摘要
Background Cardiopulmonary bypass （CPB） has been shown to be associated with a systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a good rat model of CPB to study the pathophysiology of potential complications. Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into a CPB group （n=10） and a control group （n=10）. All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. The surface of the hollow fiber oxygenator was 0.075 m~. CPB was conducted for 60 minutes at a flow rate of 100-120 ml. kg-1. min-1 in the CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Blood gas analysis, hemodynamic investigations, and lung histology were subsequently examined. Results All CPB rats recovered from the operative process without incident. Normal cardiac function after successful weaning was confirmed by electrocardiography and blood pressure measurements. Mean arterial pressure remained stable. The results of blood gas analysis at different times were within the normal range. Levels of IL-113 and TNF-a were higher in the lung tissue in the CPB group （P 〈0.005）. Histological examination revealed marked increases in interstitialcongestion, edema, and inflammation in the CPB group. Conclusion This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia
Background Cardiopulmonary bypass （CPB） has been shown to be associated with a systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a good rat model of CPB to study the pathophysiology of potential complications. Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into a CPB group （n=10） and a control group （n=10）. All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. The surface of the hollow fiber oxygenator was 0.075 m~. CPB was conducted for 60 minutes at a flow rate of 100-120 ml. kg-1. min-1 in the CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Blood gas analysis, hemodynamic investigations, and lung histology were subsequently examined. Results All CPB rats recovered from the operative process without incident. Normal cardiac function after successful weaning was confirmed by electrocardiography and blood pressure measurements. Mean arterial pressure remained stable. The results of blood gas analysis at different times were within the normal range. Levels of IL-113 and TNF-a were higher in the lung tissue in the CPB group （P 〈0.005）. Histological examination revealed marked increases in interstitialcongestion, edema, and inflammation in the CPB group. Conclusion This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia
基金
This study was supported by grants from the Capital Medical University-Clinical Research Cooperation Fund （No. l lJLS0, No. 13JL26）, the National Natural Science Foundation of China （No. 81371443, No. 81070055）, Beijing Natural Science Foundation （No. 7112046, No. 7122056）, Beijing Health System High Level Health Technical Personnel Training Plan （No. 2011-1-4）, and the Specialized Research Fund for the Doctoral Program of Higher Education （SRFDP, No. 20111107110006）.
