基础与临床研究 >文章正文
基础与临床研究 >文章正文
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> THE INFLUENCE OF EPIDURAL ANESTHESIA AND DIFFERENT GENERAL ANESTHETIC AGENT ON THROMBOXANE B2 AND 6-keto-PROSTAGLANDIN F1α 刘慧贞 李 刚 许永广 (山东省立医院麻醉科) LIU Hui-zhen,LI Gang,XU Yong-guang (Dept. of Anesthesia,Shandong Provincial Hospital) ABSTRACT Objective:To observe the influence of epidural anesthesia and different general aneshthetic a-gent on plasma thromboxane B2(TXB2)and 6-keto-prostaglandin F1α(6-keto-PGF1α concent ration before and during surgery. Methods:42 patient s undergoing elective abdominal surgery were allocated randomly in three groups:epidural anesthesia (group1,n=14),general anesthesia induced with thiopental (group2,n=14),general nesthesia induced with propofol and midazolam(group 3,n=14). Every group was also allocated randomly in group A(n=7)and group B(n=7). Venous blood samples were collected at two time :before anesthesia and 15~20 minute after anesthesia (group A were before skin incision ,group B were 5~10 minute after skin incision). |
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> Results:In group 2,plasma(TXB2)concent ration significantly increased from(179.8±44.0)pg. ml-1 to(268.7±92.9)pg. ml-1 after skin incision(P<0.05). Plasma TXB2 after skin incison was also significant higher than before skin incison(P<0.05). In group 3 ,plasma thromboxane B2(TXB2)concent ration significantly decreased from(168.4±79.7)pg. ml-1 to(108.8±43.9)pg. ml-1 after anesthesia(P<0.05),plasmaTXB2 level before skin incison were lower than after skin incison(P<0105). After skin incison,TXB2 was higher in group 2 than in group 3(P<0.05). Conclusion:Plasma TXB2 concent ration is increased during surgical st ress ,which is inhibited by epidural anesthesia in some degree. Propofol and midazolam siginficantly decreases TXB2 level. KEY WORDS:Anesthesia,epidural;Anesthesia,general;ProstaglandingsF;Thromboxana B2 探讨硬膜外阻滞及不同全麻诱导药物对手术患者血浆TXA2及PGI2的影响,从而为选择麻醉方法及全麻诱导药物提供依据。
资料与方法 1. 资料 腹部手术患者42例,29~68岁,44~91kg,ASA分级1~3级,无内分泌、血液及心血管系统合并症,术前无大出血,未用过影响血小板功能的药物。42例随机分为3组:硬膜外麻醉组(1组)14例,以硫喷妥钠诱导全麻组(2组)14例,以异丙酚加咪唑安定诱导全麻组(3组)14例。每组又随机分为A、B两个小组,各7例,A组为手术切皮前,B组为切皮5~10min。试剂盒由北京北方生物技术研究所(苏州医学院监制)提供。 2. 麻醉方法及采样 术前常规应用鲁米那钠、阿托品。诱导方法:1组选择中下胸段椎间隙(胸8~12)穿刺置管,试验量为2%利多卡因5ml,首次量分次或单次注入0.75%布比卡因10ml;2组以硫喷妥钠5~7mg/kg、玻珀胆碱1.5~2mg/kg、卡肌宁0.6mg/kg、芬太尼8~10μg/kg静脉诱导后气管插管;3组以异丙酚1~1.5mg/kg、咪唑安定0.1~0.15mg/kg取代2组硫喷妥钠,余同2组。采样:麻醉诱导前静脉采第1个血样,诱导后15~20min(A组为手术切皮前,B组为切皮5~10min)采第2个血样。血浆血栓素B2(TXB2)及6-酮-前列腺素F1α(6-keto-PGF1α)以放免法测定。 |
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> 3. 统计学分析 各结果以x±s表示。组内自身前后比较用配对t检验;组间差异用两样本均数比较的t检验;方差不齐时间用t′检验。P<0.05为差异显著。 结 果 1. 各组患者年龄、体重、性别比及手术种类 见表1。 2. 各组病人血浆TXB2、6-keto-PGF1α及T/K水平 见表2。
讨 论 血栓素A2(TXA2)与前列腺环素(PGI2)为花生四烯酸代谢产物。正常情况下,TXA2与PGI2保持平衡。两者均不稳定,迅速变为血栓素B2(TXB2)和6-酮-前列腺素F1(6-keto-PGF1α)。TXB2主要来源于血小板[1],手术过程中应激激素升高,血小板被激活[2,3]。本研究显示,以硫喷妥钠诱导全麻组手术切皮后血浆TXB2浓度较诱导前显著升高,两种全麻诱导方法诱导后同一时点血浆TXB2浓度切皮组较未切皮组也明显增高,说明手术应激对TXB2浓度的影响。 麻醉方法本身对血小板活性并无影响。手术中TXB2浓度的改变是由手术应激造成的,这种应激反应能被大剂量的麻醉性镇痛药减弱;硬膜外麻醉阻滞了交感神经,减少了手术创伤传入神经节的传入信号,消除了神经内分泌反应,能显著抑制应激激素的升高[2,3],可见麻醉方法对其影响是通过调控应激程度实现的。切皮后比较,硬膜外麻醉组TXB2浓度虽然偏低,但无统计学意义(0.05 < P<0.1),分析原因,一方面由于硬膜外阻滞并不能完全消除神经内分泌反应;另一方面与全麻诱导应用大剂量芬太尼抑制手术应激有关。 麻醉药物也在不同环节影响TXB2的合成。异丙酚可以降低血小板内Ca2+浓度从而抑制血小板功能[4],使血浆TXB2浓度降低,咪唑安定结构有咪唑环,能抑制血栓素合成酶的活性,因此直接抑制血小板TXB2的合成。异丙酚加咪唑安定组诱导后TXB2明显下降;诱导后及切皮后血浆TXB2浓度均低于硫喷妥钠组的对应时点,也表明异丙酚及咪唑安定对TXB2的产生有抑制作用,而这一抑制作用在术中恰好“抵消”了应激过程对血小板的激活。 因此硬膜外麻醉和异丙酚加咪唑安定诱导在术中能使血浆TXB2浓度及T/K比值保持稳定,对有缺血性心脏病及行外周血管手术的病人是有利的。 参考文献 1. 李永荣,姚德厚,郭贵林. 吸入麻醉药对人血浆和血小板血栓素B2生成与血小板聚集的影响[J]. 中华麻醉学杂志,1997,17(2):77 2. Thwaites BK,Nigus DB,Bouska GW,et al. Intravanous Ketorolac Tromethemine worsens platelet function during knee arthroscopy under spinal anesthesia [J]. Anesth Analg,1996,82:1176 3. Thwaites BK,Nigus DB,Bouska GW,et al. Intravenous Ketorolac Tromthemine dose not worsen platelet function during knee arthroscopy under general anesthesia [J]. Anesth Analg,1995,81:119 4. Aoki H,Mizobe T,Nozuchi S,et al. In vivo and in vitro studies of the inhibitory effect of propofol on human platelet aggregation [J]. Anesthesiology,1998,81:362 |