心内手术患者围体外循环期肺内一氧化碳和一氧化氮的变化及意义

Role of pulmonary carbon monoxide and nitric oxide in patients undergoing elective cardiac surgery with cardiopulmonary bypass

目的研究心脏瓣膜置换术患者围体外循环期肺内一氧化碳和一氧化氮的变化及意义。方法20例体外循环下行心脏瓣膜置换术患者,A SAII￣III级。分别测定患者体外循环(C PB)前(T)及主动脉开放后50m in(T1)、15m in(T2)、30m in(T3)、1h(T)、3h(T5)及24h(T6)左、右心房血一氧化碳(C O)、一氧化氮4(N O)、肿瘤坏死因子(TN F-α)浓度及中性粒细胞(PM N s)数目。结果T～T时点患者左右心房血C O25含量均明显高于C PB前(P<0.05);除T6时点,左房血C O含量均明显高于同时点右房血(P<0.05);T～T4时1点患者左右心房血N O含量均明显高于C PB前(P<0.05);同一时点左右房血N O含量差异无显著性(P>0.05);T～T时点患者左右心房血PM N s数目均明显高于C PB前(P<0.05);T、T时点,左、右房血PM N s数目1612有明显差异(P<0.05);T～T时点患者血浆T N F-α值均明显高于C PB前(P<0.05),T时点左房血T N F-α141明显高于右房(P<0.05)。结论体外循环心脏瓣膜置换术中肺内存在炎性反应,C O和N O在C PB应激下增高,可能作为两种内源性保护因子起作用。

To study the role of pulmonary CO and NO in patients undergoing elective cardiac valve replacement surgery with cardiopulmonary bypass. From 20 patients undergoing elective valve replacement surgery, blood samples were obtained from left and right atria , pre-CPB, 5, 15, 30 min, 1, 3 and 24 h after release of the aortic cross-clamp ,respectively, to measure the levels of carbon monoxide (CO), nitric oxide (NO), tumor necrosis factor-α (TNF-α) and polymorphonuclear leukocytes (PMNs). Blood CO concentration increased at T2～T5 than that of pre-CPB in all patients (P <0.05); the left atria CO was significantly higher than that in the right atria except T6 (P <0.05); Plasma NO concentration increased significantly at T1～T4 than that of pre-CPB in all patients (P <0.05); but there was no difference between the left atria and the right atria at each time point(P >0.05); Blood PMNs count increased significantly at T1～T6 than that of pre-CPB in all patients (P <0.05); PMNs count in the left atria was significantly different from that in the right atria at T1, T2 (P <0.05); Plasma TNF-α concentration increased significantly at T1 ～T4 than that of pre-CPB in all patients (P <0.05), TNF-α concentration in the left atria was significantly higher than that in the right atria at T1. [Conclusions] Increased concentration of endogenous CO and NO in lung may play a protective role in the pathogenesis of CPB-induced pulmonary injury.