摘要
目的 观察缺血预处理对全膝关节置换术(TKA)后患者脑氧合以及血清肌酸磷酸激酶(CK)、乳酸脱氢酶(LDH)水平的影响。方法 选择2015年1月—2017年5月乌鲁木齐市友谊医院骨一科收治并行TKA治疗的患者84例,按照随机数字表法分为研究组和对照组,每组42例,2组患者均在腰硬联合阻滞下接受TKA治疗,并应用充气式止血带止血,研究组在麻醉诱导前进行缺血预处理,对照组不进行缺血预处理。观察2组麻醉诱导前、术毕颈静脉血氧饱和度(S.jv02)、颈静脉球部氧分压(PjO_2)及脑氧摄取分数(OEF);比较2组麻醉诱导前、术毕、术后12 h、术后24 h血清CK、LDH、炎性因子、丙二醛(MDA)和超氧化物歧化酶(SOD)水平。结果 手术毕,对照组患者PjO_2较麻醉诱导前显著降低(t=3.070,P<0.01),研究组SjvO_2、PjO_2、OEF与麻醉诱导前比较无统计学差异(P>0.05),术毕研究组SjvO_2、PjO_2、OEF显著高于对照组(t=2.068、2.734、2.035,P均<0.05)。2组患者术毕、术后12 h、术后24h血清CK、LDH较麻醉诱导前显著升高(对照组:F=37.521、18.349,P均=0.000,研究组:F=13.297、15.438,P均=0.000),研究组患者血清CK、LDH显著低于对照组(t=39.663、21.348、10.087、18.221、23.143、20.318,P均<0.01)。术毕、术后12 h、术后24 h研究组患者血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)、MDA显著低于对照组,SOD显著高于对照组(t=3.265、8.480、7.783,2.060、2.169、2.382,5.160、4.427、3.649,15.453、14.391、17.983,2.455、6.906、7.319,P均<0.01)。住院期间2组患者不良反应发生率比较无统计学差异(P>0.05)。结论 缺血预处理可以有效降低TKA患者术后血清CK和LDH水平、机体炎性反应和氧化应激损伤,降低缺血再灌注损伤对脑氧合的影响。
Objective To investigate the effect of ischemic preconditioning on cerebral oxygenation, serum creatine phosphokinase (CK) and lactate dehydrogenase (LDH) level in patients with total knee arthroplasty (TKA). Methods Eighty-four patients with TKA in Department of orthopedics, Urumqi Friendship Hospital from January 2015 to May 2017 were selected, they were divided into study group and control group according to the random number table, 42 cases in each group, two groups were treated with TKA in combined spinal epidural anesthesia, and the pneumatic tourniquet was used to stop bleeding, the study group underwent ischemic preconditioning prior to anesthesia induction, the ischemic preconditioning was not performed in the control group. The jugular venous oxygen saturation (SjvO 2), jugular bulb oxygen pressure (PjO 2) and cerebral oxygen uptake fraction (OEF) were observed before and after anesthesia induction in two groups, the levels of CK, LDH, inflammatory factors, malondialdehyde (MDA) and superoxide enzyme (SOD) were compared between the two groups before anesthesia induction, after operation, after 12 h operation and after 24 h operation. Results The PjO 2 in the control group after operation was significantly lower than that before anesthesia induction ( t =3.070, P 〈0.05), compared with before anesthesia induction, there were no statistical differences between SjvO 2, PjO 2 and OEF in the study group after operation ( P 〉0.05), the levels of SjvO 2, PjO 2 and OEF in the study group were significantly higher than those in the control group ( t =2.068, t =2.734, t =2.035, P 〈0.05). The levels of serum CK and LDH in the two groups after operation, after 12 h operation and after 24 h operation were significantly higher than those before anesthesia induction ( P 〈0.05), the serum CK and LDH in the study group were significantly lower than those in the control group ( t =39.663, t =21.348, t =10.087, t =18.221, t =23.143, t =20.318, P 〈0.01). The serum levels of interleukin 6 (IL-6), tumor necrosis factorα (TNF-α), interleukin 8 (IL 8) and MDA in the study group after operation, after 12 h operation and after 24 h operation were significantly lower than those in the control group, and SOD was significantly higher than that in the control group ( t =3.265, t = 8.480, t =7.783, t =2.060, t =2.169, t =2.382, t =5.160, t =4.427, t =3.649, t =15.453, t =14.391, t = 17.983 , t =2.455, t =6.906, t =7.319, P 〈0.01). There was no statistical difference in the incidence of adverse reactions between the two groups during hospitalization ( P 〉0.05). Conclusion Ischemic preconditioning can effectively reduce the serum levels of CK and LDH, inflammatory reaction and oxidative stress in patients with TKA, and reduce the effect of ischemia reperfusion injury on cerebral oxygenation.
作者
赵之颢
洪凯峰
梁振
李瑞
ZHAO Zhihao;HONG Kaifeng;LIANG Zhen;LI Rui(Department of Orthopedics,Urumqi Friendship Hospital,Urumqi 830049,China)
出处
《疑难病杂志》
CAS
2018年第9期922-926,共5页
Chinese Journal of Difficult and Complicated Cases
关键词
缺血预处理
全膝关节置换术
脑氧合
肌酸磷酸激酶
乳酸脱氢酶
Isehemie preconditioning
Total knee arlhroplasty
Cerebral oxygenation
Creatine phosphokinase
Lactate dehydrogenase