Impact of dexmedetomidine preconditioning and postconditioning on acute lung injury by lung ischemia-reperfusion in rats
Jiefang Zhu
Abstract
Jiefang Zhu
Abstract
Objective To study the effect of dexmedetomidine preconditioning and postconditioning on acute lung injury by lung ischemia-reperfusion (I/R) in rats. Methods 32 SD rats were divided into control group, I/R group, preconditioning group, postconditioning group. All the groups establish the model of acute lung injury by lung ischemia-reperfusion, except the control group. Arterial blood oxygen partial pressure, lung coefficient, oxidative stress and inflammation mediator content, the expression of apoptosis molecule were measured. Results The lung tissue wet / dry weight ratio (W/D), malondialdehyde (MDA), C-reactive protein (CRP) and tumor necrosis factor-α (TNF- α), monocyte chemotaxis protein-1 (MCP-1) content and bax, Caspase-3 expression were decreased from I/R group to preconditioning group, and to postconditioning group, respectively [5.97±0.74, 4.42±0.62, 3.88±0.44; (20.35±2.65, 15.54±1.73, 11.21±1.36) nmol/L; (7.21±0.89, 4.14±0.54, 3, 56±0.44) mg/L; (66.51±7.38, 49.59±5.27, 44.25±4.63) ng/L; (38.28±4.76, 25.39±3.49, 21.24±3.12) ng/L; 236.75±28.48, 176.59±18.39, 155.35±14.68; 194.78±20.35, 148.54±15.86, 130.15±12.45]. While the arterial oxygen pressure (PaO2), superoxide dismutase (SOD), glutathione (GSH) content and bcl-2 expression were increased from I/R group to preconditioning group, and to postconditioning group, respectively [(68.73±7.13, 80.53±7.35, 88.65±7.75) mmHg (1 mmHg=0.133 kPa); (24.48±3.25, 32.65±3.24, 36.42±3.36) U/L; (30.45±3.51, 45.97±5.13, 53.12±5.45) U/L; 36.65±4.12, 66.76±7.38, 74.65±7.24]. Conclusion Dexmedetomidine preconditioning and postconditioning have a protective effect on acute lung injury by lung ischemia-reperfusion in rats and can reduce cell injury and apoptosis induced by oxidative stress injury and inflammation, and the protective effect of dexmedetomidine postconditioning is better. Key words: Acute lung injury; Reperfusion injury; Dexmedetomidine; Preconditioning; Postconditioning
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Objective To study the effect of dexmedetomidine preconditioning and postconditioning on acute lung injury by lung ischemia-reperfusion (I/R) in rats. Methods 32 SD rats were divided into control group, I/R group, preconditioning group, postconditioning group. All the groups establish the model of acute lung injury by lung ischemia-reperfusion, except the control group. Arterial blood oxygen partial pressure, lung coefficient, oxidative stress and inflammation mediator content, the expression of apoptosis molecule were measured. Results The lung tissue wet / dry weight ratio (W/D), malondialdehyde (MDA), C-reactive protein (CRP) and tumor necrosis factor-α (TNF- α), monocyte chemotaxis protein-1 (MCP-1) content and bax, Caspase-3 expression were decreased from I/R group to preconditioning group, and to postconditioning group, respectively [5.97±0.74, 4.42±0.62, 3.88±0.44; (20.35±2.65, 15.54±1.73, 11.21±1.36) nmol/L; (7.21±0.89, 4.14±0.54, 3, 56±0.44) mg/L; (66.51±7.38, 49.59±5.27, 44.25±4.63) ng/L; (38.28±4.76, 25.39±3.49, 21.24±3.12) ng/L; 236.75±28.48, 176.59±18.39, 155.35±14.68; 194.78±20.35, 148.54±15.86, 130.15±12.45]. While the arterial oxygen pressure (PaO2), superoxide dismutase (SOD), glutathione (GSH) content and bcl-2 expression were increased from I/R group to preconditioning group, and to postconditioning group, respectively [(68.73±7.13, 80.53±7.35, 88.65±7.75) mmHg (1 mmHg=0.133 kPa); (24.48±3.25, 32.65±3.24, 36.42±3.36) U/L; (30.45±3.51, 45.97±5.13, 53.12±5.45) U/L; 36.65±4.12, 66.76±7.38, 74.65±7.24]. Conclusion Dexmedetomidine preconditioning and postconditioning have a protective effect on acute lung injury by lung ischemia-reperfusion in rats and can reduce cell injury and apoptosis induced by oxidative stress injury and inflammation, and the protective effect of dexmedetomidine postconditioning is better. Key words: Acute lung injury; Reperfusion injury; Dexmedetomidine; Preconditioning; Postconditioning
Key concepts: Malondialdehyde, Lung, Reperfusion injury, Oxidative stress, Medicine, Superoxide dismutase, Anesthesia, Ischemia