2013Chinese Journal of AsthmaRequires access

Expression of CC16 in lung tissue of rabbits with ventilator induced lung injury

Boyi Liu, Xiao-Li Zheng, Xiang Zheng, Pei Liu, Zhicheng Fang, Haitao Li

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Abstract

Objective To investigate the role of clara ceil secretory 16-kD protein (CC16) in mechanism of ventilator induced lung injury (VILI). Methods 20 healthy adult male Japanese white rabbits were randomly divided into control group (without mechanical ventilation after intubation) and experimental group (mechanical ventilation after intubatiom tidal volume was 20 rnl/kg, frequency was 30 times/min, respiratory absorption ratio was 1 = 3, FiOa was 21%, ventilation time was 24 hours). The changes of arterial pressure of oxygen before and after experiment were observed. The central part of the left lung tissue was collected, lung tissue homogenate was prepared. The level of CC16 in the supernatant of lung tissues was detected by double antibody sandwich ELISA. The left lung tissue was collected,embedded by paraffin, and stained~by HE. Lung tissue sections were prepared for biopsies. Results There was no significant difference in arterial pressure of oxygen between the two groups ( P 0.05). The level of CC16 in lung tissues was 1. 108 ± 0. 072 in control group, 0. 621±0. 056 in experimental group, there was significant difference between the two groups ( P d0.01). Lung tissue edema could be found in lung tissue biopsy of experimental group. Conclusions The expression of CC16 decreases in rabbits with VILI, CC16 may play an important role in the occurrence and development of VILI. Key words: CC16 Mechanical ventilation; Lung injury Mechanism

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Objective To investigate the role of clara ceil secretory 16-kD protein (CC16) in mechanism of ventilator induced lung injury (VILI). Methods 20 healthy adult male Japanese white rabbits were randomly divided into control group (without mechanical ventilation after intubation) and experimental group (mechanical ventilation after intubatiom tidal volume was 20 rnl/kg, frequency was 30 times/min, respiratory absorption ratio was 1 = 3, FiOa was 21%, ventilation time was 24 hours). The changes of arterial pressure of oxygen before and after experiment were observed. The central part of the left lung tissue was collected, lung tissue homogenate was prepared. The level of CC16 in the supernatant of lung tissues was detected by double antibody sandwich ELISA. The left lung tissue was collected,embedded by paraffin, and stained~by HE. Lung tissue sections were prepared for biopsies. Results There was no significant difference in arterial pressure of oxygen between the two groups ( P 0.05). The level of CC16 in lung tissues was 1. 108 ± 0. 072 in control group, 0. 621±0. 056 in experimental group, there was significant difference between the two groups ( P d0.01). Lung tissue edema could be found in lung tissue biopsy of experimental group. Conclusions The expression of CC16 decreases in rabbits with VILI, CC16 may play an important role in the occurrence and development of VILI. Key words: CC16 Mechanical ventilation; Lung injury Mechanism

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Available abstract

Objective To investigate the role of clara ceil secretory 16-kD protein (CC16) in mechanism of ventilator induced lung injury (VILI). Methods 20 healthy adult male Japanese white rabbits were randomly divided into control group (without mechanical ventilation after intubation) and experimental group (mechanical ventilation after intubatiom tidal volume was 20 rnl/kg, frequency was 30 times/min, respiratory absorption ratio was 1 = 3, FiOa was 21%, ventilation time was 24 hours). The changes of arterial pressure of oxygen before and after experiment were observed. The central part of the left lung tissue was collected, lung tissue homogenate was prepared. The level of CC16 in the supernatant of lung tissues was detected by double antibody sandwich ELISA. The left lung tissue was collected,embedded by paraffin, and stained~by HE. Lung tissue sections were prepared for biopsies. Results There was no significant difference in arterial pressure of oxygen between the two groups ( P 0.05). The level of CC16 in lung tissues was 1. 108 ± 0. 072 in control group, 0. 621±0. 056 in experimental group, there was significant difference between the two groups ( P d0.01). Lung tissue edema could be found in lung tissue biopsy of experimental group. Conclusions The expression of CC16 decreases in rabbits with VILI, CC16 may play an important role in the occurrence and development of VILI. Key words: CC16 Mechanical ventilation; Lung injury Mechanism

Key concepts: Lung, Medicine, Mechanical ventilation, Ventilation (architecture), Respiratory system, Tidal volume, Pathology, Edema

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