A rat model of cardiopulmonary bypass with cardioplegic arrest and hemodynamic assessment by conductance catheter technique.
BACKGROUND
Cardiopulmonary bypass (CPB) is known to induce systemic inflammation and cardiac dysfunction associated with a significant morbidity. Aim of the study was to develop an in vivo model of rat CPB with hypothermic cardiac arrest and the use of cardioplegia.


METHODS
The CPB circuit consisted of a venous reservoir, membrane oxygenator, heat exchanger, and roller pump. CPB was instituted in adult male Wistar rats (400-500 g) for 60 min at a flow rate of 120 ml x kg(-1) x min(-1), including 15 min cooling to 32 degrees C, 30 min cardiac arrest with the use of cold crystalloid cardioplegia after aortic cross clamping, and 15 min of reperfusion and rewarming to 37 degrees C. Arterial blood pressure (MAP) and heart rate (HR) were monitored, arterial blood samples were analyzed. Left ventricular (LV) function parameters were assessed by intraventricular conductance catheter. Important technical aspects are: ventilation is required during partial bypass; anticoagulation should be performed immediately prior to CPB to reduce blood loss; active suction on venous drainage allows higher pump flows; and the small priming volume of the extracorporeal circuit (8 ml) avoids the need for donor blood.


RESULTS
MAP remained stable prior to and during CPB.MAP and HR were significantly decreased 60 min after weaning from bypass. Hct was significantly lowered after hemodilution, but remained stable during CPB and 60 min after weaning from bypass. BE and pH remained stable throughout the experiment.Without inotropic support diastolic and systolic LV function parameters were impaired after 30 min of cardioplegic arrest followed by 15 min of reperfusion. Myocardial TNF-alpha mRNA levels were slightly increased (1.28-fold, p = 0.71), and IL-6 mRNA was significantly increased in the cardioplegia group (90.3-fold, p = 0.001). Both IL-6 and TNF-alpha plasma levels were significantly elevated in the cardioplegia group (TNF-alpha: 4.6-fold increase,p < 0.05; IL-6: 426.8-fold increase, p < 0.001).


CONCLUSIONS
We have developed a rat CPB with mild hypothermic cardioplegic arrest. This rodent model is suitable to study clinically relevant problems related to CPB,myocardial protection and systemic inflammation.
Günzinger
Ralf
R
Dept of Cardiovascular Surgery, German Heart Center Munich, Technical University of Munich, Munich, Germany.
Wildhirt
Stephen M
SM
Schad
Hubert
H
Heimisch
Werner
W
Gurdan
Manuela
M
Mendler
Nikolaus
N
Grammer
Joachim
J
Lange
Rüdiger
R
Bauernschmitt
Robert
R
D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006328:Cardiac Catheterization / Q000379:methods*; D002315:Cardiopulmonary Bypass / Q000379:methods*; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced / Q000379:methods*; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000503:physiopathology; D007036:Hypothermia, Induced; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013525:Surgical Instruments; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha