CSEA分娩镇痛对产程和母儿血IL-6、NO的影响
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
  • 英文题名:The Influence of Combined Spinal-Epidural Analgesia on Labor Progress and Serum IL-6 and NO of Maternity and Neonate
  • 作者:陈新忠
  • 论文级别:硕士
  • 学科专业名称:妇产科学
  • 学位年度:2002
  • 导师:石一复
  • 学科代码:100211
  • 学位授予单位:浙江大学
  • 论文提交日期:2002-05-01
摘要
腰麻—硬膜外联合阻滞镇痛(CSEA)被认为是目前镇痛效果最确切的分娩镇痛方法,它克服了腰麻和硬膜外阻滞镇痛各自的缺点,具有镇痛确切、起效迅速、用药量少、运动阻滞轻及时控性强等优点。CSEA分娩镇痛对产程的影响的研究较少,尤其是其对宫缩强度影响的研究到目前为止还未见有报道。本研究拟通过观察CSEA分娩镇痛时宫缩强度、胎心监护的变化及产程进展情况,并与自然分娩对照,来了解CSEA分娩镇痛对产程的影响。
     白细胞介素-6(IL-6)是一种多效性促炎细胞因子,是免疫和内分泌系统的一个重要连接介质,组织损伤、剧烈疼痛、应激、炎症等均可使IL-6升高,而IL-6的过度升高破坏促炎细胞因子和抗炎细胞因子之间的平衡,使细胞免疫抑制,导致机体免疫功能紊乱。关于CSEA分娩镇痛对IL-6的影响,目前尚没有报道。本研究拟通过测定CSEA分娩镇痛前后母儿血IL-6水平及与自然分娩对照,来了解CSEA分娩镇痛对母儿IL-6的影响,间接了解其对母儿免疫功能的影响及IL-6与产痛的关系。通过观察IL-6与宫缩强度之间的关系,来了解IL-6对宫缩的影响。
     一氧化氮(NO)生物学效应广泛。其中NO对胎盘循环的调节较受关注,NO能扩张脐血管、胎盘血管,降低胎儿—胎盘的循环阻力,保证胎儿充足的血氧供应。体外研究认为低NO是维持宫缩的主要因素,在分娩过程中,随着产程的进展NO水平降低。CSEA分娩镇痛后NO水平是否有变化,目前还无人作过研究。本研究拟测定CSEA分娩镇痛前后母儿血NO水平并与自然分娩作对照,来了解CSEA分娩镇痛对母儿NO的影响及NO与产痛的关系。通过观察NO与宫缩强度的关系,来了解NO对子宫收缩的影响。
     材料与方法:选择2001年3月~7在本院分娩室分娩的产妇(初产妇、单胎、头位、
    
     川肚丫浙;D厂NI上·f卜沦丁
     足月、无胎膜早破、无产科合并症及并发症、ASA{级、经产科医师评价宫口处在 3-4CCI
     并能阴道分娩的)50例作为研究对象c随机分为CSEA分娩镇痛组和自然分娩组各25例。
     CSEA分娩镇痛方法为:LZ-3为穿刺点,腰麻用药为3厂sing罗响卡因+25ty芬太尼,硬膜
     外用药为0*%罗赈卡因刊卜gml芬太尼。两组入选前后各做30分钟胎心宫缩监护,并记录
     产程各阶段时间。两组在宫口 3斗cm(入选时)、宫日开全、产后 2’J’时采集产妇静脉血 5ml
     及胎儿娩出时脐静脉血sml,待血液凝固后提取血清置于-80OC冰箱保存,用于检测IL-6、
     NOc绞计学方祛采用t检验和乍方检验c检验水准为:Q—005(双侧)。
     结果:(l)*SEA分娩镇嫡组镇痛后(入选后)宫缩强度、宫颈扩张速率明显高}自
     然分娩组(P、005)。两组总产程无差异,CSEA分娩镇痛组的第-二产程稍L丁自然分娩全
     \ P<0.05),两组剖宫产率、产钳率无差异c 2)CSEA分娩镇痛后母)L血 6水平显著低了
     自然分娩组o<00)。()*%A分娩镇痛组母儿血*O水平显著高于自然分娩组(P<OOI)c
     结论:(l)CSEA分娩镇痛能加强于宫收缩,提高宫颈扩张速率,缩短活跃期c但对
     第_1产程有所延缓,需要做好运用腹压的指导c(2)CSEA分娩镇痛能减轻分娩过程中应
     激反应,降低母儿血 IL6水平c(3)分娩过程中 IL6随产程的进展而升高,士要与产痛及
     产痛所致的应激有关c(4)IL6对于宫收缩可能不起主要的调节作用。(5) CSE*分娩镇
     痛能提高母儿血 \O水平。(6)NO对于宫收缩可能不起主要的调节作用c()分娩过程中
     \O随产程进展而降低,主要与产痛和应激有关。
Combined spinal-epidural analgesia is the most effective method of labor analgesia. It minimize the disadvantages of spinal and epidural analgesia. It has some advantages including excellent analgesia, rapid onset, lower total drug dosage, minimal motor block and easier time control. There are few studies about the influence of CSEA on labor progress, especially the studies about the influence of CSEA on uterine contraction, and there is no report about it up to now. The objective of this study is to evaluated the influence of CSEA on labor progress by observing the intensity of uterine contraction, fetal heart rate changes and the progress of labor compared with the changes of spontaneous labor.
    Interlerkin-6 is a pleiotropic proinflammatory cytokine and an important mediator of immune system and endocrine system. IL-6 levels increase after tissue injure, sever pain, stress and inflammation. The over-high IL-6 levels would breakdown the balance between proinflammatory cytokine and antiinflammatory cytokine and suppress the cellular immunity and lead to turbulence of the immunological function. There are no reports about the influence of CSEA on the serum IL-6 up to now. The objective of this study is to evaluate the influence of CSEA labor analgesia on serum IL-6 of maternity and neonate, the relationship between IL-6 and labor pain and the influence of IL-6 on uterine contraction by measuring the serum IL-6 of maternity and neonate pre-CSEA and post-CSEA.
    Nitric oxide (NO) has wide biological effect. The modulation of NO on feto-placental circulation is more noticeable. NO can dilate umbilical and placenta! blood vessels. It can
    
    
    2002
    decrease the resistance of feto-placental circulation and make the fetus have enough blood oxygen supply. Lower NO is the most important factor to maintain the uterine contraction in vivo, and NO levels decrease along with the progress of the labor. NO. So far there is no report about the changes of NO levels after CSEA labor analgesia. The objective of this study is to evaluate the influence of CSEA labor analgesia on the NO levels of maternity and neonate and the relationship between the NO and labor pain and the influence of NO on uterine contraction.
    Materials and methods: Fifty healthy nulliparous in spontaneous labor with singleton.
    vetex. full-term fetus. -----.ASA I -II were enrolled when their cervical dilation in 3-4cm in
    Zhejiang Women's Hospital between Mar 2001 and July 2001. The patients were randomly assigned to CSEA labor analgesia group(n = 25) or spontaneous delivery group (n = 25). The CSEA's puncture point is at L2-3 interspace . It's spina! drug is 3.75mg ropivacaine combined with 25ug fentanyl and epidural drug is 0.1% ropivacaine combined with lug ml fentanyl. Both groups" patients were routinely monitored with electronic FHR and uterine contraction monitoring for 30min before and after the time at enrolling. Data on labor progress and outcome were recorded for each patient. Blood samples were taken from the mother vein at cervical dilation at 3-4cm (time at enroll), full cervical dilation, 2h postpartum; neonatal samples were taken at birth (cord blood vein). The serum disintegrated from the coagulated blood were stored at -SOC until thawed for IL-6 and NO assay. Statistical analysis included T test and X test. Statistical significance was assumed when P<0.05 .
    Results: (1) The uterine contraction's intensity and cervical dilation rate after analgesia in the CSEA group were significantly higher than the spontaneous delivery group (P<0.05); The second stage of labor in the CSEA group was longer than the spontaneous delivery group (P<0.05); There was no difference between the two groups in whole period of labor, Cesarean section rate and instrumental vaginal delivery rate. (2) The serum IL-6 levels of maternity and neonate in CSEA group were significantly lower than the spontaneous delivery group at full cervical dilation and 2h postpartum (P<0.01). (3) The serum NO levels of maternity and neonate
    
    in CSEA group were significantly higher
引文
1. Richardson MG Regional anesthesia for obstetrics. Anesthesiol Clin North America, 2000,18(2) : 383-406
    2. Liu SS, Mckonald SB. Current issues in spinal anesthesia, Anesthesiology, 2001,94(5) :888-906
    3. Tsen LC, Thue B, Datta S, et al. Is combined spinal-analgesia associated with more rapid cervical dilation in nulliparous patients when compared with conventional epidural analgesia? Anesthesiology 1999;91(4) :920-5
    4. Norris MC. Fogel ST, Conway-Long C. Combined spinal-epidural versus epidural labor analgesia. Anesthesiology 2001 ;95(4) :913-20
    5. Nageotte MP, Larson D, Rumney PJ, et al. Epidural analgesia compared with combined spinal-epidural analgesia during labor in nulliparous women, N Engl J Med. 1997,337:1715-1719
    6. Zhang J, KJebanoff MA. DerSimonian R. Epidural analgesia in association with duration of labor and mode of delivery: a quantitative review. Am J Obstet Gynecol 1999:180(5 ):970-7
    7. Alexander JM, Lucas MJ. Ramin SM. et al. The course of labor with and without epidural analgesia. Am J Obstet Gynecol 1998;178(3) :516-20
    8. Desborough JP. The stress response to trauma and surgery. Br J Anaesth 2000:85( 1) : 109-17
    9. 王国年。细胞因子与麻醉。四外医学免疫学分册 ; 23 (3) : 149-51
    10. Paik IH, Toh K.Y, Lee C. et al. Psychological stress may induce increased humoral and decreased cellular immunity. Behav Med 2000;26(3) : 139-41
    11. Hcbisch G Grauaug AA, Neumaier-Wagner PM, et al. The relationship between cervical dilatation, interleukin-6 and interleukin-8 during term labor. Acta Obstet Gynecol Scand 2001;80(9) :840-8
    12. 牛秀敏,倪晓妍,邬瑾慧,等。白细胞介素-8和白细胞介素-6对分娩发动的影响。中国实用妇科与总务科杂志 2000(1) :32-4
    
    
    13. Steinborn A, Kuhnert M, Halberstadt E. Immunmodulating cytokines induce term and preterm parturition. J Perinat Med 1996;24(4) :381-90
    14. Friebe-Hoffmann U, chiao JP, Rauk PN. Effect of IL-lbeta and IL-6 on oxytocin secretion in human uterine smooth muscle cells. Am J Reprod Immunol 2001;46(3) :226-31
    15. Rauk PN, Friebe-Hoffmann U, Winebrenner LD, et al. Interleukin-6 up-regulates the oxytocin receptor in cultured uterine smooth muscle cells. Am J Reprod Immunol 2001;45(3) :148-53
    16. De Jongh RF. Puylaert M, bosmans E. et al. The fetomaternal dependency of cord blood interleukin-6. Am J Perinatol 1999;16(3) :121-8
    17. Zidek Z. Role of cytokines in the modulation of nitric oxide production by cyclic AMP. Eur Cytokine Netw 2001; 12( 1 ):22-32
    18. 余立凯。NO的生物代谢及检测方法。国外医学生理、病理科学与临床分册 1998; 18 (3) : 264-6
    19. Myatt L. Brewer AS, Langdon G et al. Attenuation of the vasoconstrictor effects of thromboxane and endothelin by nitric oxide in the human fetal-placental circulation. Am J Obstet Gynecol 1992; 166(1 Pt 1) :224-30
    20. Byrne BM, Howard RB, Morrow RJ, et al. Role of the L-arginine nitric oxide pathway in hypoxic fetoplacental vasoconstriction. Placenta 1997 ;18(8) :627-34
    21. Acevedo CG Huambachano AM. Bravo I, et al. Endogenous nitnc oxide attenuates ethanol-induced vasoconstriction in the human placenta. Gynecol Obstet Invest 1997;44(3) : 153-6
    22. 金镇,曲陆荣,李守柔,等。母胎血一氧化氮的测定及其临床意义。中国实用妇科与产科杂志 1999; 15 (11) : 746-8
    23. Yanik FF, Amanvermez R, Kocak I, et al. Serum nitric oxide and glutathione levels in preeclamptic and normaotensive women during labor. Gynecol Obstet Invest 2001;51(2) :110-5
    
    
    24. Yallampalli C, Izumi H, Byam-Smith M,et al. An L-arginine-nitric oxide-cyclic guanosine monophosphate system exists in the uterus and inhibits contractility during pregnancy. Am J Obstet Gynecol, 1994; 170( 1) : 175
    25. Chanrachakul B, Herabutya Y, Punyavachira P. Potential efficacy of nitric oxide for cervical ripening in pregnancy at term. Int J Gynaecol Obstet 2000;71(3) :217-9
    26. Campbell DC, Camann WR, Datta S: The addition of bupivacaine to intrathecal sufentanil for labor analgesia. Anesth Analg 1995;81:305-9
    27. Thorp JA. Hu DH. Albin RM. et al. The effect of intrapartum epidural analgesia on nulliparous labor: A randomized, controlled, prospective trial. Am J Obstet Gynecol 1993:169:851-8
    28. Lederman RP, Lederman E, Work B Jr, et al. Anxiety and epinephrine in multiparous women in labor. Relationship to duration of labor and fetal heart rate pattern. Am J Obstet Gynecol 1985:153:870-7
    29. Hata T. Manabe A, Makihara K,et al. Plasma catecholamines and doppler-derived cardiac time intervals in vaginally and cesarean delivered neonates. Gynecol Obstet Invest 1997:44(3) : 173-6
    30. Cascio M, Pygon B, Bernert C, et al.Labour analgesia with intrathecal decreases maternal stress. Can J Anaesth 1997; 44:605-9
    31. Segal S,Csavoy A. Datta S. The tocolytic effect of catecholamines in the gravid rat uterus. Anesth analg 1998;87:864-9
    32. Lederman RP, Lederman E. The relationship of maternal anxiety, plasma catecholamines, and plasmacortisol to progress in labor. Am J Obstet Gynecol 1978;87:864-9
    33. Arntzen KJ, Lien E, Austagulean R. Maternal serum levels of IL-6 and clinical characteristics of normal delivery at term. Act Obstet Gynecol Scand 1997;76(8) :499
    34. Nukina H, Sudo N, Aiba Y, et al. Restraint stress elevates the plasma interleukin-6 levels in germ-free mice. J Neuroimmunol 2001;115(1-2) :46-52.
    
    
    35. Goebel MU, Mills PJ, Irwin MR, et al. Interleukin-6 and tumor necrosis factor-alpha production after acute psychological stress, exercise, and infused isoproterenol: differential effects and pathways. Psychosom Med 2000;62(4) :591-8
    36. Crozier TA, Muller JE, Quttkat D, et al. Errect of anesthesia on the cytokine responses to abdominal surgery. Br J anaesth, 1994;72:280-5
    37. Mirabile CP, Massmann GA, Figueroa JP. Physiologic role of nitric oxide in the maintenance of uterine quiescence in nonpregnant and pregnant sheep. Am J Obstet Gynecol 2000;183(l):191-8
    38. Salkowsk CA. Detore G Mcnally r. et al. Regulation of inducible nitric oxide synthase messenger RNA expression and nitric oxide production by lipopolysaccharide in vivo: the roles of macrophages, endogenous IFN-gamma, and TNF-receptor-1-mediated signaling. J Immunol 1997;158(2) :839
    39. 董有静,孟凌新,崔健君。两种不同脊神经阻滞对妊娠高血压综合征患者血浆一氧化氮水平影响的比较。中国疼痛医学杂志 2001; 7 (2) : 97-100

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700