]. In addition, the release of proteolytic enzymes will be facilitated and the imbalance of oxidative stress will be triggered by the severe inflammation, which finally contributes to the injuries on lung tissues [ 9 ].…”