浅低温心脏不停跳与低温冷停跳对心肌保护效果比较

目的比较浅低温心脏不停跳及低温冷停跳心内直视手术对心肌保护的效果。方法20例需行二尖瓣置换术的患者随机分成两组,一组为不停跳体外循环心肌保护组(BH组),另一组为低温晶体心停搏液心肌保护组(CCP组),每组各10例。分别在转流前、开放主动脉后1h(BH组为开放上下腔静脉后1h,下同),术后6、24、48、72h采静脉血测定心肌肌钙蛋白I(cTnI)、磷酸肌酸激酶同功酶(CK-MB)、血清超氧化物歧化酶(SOD)。结果两组间比较cTnI、CK-MB及SOD在开放主动脉后1h、术后6、24、48h均有显著性差异(P<0.05,P<0.01或P<0.001),cTnI于术后24h达到峰值,术后72h降至正常水平(P>0.05);SOD水平开放主动脉后1h为最低,后逐渐升高,至术后72h降至正常水平(P>0.05)。结论心脏不停跳体外循环心肌保护基本能避免缺血损害和缺血再灌注损伤,较之低温冷停跳是一种更安全、更接近于生理的心肌保护方法。

Clinical comparison of myocardial protection of warm beating heart with cold crystalloid cardioplegia

Objective To compare the effects of warm beating heart with cold crystalloid cardioplegia on the ischemic damage, reperfusion injury, arithmia and ultrastruture changes, and to investigate the theoretical basis of myocardial protection of warm beating heart.Methods Twenty patients undergone mitral valve replacement were selected and randomly divided into two groups: group of warn beating heart (BH,n=10) and group of cold crystalloid cardioplegia (CCP,n=10). Venous blood examples were taken to assess myocardialtroponin I(cTnI),creatinekinase-MB(CK-MB) and superoxidedismutase(SOD) before pre-cardiopulmonary bypass, 1 hour after aortic unclamp (1 hour after superior and inferior vena cava unclamp in group BH) and post-operative 6,24,48,72 hours. Electrical cardiography was recorded 3 hours before and after operation. Right atrial specimens were taken 10 minutes before aortic clamp and 30 minutes after aortic unclamp for electropic microscopic examination.Results cTnI, CK-MB and SOD levels in two groups 1 hour after aortic unclamp, 6,24, and 48 hours after operation were significantly different(P<0.05,P<0.01, or P<0.001). cTnI reached to a climax 24 hours after operation, and decreased to normal 72 hours after operation. SOD reached to a minimum 1 hour after operation, and increased to normal 72 hours after operation. Newly occurred arithmia in group BH was less than that in group CCP (1/10 vs 4/10). Myocardial ultrastructure changes in group BH were slighter than in group CCP. Plasma cTnI and myocardial enzymes in group BH were remarkbly lower than in group CCP. Ischemic-reperfusion damages in group BH was less than in group CCP. Occurrence of arithmia in patients with warm beating hearts was less than that in group CCP. Inotropics applied postoperatively in group BH were less than that in group CCP. Myocardial ultrastructure changes in group BH were lighter than in group CCP. Conclusion Myocardial protection of warm beating heart can essentially avoid ischemic-reperfusion damages and is a kind of safer and closer to physiogical way of myocardial protection.