Investigation of the biological effects of artificial perfusion using rat extracorporeal circulation model

Extracorporeal circulation (ECC) is indispensable for cardiac surgery. Since difficulty in clinical research keeps the knowledge insufficient, it is desirable to have a miniature ECC system for small animals. We aimed to establish a miniature ECC system and apply the system to the rat for investigating biochemical changes. The ECC system consisted of a membranous oxygenator (polypropylene, 0.03 m2), tubing line (polyvinyl chloride) and roller pump. Priming volume of this system is only 15 ml. Rats were divided into the SHAM group and the ECC group. ECC pump flow was initiated and maintained at 70 ml/kg/min. We measured the serum cytokine levels of tumor necrosis factor-a, interleukin (IL)-6, and IL-10, and biochemical markers (lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase) before, 60, and 120 min after the initiation of ECC. In addition, we measured the wet-to-dry weight (W/D) ratio of the left lung tissues. During ECC, blood pressure and Hb were maintained around 80 mmHg and 10g/dl, the serum cytokine levels and biochemical markers were significantly elevated in the ECC group compared with the SHAM group. The W/D ratio increased significantly more in the ECC group compared with that in the SHAM group. These data suggest that ECC promotes organ damages and systemic inflammatory response. This rat ECC model is considered to be equivalent to the already established human ECC and useful for studying the mechanism of pathophysiological changes during artificial perfusion.

[1]  A Haverich,et al.  Systemic inflammatory response syndrome after cardiac operations. , 1996, The Annals of thoracic surgery.

[2]  M. Ovize,et al.  Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recovery. , 2006, American journal of physiology. Heart and circulatory physiology.

[3]  Uwe Mehlhorn,et al.  Cardioplegic arrest induces apoptosis signal-pathway in myocardial endothelial cells and cardiac myocytes. , 2003, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.

[4]  S. Kirchner,et al.  Endothelial apoptosis is induced by serum of patients after cardiopulmonary bypass. , 2000, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.

[5]  Eisuke Tatsumi,et al.  Insufflation of hydrogen gas restrains the inflammatory response of cardiopulmonary bypass in a rat model. , 2013, Artificial organs.

[6]  M. Liddell,et al.  Extracorporeal life support - state of the art. , 2003, Paediatric respiratory reviews.

[7]  F E Schmidt,et al.  Leukocyte depletion of blood cardioplegia attenuates reperfusion injury. , 1996, The Annals of thoracic surgery.

[8]  Yasuyuki Sasaki,et al.  Impact of non-di-(2-ethylhexyl)phthalate cardiopulmonary bypass tubes on inflammatory cytokines and coagulation-fibrinolysis systems during cardiopulmonary bypass , 2009, Journal of Artificial Organs.

[9]  S Westaby,et al.  Inflammatory response to cardiopulmonary bypass. , 1993, The Annals of thoracic surgery.

[10]  D. Das,et al.  Influence of steroids on complement and cytokine generation after cardiopulmonary bypass. , 1995, The Annals of thoracic surgery.

[11]  John G. Laffey,et al.  The Systemic Inflammatory Response to Cardiac Surgery: Implications for the Anesthesiologist , 2002, Anesthesiology.

[12]  E D Verrier,et al.  Endothelial cell injury in cardiovascular surgery: the systemic inflammatory response. , 1997, The Annals of thoracic surgery.