Abstract
OBJECTIVES:Hypertonic saline has been proposed to modulate the inflammatory cascade in certain experimental conditions, including pulmonary inflammation caused by inhaled gastric contents. The present study aimed to assess the potential anti-inflammatory effects of administering a single intravenous dose of 7.5% hypertonic saline in an experimental model of acute lung injury induced by hydrochloric acid.METHODS:Thirty-two pigs were anesthetized and randomly allocated into the following four groups: Sham, which received anesthesia and were observed; HS, which received intravenous 7.5% hypertonic saline solution (4 ml/kg); acute lung injury, which were subjected to acute lung injury with intratracheal hydrochloric acid; and acute lung injury + hypertonic saline, which were subjected to acute lung injury with hydrochloric acid and treated with hypertonic saline. Hemodynamic and ventilatory parameters were recorded over four hours. Subsequently, bronchoalveolar lavage samples were collected at the end of the observation period to measure cytokine levels using an oxidative burst analysis, and lung tissue was collected for a histological analysis.RESULTS:Hydrochloric acid instillation caused marked changes in respiratory mechanics as well as blood gas and lung parenchyma parameters. Despite the absence of a significant difference between the acute lung injury and acute lung injury + hypertonic saline groups, the acute lung injury animals presented higher neutrophil and tumor necrosis factor alpha (TNF-α), interleukin (IL)-6 and IL-8 levels in the bronchoalveolar lavage analysis. The histopathological analysis revealed pulmonary edema, congestion and alveolar collapse in both groups; however, the differences between groups were not significant. Despite the lower cytokine and neutrophil levels observed in the acute lung injury + hypertonic saline group, significant differences were not observed among the treated and non-treated groups.CONCLUSIONS:Hypertonic saline infusion after intratracheal hydrochloric acid instillation does not have an effect on inflammatory biomarkers or respiratory gas exchange.
Highlights
The aspiration of acid gastric contents is the second most common cause of direct acute lung injury (ALI) [1], and it accounts for 10% of all acute respiratory distress syndrome (ARDS) cases [2]
Hemodynamic and respiratory data The hemodynamic measurements were similar for each of the investigated groups throughout the period of observation, and significant changes were not observed in the mean arterial pressure (MAP), central venous pressure (CVP), or systemic vascular resistance index (SVRI) values
The PaO2/FiO2 ratio exhibited a significant reduction at T30 in injured animals, or those in the ALI and ALI+hypertonic saline (HS) groups (240±40 and 244±51, respectively, po0.001), compared with those in the control animals, or the Sham and HS groups (467±37 and 445±57, respectively), and this ratio remained low throughout the observation period (Figure 2)
Summary
The aspiration of acid gastric contents is the second most common cause of direct acute lung injury (ALI) [1], and it accounts for 10% of all acute respiratory distress syndrome (ARDS) cases [2]. In addition to the potential risk of developing ARDS [5], the inhalation of gastric contents is a common cause of donor lung rejection [6]. Hyperosmolar solutions, such as hypertonic saline, have been tested in an attempt to reduce inflammation in ALI [7,8,9]. Previous results are contradictory and indicate that the effects of hypertonic saline depend on the type and agent of lung injury and timing of administration [10,11]
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