Literature DB >> 15257087

Use of low tidal volume in septic shock may decrease severity of subsequent acute lung injury.

Fuhong Su1, Nam Duc Nguyen, Jacques Creteur, Ying Cai, Nathalie Nagy, Hoang Anh-Dung, Andre Amaral, Frederico Bruzzi de Carvalho, Didier Chochrad, Jean-Louis Vincent.   

Abstract

Recent studies have indicated that protective lung strategies may improve outcomes in acute lung injury. We hypothesized that the use of a lower tidal volume early during septic shock may protect against the subsequent development of acute lung injury. Fourteen fasted, anesthetized, invasively monitored, mechanically ventilated, female sheep (26.4 +/- 4.5 kg) underwent cecal ligation and perforation to induce sepsis. Sheep were then randomized to ventilation with low (6 mL/kg) or high (12 mL/kg) tidal volumes. A positive end-expiratory pressure of 10 cm H(2)O was applied in each case. Ringer's lactate was titrated to maintain pulmonary artery occlusion pressure at baseline levels. No vasoactive agents or antibiotics were used. Survival time was longer in the low- than in the high-tidal-volume group (21.8 +/- 2.4 vs. 17.6 +/- 4.1 h, respectively, P < 0.05). The times to develop hypotension and anuria were longer in the low-tidal-volume group (18.1 +/- 3.1 vs. 12.0 +/- 2.8 h, P < 0.05, and 17.6 +/- 1.6 vs. 14.1 +/- 3.8 h, P < 0.05). Although the Pao2/Fio2 tended to be lower in the low- than in the high-tidal-volume group (P = 0.06), postmortem examination showed a lower lung tissue wet/dry ratio in the low- than in the high-tidal-volume group (7.1 +/- 0.5 vs. 9.1 +/- 0.7, P < 0.05). A low-tidal-volume ventilation strategy applied early during septic shock may be beneficial in terms of reducing the amount of lung edema and prolonging survival time.

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Year:  2004        PMID: 15257087     DOI: 10.1097/01.shk.0000131488.89874.8a

Source DB:  PubMed          Journal:  Shock        ISSN: 1073-2322            Impact factor:   3.454


  7 in total

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2.  CD11c+ alveolar macrophages are a source of IL-23 during lipopolysaccharide-induced acute lung injury.

Authors:  Markus Bosmann; Jamison J Grailer; Norman F Russkamp; Robert Ruemmler; Firas S Zetoune; J Vidya Sarma; Peter A Ward
Journal:  Shock       Date:  2013-05       Impact factor: 3.454

3.  Role of arginine vasopressin and terlipressin as first-line vasopressor agents in fulminant ovine septic shock.

Authors:  Sebastian Rehberg; Christian Ertmer; Gabriele Köhler; Hans-Ulrich Spiegel; Andrea Morelli; Matthias Lange; Katharina Moll; Katrin Schlack; Hugo Van Aken; Fuhong Su; Jean-Louis Vincent; Martin Westphal
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Review 4.  Bench-to-bedside review: Biotrauma and modulation of the innate immune response.

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5.  Adjusting tidal volume to stress index in an open lung condition optimizes ventilation and prevents overdistension in an experimental model of lung injury and reduced chest wall compliance.

Authors:  Carlos Ferrando; Fernando Suárez-Sipmann; Andrea Gutierrez; Gerardo Tusman; Jose Carbonell; Marisa García; Laura Piqueras; Desamparados Compañ; Susanie Flores; Marina Soro; Alicia Llombart; Francisco Javier Belda
Journal:  Crit Care       Date:  2015-01-13       Impact factor: 9.097

6.  Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung.

Authors:  Lucio Pavone; Scott Albert; Joseph DiRocco; Louis Gatto; Gary Nieman
Journal:  Crit Care       Date:  2007       Impact factor: 9.097

7.  Protective effect of S-nitrosoglutathione pretreatment on acute lung injury in septic rats.

Authors:  Zhou-Feng Wang; Yu-Min Yang; Heng Fan
Journal:  Iran J Basic Med Sci       Date:  2020-08       Impact factor: 2.699

  7 in total

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