Abstract
Purpose: To study the effect of different doses of dexmedetomidine on lung function and lung tissue cell apoptosis in a rat model of hyperoxic acute lung injury.
 Methods: Five groups of healthy male Sprague-Dawley rats were used: normal rats, untreated hyperoxic rats, and hyperoxic rats given 3 different doses of dexmedetomidine, with 20 rats in each group. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined usingenzyme-linked immunosorbent assay (ELISA). Parietal paraffin cuts were taken from the right upper lobe for measurement of apoptosis using in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and the apoptosis index was calculated.
 Results: At 24 and 48 h, the levels of IL-6 and TNF-α in the hyperoxia model group were significantly higher than those in the normal control group, and their levels in the middle- and high-dose groups were markedly lowered, relative to untreated hyperoxia rats (p < 0.05). Apoptosis index in the hyperoxia model rats significantly increased, relative to normal rats (p < 0.05). The apoptosis index in the mediumand high-dose groups decreased significantly (p < 0.05).
 Conclusion: Dexmedetomidine inhibits inflammatory responses caused by high concentration of oxygen inhalation, minimizes lung injury, improves lung function and inhibits lung apoptosis.
 Keywords: Dexmedetomidine, Hyperoxia, Acute lung injury, Lung function, Apoptosis
Highlights
Inhalation of high concentration of oxygen is one of the most common and necessary treatments in clinical rescue, and it plays an important role in maintaining stable organ function, preventing organ failure, gaining time for clinical treatment, and saving patients' lives [1]
It has been found that long-term inhalation of high oxygen concentration causes significant adverse reactions to organs, with the lungs as the most prone to hyperoxia-type acute injury
This study was carried out to investigate the effect of dexmedetomidine on lung function and apoptosis in a rat model of hyperoxic acute lung injury
Summary
Inhalation of high concentration of oxygen is one of the most common and necessary treatments in clinical rescue, and it plays an important role in maintaining stable organ function, preventing organ failure, gaining time for clinical treatment, and saving patients' lives [1]. It has been found that long-term inhalation of high oxygen concentration causes significant adverse reactions to organs, with the lungs as the most prone to hyperoxia-type acute injury. Studies have shown that acute lung injury is closely related to oxidative stress, inflammatory response and apoptosis [3]. Research has shown that dexmedetomidine protects the lungs by controlling inflammatory response, reducing oxidative stress, and improving lung oxygenation. This study was carried out to investigate the effect of dexmedetomidine on lung function and apoptosis in a rat model of hyperoxic acute lung injury. The lungs of each group of rats were separated, the upper lobes of the left lungs were subjected to H&E staining for determination of pathological changes. Values of p < 0.05 were taken as indicative of statistical significance of difference
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