Abstract
Background: A growing body of evidence demonstrates discretely the difference of open endotracheal suctioning (OES) and closed endotracheal suctioning (CES) on the respiratory and hemodynamic parameters in acute respiratory distress syndrome (ARDS). Endothelin-1 (ET-1), a mediator of vascular inflammation, cell proliferation, and fibrosis in addition to being a potent vasoconstrictor has been potentially implicated in the pathogenesis of ARDS. Here, we investigated the effects of repeated OES vs. CES during mechanical ventilation on circulatory and pulmonary levels of ET-1 in ARDS. Methods: Briefly, 22 Japanese White Rabbits were intubated with a 3.5-mm endotracheal tube. Normal saline was instilled into lung and washed mildly. After instillation, rabbits were ventilated at definite setting; OES and CES duration was for 6 hours and performed every 30 minutes from protocol start. Results: At circulatory level, either OES or CES did not alter plasma ET-1 level compared to the ET-1 level in ARDS before the initiation of endotracheal suctioning (OES 4.7 ± 1.3 pg/ml vs. CES 4.8 ± 1.5 pg/ml, p=0.839). In contrast, pulmonary ET-1 level was significantly higher in CES group compared to OES group after 6 hours of repeated suctioning in ARDS (OES 26.9 ± 2.2 pg/mg vs. CES 29.9 ± 3.3 pg/mg, p=0.018). This change in pulmonary ET-1 level could maintain a parallel relation with PaO2 level. Conclusion: At this moment, we cannot clarify the mechanism and effects of the observed change in ET-1 in a rabbit model of ARDS as well as its clinical impact.
Highlights
Mechanical ventilation is an important support for patients with acute respiratory distress syndrome (ARDS), it can cause ventilator-induced lung injury (VILI) [1,2,3]
After lung injury was induced, PaO2 was reduced to a mean of 66 ± 19 mmHg and 67 ± 14 mmHg for the closed endotracheal suctioning (CES) and open endotracheal suctioning (OES) groups, OES group n = 9 CES group n = 9 p Value
The key findings of the present study are that: a) repeated open endotracheal suctioning causes gradual and time-dependent reductions in arterial oxygenation over the course of endotracheal suctioning; b) there was no distinct difference in lung injury severity and extent between OES and CES groups; c) at circulatory level, either OES or CES did not alter plasma ET-1 level
Summary
Mechanical ventilation is an important support for patients with acute respiratory distress syndrome (ARDS), it can cause ventilator-induced lung injury (VILI) [1,2,3]. The key to a successful clinical management of patients with ARDS is avoidance of further advancement of VILI [1,2,3] For this reason, prevention of alveolar overdistension and derecruitment are the goals of recently proposed lung protective ventilation strategies. A growing body of evidence demonstrates discretely the difference of OES and CES on the respiratory and hemodynamic parameters in ARDS. A growing body of evidence demonstrates discretely the difference of open endotracheal suctioning (OES) and closed endotracheal suctioning (CES) on the respiratory and hemodynamic parameters in acute respiratory distress syndrome (ARDS). We investigated the effects of repeated OES vs. CES during mechanical ventilation on circulatory and pulmonary levels of ET-1 in ARDS
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