Myocardial Injury After Cardiopulmonary Bypass In Rats Model Is Protected By P38MAPK Inhibitor CBS3830

Objective In this study, by using CBS3830Pretreatment of rats beforecardiopulmonary bypass(CPB), discuss the p38MAPK inhibitor myocardial injury andshort-term effects to SD rats after cardiopulmonary bypass.Methods Twenty-four Male Sprague-Dawley rats (rats age:14though16weeks,weight between300-350g)were randomly divided into three groups：sham group（n=8），CPB group（n=8） and drugs group（n=8）. Tail artery is used for arterialblood perfusion. The venous cannula in the right internal jugular vein was allowed forcomplete drainage of the right atrium, superior vena cava, as well as the inferior vena.The CPB circuit was primed with blood. Extracorporeal circulation was slowly initiatedto a final flow rate of100–120(ml/kg)/min. CPB group and drugs group underwent60-minute cardiopulmonary bypass. To maintain spontaneous breathing during surgery.Drugs group through a gastric tube poured of P38MAPK inhibitor CBS3830one hourbefore surgery and the control group underwent cannulation and heparinization only.Arterial blood pressure and blood gas were monitored in preoperative, intraoperativeand postoperative. Plasma was collected in each group about1ml at baseline,afterCPB,and after CPB three days for IL-1β and cTnI analysis.The rats were killed aftersurgery three days，the Myocardial tissue was then isolated and stored at-80°untilTNF-α and p-p38MAPK analysis were performed. The remaining was fixed by4%formaldehyde solution for light microscopy observation. Results①CPB model after such minimally invasive peripheral cannulation treatment,3groups of experimental rats survived for three days. According to the preoperative,intraoperative and postoperative invasive blood pressure monitoring and blood gasanalysis results,blood pressure was stable and oxygenation was well, basically meet therequirement of CPB.②Myocardial tissue TNF-α and p-p38MAPK were significantlyincreased in the CPB group compared to the Sham group. Histopathology revealed therewas more myocardial injury in the CPB group compared to the Sham group. The CPBgroup had significantly increased in plasma IL-1β and cTnI compared to the Shamgroup.③Myocardial tissue TNF-α and p-p38MAPK were significantly decreased in thedrugs group compared to the CPB group. Histopathology revealed there was lessmyocardial injury in the drugs group compared to the CPB group. The drugs group hadsignificantly decreased in plasma IL-1β and cTnI compared to the CPB group.Conclusion①Establishment of cardiopulmonary bypass model in the j rats throughthis method is stable and practical. Using peripheral cannulation, maintainspontaneous breathing during surgery, relatively aseptic surgery, maintain higher arterialblood pressure are the key to successful postoperative survival.②T heCPB hadincreased plasma IL-1β, cTnI.and Myocardial tissul TNF-α, p-p38MAPK, result inmyocardial injury after cardiopulmonary bypass.③Through a gastric tube poured ofP38MAPK inhibitor CBS3830one hour before surgery can reduce the inflammatoryresponse from CPB,thus reduces the amount of myocardial injury.