再灌注初期控制性降压对肝叶切除术病人肝缺血再灌注损伤的影响

Effect of controlled hypotension at the beginning of reperfusion on ischemia-reperfusion injury of Hver in patients undergoing hepatectomy

目的评价再灌注初期控制性降压对肝叶切除术病人肝缺血再灌注损伤的影响。方法择期行肝叶切除术病人40例，性别不限，年龄30～60岁，体重40．70kg，ASA分级Ⅱ或Ⅲ级，将病人按分层随机方法分为2组（n=20），对照组（C组）开放肝门后10min期间维持MAP75～100mmHg，控制性降压组（H组）于开放肝门前2min开始静脉输注硝酸甘油3—6μg·kg^-1·min^-1实施控制性降压，再灌注10min期间维持MAP60～70mmHg。分别于缺血前（基础状态）、缺血15min和再灌注25min时采集静脉血样，测定血浆内皮素（ET）、一氧化氮（NO）、TNF-α和IL-1的浓度。结果与基础值比较，两组缺血15min和再灌注25min时血浆ET、TNF-α和IL-1的浓度升高，血浆NO浓度降低（P〈0．05）；与C组比较，H组再灌注25min时血浆ET、TNF-α和IL-1的浓度降低，血浆NO浓度升高（P〈0．05）。结论再灌注初期控制性降压10min可减轻肝叶切除术病人肝缺血再灌注损伤，其机制与调节肝窦内皮细胞ET和NO的平衡及抑制炎性反应有关。

Objective To evaluate the effect of controlled hypotension at the beginning of reperfusion on isehemia-reporfusion （I/R） injury of the liver in patients undergoing hepatectomy. Me/hods Forty ASA Ⅱ or Ⅲ patients aged 30-60 yr weighing 40-70 kg undergoing elective partial hepatectomy for liver cancer were randomly divided into 2 groups （ n = 20 eaeh） ： group C normal BP and group H controlled hypotension. Hepatic portal was occluded during operation. In group C normal BP was maintained during reperfusion while in group H controlled hypotension （MAP was maintained at 60-70 mm Hg） was performed for 10 min since the beginning of reperfusion. Venous blood samples were taken before hepatic ischemia （To , baseline） and at 15 rain of ischemia （Ti） and 25 min of reperfusion （T2） for determination of plasma endothelin （ET）, nitric oxide（NO）, TNF-α and IL-1 concen- trations. Resulls I/R of the liver led to significant increase in plasma ET, TNF-α and IL-1 concentrations and decrease in plasma NO concentration at T1,2 as compared with the baseline values at To in both groups. Plasma ET, TNF-α and IL-1 concentrations were significantly lower while plasma NO concentration was significantly higher at T2 in group H than in group C. Conclusion Ten minutes controlled hypotension in the initial stage of reperfusion can attenuate I/R-induced injury to the liver in patients undergoing hepatectomy by balancing ET with NO and inhibiting inflammation response.