Fei Lin1, Ling-Hui Pan2, Lin Ruan1, Wei Qian1, Rui Liang1, Wan-Yun Ge1, Bin Huang1. 1. Department of Anesthesiology, Affiliated Cancer Hospital, Guangxi Medical University, Nanning, China. 2. Department of Anesthesiology, Affiliated Cancer Hospital, Guangxi Medical University, Nanning, China. Electronic address: linghuipancn@163.com.
Abstract
AIMS: One-lung ventilation (OLV) is a standard practice in thoracic surgery. However, OLV can give rise to arterial hypoxemia. Hypoxia-inducible transcription factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and aquaporin-1 (AQP-1) may be involved in arterial hypoxemia and contribute to cellular injury. Therefore, in the present study, these moieties were investigated in an OLV rat model. MAIN METHODS: Forty Sprague-Dawley (S-D) rats were randomly divided into four groups: right lung mechanical ventilation for 0.5 h (Group A); 1 h (Group B); 2 h (Group C) and mechanical ventilation of both lungs (control group). Rat lung tissue was examined using electron microscopy. Serum and lung tissue levels of VEGF were measured by ELISA, Western blot analyses were used to detect the protein expression of HIF-1α and immunohistochemical staining and real-time polymerase chain reaction (PCR) were performed to examine protein expression and gene levels, respectively, of VEGF and AQP-1 after hypoxia. KEY FINDINGS: Electron microscopy revealed that increased duration of OLV was correlated with greater destruction of the non-ventilated lung. The protein expression of HIF-1α was significantly increased in the non-ventilated lungs of the experimental hypoxia groups (A-C) compared to the control group, whereas VEGF and AQP-1 protein expression and gene levels were decreased in the non-ventilated lungs of the hypoxia groups (A-C) compared to the control group. SIGNIFICANCE: The OLV caused hypoxia in the non-ventilated lung and subsequent injury. The altered expression of HIF-1α, VEGF, and AQP-1 may be involved in the pathological process of lung injury caused by hypoxia.
AIMS: One-lung ventilation (OLV) is a standard practice in thoracic surgery. However, OLV can give rise to arterial hypoxemia. Hypoxia-inducible transcription factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and aquaporin-1 (AQP-1) may be involved in arterial hypoxemia and contribute to cellular injury. Therefore, in the present study, these moieties were investigated in an OLV rat model. MAIN METHODS: Forty Sprague-Dawley (S-D) rats were randomly divided into four groups: right lung mechanical ventilation for 0.5 h (Group A); 1 h (Group B); 2 h (Group C) and mechanical ventilation of both lungs (control group). Rat lung tissue was examined using electron microscopy. Serum and lung tissue levels of VEGF were measured by ELISA, Western blot analyses were used to detect the protein expression of HIF-1α and immunohistochemical staining and real-time polymerase chain reaction (PCR) were performed to examine protein expression and gene levels, respectively, of VEGF and AQP-1 after hypoxia. KEY FINDINGS: Electron microscopy revealed that increased duration of OLV was correlated with greater destruction of the non-ventilated lung. The protein expression of HIF-1α was significantly increased in the non-ventilated lungs of the experimental hypoxia groups (A-C) compared to the control group, whereas VEGF and AQP-1 protein expression and gene levels were decreased in the non-ventilated lungs of the hypoxia groups (A-C) compared to the control group. SIGNIFICANCE: The OLV caused hypoxia in the non-ventilated lung and subsequent injury. The altered expression of HIF-1α, VEGF, and AQP-1 may be involved in the pathological process of lung injury caused by hypoxia.