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Abstract：
BACKGROUND: Ischemia-reperfusion (IR) injury is a major concern that frequently occurs during vascular surgeries. Hydrogen-rich saline (HRS) solution exhibits antioxidant and anti-inflammatory properties. This study aimed to examine the effects of HRS applied before ischemia in the lungs of rats using a lower extremity IR model.
METHODS: After approval was obtained from the ethics committee, 18 male Wistar albino rats weighing 250-280 g were randomly divided into three groups: control (C), IR and IR-HRS. In the IR and IR-HRS groups, an atraumatic microvascular clamp was used to clamp the infrarenal abdominal aorta, and skeletal muscle ischemia was induced. After 120 min, the clamp was removed, and reperfusion was achieved for 120 min. In the IR-HRS group, HRS was administered intraperitoneally 30 min before the procedure. Lung tissue samples were examined under a light microscope and stained with hematoxylin-eosin (H&E). Malondialdehyde (MDA) levels, total sulfhydryl (SH) levels, and histopathological parameters were evaluated in the tissue samples.
RESULTS: MDA and total SH levels were significantly higher in the IR group than in the control group (p < 0.0001 and p = 0.001, respectively). MDA and total SH levels were significantly lower in the IR-HRS group than in the IR group (p < 0.0001 and p = 0.013, respectively). A histopathological examination revealed that neutrophil infiltration/aggregation, alveolar wall thickness, and total lung injury score were significantly higher in the IR group than in the control group (p < 0.0001, p = 0.001, and p < 0.0001, respectively). Similarly, alveolar wall thickness and total lung injury scores were significantly higher in the IR-HRS group than in the control group (p = 0.009 and p = 0.004, respectively). A statistically significant decrease was observed in neutrophil infiltration/aggregation and total lung injury scores in the IR-HRS group compared to those in the IR group (p = 0.023 and p = 0.022, respectively).
CONCLUSIONS: HRS at a dose of 20 mg/kg, administered intraperitoneally 30 min before ischemia in rats, reduced lipid peroxidation and oxidative stress, while also reducing IR damage in lung histopathology. We believe that HRS administered to rats prior to IR exerts a lung-protective effect.
METHODS: After approval was obtained from the ethics committee, 18 male Wistar albino rats weighing 250-280 g were randomly divided into three groups: control (C), IR and IR-HRS. In the IR and IR-HRS groups, an atraumatic microvascular clamp was used to clamp the infrarenal abdominal aorta, and skeletal muscle ischemia was induced. After 120 min, the clamp was removed, and reperfusion was achieved for 120 min. In the IR-HRS group, HRS was administered intraperitoneally 30 min before the procedure. Lung tissue samples were examined under a light microscope and stained with hematoxylin-eosin (H&E). Malondialdehyde (MDA) levels, total sulfhydryl (SH) levels, and histopathological parameters were evaluated in the tissue samples.
RESULTS: MDA and total SH levels were significantly higher in the IR group than in the control group (p < 0.0001 and p = 0.001, respectively). MDA and total SH levels were significantly lower in the IR-HRS group than in the IR group (p < 0.0001 and p = 0.013, respectively). A histopathological examination revealed that neutrophil infiltration/aggregation, alveolar wall thickness, and total lung injury score were significantly higher in the IR group than in the control group (p < 0.0001, p = 0.001, and p < 0.0001, respectively). Similarly, alveolar wall thickness and total lung injury scores were significantly higher in the IR-HRS group than in the control group (p = 0.009 and p = 0.004, respectively). A statistically significant decrease was observed in neutrophil infiltration/aggregation and total lung injury scores in the IR-HRS group compared to those in the IR group (p = 0.023 and p = 0.022, respectively).
CONCLUSIONS: HRS at a dose of 20 mg/kg, administered intraperitoneally 30 min before ischemia in rats, reduced lipid peroxidation and oxidative stress, while also reducing IR damage in lung histopathology. We believe that HRS administered to rats prior to IR exerts a lung-protective effect.
摘要：
背景：缺血再灌注（IR）损伤是血管手术中经常发生的主要问题。富氢盐水(HRS)溶液具有抗氧化和抗炎特性。本研究旨在使用下肢IR模型检查在大鼠肺缺血前应用HRS的影响。
方法：获得伦理委员会批准后，18只体重250-280g的雄性Wistar白化病大鼠随机分为三组：对照组（C），IR和IR-HRS。在IR和IR-HRS组中，使用无创伤微血管钳夹住肾下腹主动脉，并诱发骨骼肌缺血。120分钟后，夹具被移除，再灌注120分钟。在IR-HRS组中，手术前30分钟腹膜内给予HRS。在光学显微镜下检查肺组织样品并用苏木精-伊红(H&E)染色。丙二醛（MDA）水平，总巯基(SH)水平，并在组织样本中评估组织病理学参数。
结果：IR组的MDA和总SH水平明显高于对照组（分别为p<0.0001和p=0.001）。IR-HRS组的MDA和总SH水平显著低于IR组(分别为p<0.0001和p=0.013)。组织病理学检查显示中性粒细胞浸润/聚集，肺泡壁厚度，IR组的肺损伤评分和总肺损伤评分明显高于对照组（分别为p<0.0001，p=0.001和p<0.0001）。同样，IR-HRS组的肺泡壁厚度和总肺损伤评分明显高于对照组(分别为p=0.009和p=0.004).与IR组相比，IR-HRS组的嗜中性粒细胞浸润/聚集和总肺损伤评分具有统计学上的显着降低（分别为p=0.023和p=0.022）。
结论：HRS剂量为20mg/kg，在大鼠缺血前30分钟腹膜内给药，减少脂质过氧化和氧化应激，同时减少肺组织病理学中的IR损伤。我们认为在IR之前对大鼠施用HRS具有肺保护作用。
方法：获得伦理委员会批准后，18只体重250-280g的雄性Wistar白化病大鼠随机分为三组：对照组（C），IR和IR-HRS。在IR和IR-HRS组中，使用无创伤微血管钳夹住肾下腹主动脉，并诱发骨骼肌缺血。120分钟后，夹具被移除，再灌注120分钟。在IR-HRS组中，手术前30分钟腹膜内给予HRS。在光学显微镜下检查肺组织样品并用苏木精-伊红(H&E)染色。丙二醛（MDA）水平，总巯基(SH)水平，并在组织样本中评估组织病理学参数。
结果：IR组的MDA和总SH水平明显高于对照组（分别为p<0.0001和p=0.001）。IR-HRS组的MDA和总SH水平显著低于IR组(分别为p<0.0001和p=0.013)。组织病理学检查显示中性粒细胞浸润/聚集，肺泡壁厚度，IR组的肺损伤评分和总肺损伤评分明显高于对照组（分别为p<0.0001，p=0.001和p<0.0001）。同样，IR-HRS组的肺泡壁厚度和总肺损伤评分明显高于对照组(分别为p=0.009和p=0.004).与IR组相比，IR-HRS组的嗜中性粒细胞浸润/聚集和总肺损伤评分具有统计学上的显着降低（分别为p=0.023和p=0.022）。
结论：HRS剂量为20mg/kg，在大鼠缺血前30分钟腹膜内给药，减少脂质过氧化和氧化应激，同时减少肺组织病理学中的IR损伤。我们认为在IR之前对大鼠施用HRS具有肺保护作用。
