Low tidal volume protects pulmonary vasomotor function from -second-hit- injury in acute lung injury ratsReportar como inadecuado

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Respiratory Research

, 13:77

First Online: 06 September 2012Received: 03 April 2012Accepted: 24 August 2012


BackgroundSepsis could induce indirect acute lung injuryALI, and pulmonary vasomotor dysfunction. While low tidal volume is advocated for treatment of ALI patients. However, there is no evidence for low tidal volume that it could mitigate pulmonary vasomotor dysfunction in indirect ALI. Our study is to evaluate whether low tidal volume ventilation could protect the pulmonary vascular function in indirect lipopolysaccharide LPS induced acute lung injury rats.

MethodsAn indirect ALI rat model was induced by intravenous infusion of LPS. Thirty rats n = 6 in each group were randomly divided into 1Control group; 2 ALI group; 3 LV group tidal volume of 6mL-kg; 4 MV group tidal volume of 12mL-kg; 5VLV group tidal volume of 3mL-kg. Mean arterial pressure and blood gas analysis were monitored every 2 hours throughout the experiment. Lung tissues and pulmonary artery rings were immediately harvested after the rats were bled to be killed to detect the contents of endothelin-1 ET-1, endothelial nitric oxide synthase eNOS and TNF-α. Acetylcholine Ache-induced endothelium-dependent and sodium nitroprusside SNP-induced endothelium-independent relaxation of isolated pulmonary artery rings were measured by tensiometry.

ResultsThere was no difference within groups concerning blood pressure, PaCO2 and SNP-induced endothelium-independent relaxation of pulmonary artery rings. Compared with MV group, LV group significantly reduced LPS-induced expression of ET-1 level 113.79 ± 7.33pg-mL vs. 152.52 ± 12.75pg-mL, P < 0.05 and TNF-α 3305.09 ± 334.29pg-mL vs.4144.07 ± 608.21pg-mL, P < 0.05, increased the expression of eNOS IOD: 15032.05 ± 5925.07 vs. 11454.32 ± 6035.47, P < 0.05. While Ache 10mol-L-10mol-L-induced vasodilatation was ameliorated 30% more in LV group than in MV group.

ConclusionsLow tidal volume could protect the pulmonary vasodilative function during indirect ALI by decreasing vasoconstrictor factors, increasing expressions of vasodilator factors in pulmonary endothelial cells, and inhibiting inflammation injuries.

KeywordsEndothelium Mechanical ventilation Vascular reactivity Vascular injury Lung injury Pulmonary hypertension Electronic supplementary materialThe online version of this article doi:10.1186-1465-9921-13-77 contains supplementary material, which is available to authorized users.

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Autor: Chun Pan - Jianqiang Wang - Wei Liu - Ling Liu - Liang Jing - Yi Yang - Haibo Qiu

Fuente: https://link.springer.com/

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