A novel, recovery, and reproducible minimally invasive cardiopulmonary bypass model with lung injury in rats

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-reperfusion injury in vivo.

A novel rat model of cardiopulmonary bypass for deep hypothermic circulatory arrest without blood priming

Background Large animal cardiopulmonary bypass （CPB） models are expensive,and prevent assessment of neurocognitive function,and difficulties with long-term recovery.The purpose of this study was to establish a novel rat model of cardiopulmonary bypass for deep hypothermic circulatory arrest without blood priming.Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomized to CPB with deep hypothermic circulatory arrest （DHCA） and control groups,with 10 rats each.The experimental protocols,including blood and crystalloid fluid administration,anesthesia,orotracheal intubation,ventilation,cannulation,and heparinization were identical in both groups.After inducing cardiac arrest,the circuit was turned off and rats were left in a DHCA state for 15 minutes.Rats were rewarmed to 34℃ to 35℃ over a period of 36 to 42 minutes using CPB-assisted rewarming,a heating blanket,and a heating lamp along with administration of 0.1 mEq of sodium bicarbonate and 0.14 mEq of calcium chloride.The remaining priming volume was reinfused and animals were weaned from CPB.Results All CPB with DHCA processes were successfully achieved.Blood gas analysis and hemodynamic parameters were in the normal range.The vital signs of all rats were stable.Conclusions Our CPB circuit has several novel features,including a small priming volume,active cooling/rewarming processes,vacuum-assisted venous drainage,peripheral cannulation without thoracotomy or stemotomy,and an accurate means of monitoring peripheral tissue oxygenation.

A novel, minimally invasive rat model of normothermic cardiopulmonary bypass model without blood priming

Background Cardiopulmonary bypass （CPB） has been shown to be associated with 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 novel, minimally invasive rat model of normothermic CPB model without blood priming. Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into CPB group （n=10） and 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 further transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. The volume of the priming solution, composed of 6% HES130/0.4 and 125 IU heparin, was less than 12 ml. The surface of the hollow fiber oxygenator was 0.075 m2. CPB was conducted for 60 minutes at a flow rat of 100-120 ml. kg -1. min-1 in CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Results All CPB processes were successfully achieved. Blood gas analysis and hemodynamic parameters of each time point were in accordance with normal ranges. The vital signs of all rats were stable. Conclusions The establishment of CPB without blood priming in rats can be achieved successfully. The nontransthoracic model should facilitate the investigation of pathophysiological processes concerning CPB-related multiple organ dysfunction and possible protective interventions. This novel, recovery, and reproducible minimally invasive CPB model may open the tield tor various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.