体外循环中应用吡咯烷二硫氨基甲酸酯对犬心肌能量代谢的影响

目的 观察抗氧化剂吡咯烷二硫氨基甲酸酯(PDTC)对犬体外循环(CPB)中心肌能量代谢的影响.方法 12只犬随机分为对照组(C组,n=6)和PDTC组(P组,n=6),腹腔内注射戊巴比妥钠25 mg/kg麻醉后建立CPB心肌缺血再灌注模型.P组于CPB前静脉注射PDTC 30mg/kg,C组静脉注射等量生理盐水.分别于CPB前、阻断主动脉60 min和开放主动脉60min时,取心肌测定腺苷酸(ATP、ADP、AMP、TAN、EC)、丙二醛(MDA)含量、总抗氧化能力(T-AOC)和线粒体肿胀度(MSD).于CPB前、开放主动脉30min和开放主动脉60min时测定心率(HR)、平均动脉压(MAP)和心输出量(CO).结果 与CPB前比较,两组阻断升主动脉后ATP、TAN、EC含量及T-AOC均降低(P＜0.01),MSD和MDA含量均升高;开放主动脉后C组ATP、TAN、EC含量及T-AOC均降低(P＜0.01),MSD和MDA含量均升高(P＜0.01);P组在开放主动脉60min时ATP、TAN、EC、MDA含量、T-AOC和MSD差异无统计学意义(P＞0.05).P组在阻断主动脉60 min时和开放主动脉后ATP、TAN、EC含量及T-AOC均显著高于C组(P＜0.01).MSD和MDA含量均显著低于C组(P＜0.01).P组在开放主动脉30 min和开放主动脉60 min时HR、MAP和CO较C组恢复迅速(P＜0.01).结论 CPB可引起心肌能量代谢受损及恢复延迟,PDTC能够明显改善缺血心肌的能量代谢,保护心肌线粒体的结构,从而减轻心肌缺血冉灌注损伤.

Effects of pyrrolidine dithiocarbamate pretreatment on canine myocardial energy metabolism during cardiopulmonary bypass

OBJECTIVE: To develop a technology for production of recombinant SAG1 of Toxoplasma gondii(T.g) in batches. METHODS: Twelve healthy mongrel dogs undergoing CPB were randomly allocated into control group (group C, n=6) and PDTC pretreatment group (group P, n=6). In group P, the dogs received intravenous injection of PDTC at 30 mg/kg before CPB, while in group C, normal saline was given instead. The myocardial tissues were obtained before CPB, 60 min after aortic cross-clamping (AC) and 60 min after declamping (DC) for determining the myocardial contents of adenine nucleotides (ATP, ADP, AMP, TAN, EC) and malondialdehyde (MDA) and evaluating the total anti-oxidation capacity (T-AOC) and mitochondrial swelling degree (MSD). The heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were monitored before CPB, 30 min and 60 min after DC. RESULTS: In both groups, the myocardial contents of ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after AC as compared to the values before CPB (P<0.01). In group C, ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after DC as compared to the values before CPB (P<0.01). At 60 min after DC, the dogs in group P showed no significant variation in the contents of ATP, TAN, EC, MDA, T-AOC or MSD (P>0.05). ATP, TAN, EC and T-AOC were significantly lowered while MDA and MSD increased at 60 min after AC and after DC in group P in comparison with the measurements in group C (P<0.01). HR, MAP and CO of group P recovered rapidly at 30 min and 60 min after DC as compared with those in group C (P<0.01). CONCLUSION: CPB can induce serious energy exhaustion and delay in the recovery of energy metabolism. PDTC pretreatment can substantially ameliorate myocardial energy depletion and protect the myocardial mitochondria to attenuate myocardial ischemia/reperfusion injury.