外伤应激时机体血液生化指标与血常规的变化
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
应激是机体在受到内外环境因素及社会、心理因素刺激时所出现的全身性非特异性适应反应,为一种重要的防御代偿。适当的应激有利于调动机体潜能而维持机体内环境的稳定,若应激负荷过强或应激时间过长,将会引起机体的应激副损伤,甚至导致应激性疾病。应激是机体内神经、内分泌、免疫等多系统参与的整体反应。应激时一些激素、细胞因子分泌过多,会引起机体代谢率明显增高以及器官功能的改变,可能导致血液生化及血液指标的相应变化。因骨折外伤诊断易明确,所致应激已肯定,适合于应激反应的观察,本文试图通过观察在骨折外伤应激状态下,机体血液、肝、肾功能及相关指标的变化,寻找应激相关标志物,初步探讨应激时机体生理生化变化规律,为进一步研究应激所致的后续性病理变化和应激性疾病的预防及治疗提供参考。
     方法
     1.实验分组及方法:选择年龄在20~46岁之间的复合骨折外伤住院患者34人(男24人,女10人)作为外伤应激组。同时,选择年龄、性别均与应激组相同的健康体检者作为对照组。两组均空腹静脉取血,并在同一实验室检测血液生化、血常规项目。
     2.检测指标:超敏C-反应蛋白、血糖、总蛋白、白蛋白、总胆红素、直接胆红素、间接胆红素、总胆汁酸、谷丙转氨酶、谷草转氨酶、碱性磷酸酶、血清肌酐、血清尿素、血清尿酸、血清总钙、血清磷、血清镁、白细胞数、中性粒细胞绝对值、淋巴细胞绝对值、红细胞数、血红蛋白、血小板数。
     结果外伤应激组血液中超敏C-反应蛋白、血糖、直接胆红素、总胆汁酸、谷草转氨酶、白细胞数、中性粒细胞绝对值水平增高,与正常对照组比较,有统计学显著性差异(P<0.05)。
     外伤应激组与对照组比较:总蛋白、白蛋白、碱性磷酸酶、血尿酸、血钙、血镁、红细胞计数、血红蛋白、淋巴细胞绝对值、血小板计数降低,有统计学显著差异(P<0.05)。
     其他指标无统计学显著差异。
     结论
     1.应激可以引起血液生化、血液指标的改变,该变化可能与神经内分泌有关。
     2.应激时肝功能、肾功能的改变可能受神经、内分泌调控。
     3.血液生化、血常规指标有可能作为应激标志物。主要包括:血糖、C-反应蛋白、白蛋白、碱性磷酸酶、总胆汁酸、尿酸、血钙、血镁、白细胞数、中性粒细胞数。
Stress is a kind of general physical and adaptive response during the body is stimulated by a stressor, it can produce a significant defense and compensation system in the body. It is well-known that adequate stress is profit to the body, ensure the potency of the body be activated to meet the alternation of internal environment. However, prolonged or increased magnitude stress responses could cause the tissue injury with a significant cost to the health of the individual, moreover, lead to some stress diseases. Stress response is regulated by the interactions of nervous system, endocrine system and immune system, the response is also related to many other systems. The increased secretion of certain hormones and cytokines when the individual is under stress which ultimately alter the function and metabolism of virtually all organ system and may lead to the changes of biochemistry and routine parameters in blood. Fracture trauma is easy to diagnose, and the stress caused by fracture trauma is considered as an approval model of stress. This model is available to research the mechanism of stress response perfectly. We try to find the correlated markers of stress through studying the coherent parameters of blood, hepatic function and renal function of the individuals who got fracture trauma. Meanwhile, we’ll make a reasonable evindence of the precaution and therapia of stress diseases through the research the rules of the changes of biochemistry and physiology, and the followed pathologic alteration.
     Method
     1. Groups and methods: 34 patients (male 24, female 10) of the multiple fracture trauma, aged between 20- 46, were selected as the trauma stress group. And 34 healthy person whose sex and age were same with the stress group ,were defined as the control group. All of those were took venous blood on an empty stomach, and finished the examination of biochemical and rout parameters in the same laboratory.
     2.The parameters: high-sensitive C– reactive protein(hs-CRP), blood glucose(BG), total protein(TP), albumen(AL), total bilirubin(BRT), direct bilirubin(BRD), indirect bilirubin(BRID), total bile acid(TBA), GPT,GOT, alkaline phosphatase(ALP), serum creatinine, urea of serum, serum uric acid, serum total calcium, serum phosphorus, serum magnesium, WBC, absolute value of neutrophilic leucocyte, absolute value of lymphocyte, RBC, HB and PLT.
     Result:The levels of CRP, BG, TBA, GOT, WBC, and absolute value of nutrophilic leucocyte of the trauma stress group is increased, compared with the control group, there is a statistic significance between those groups (P<0.05) .
     The levels of TP, AL,ALP, serum uric acid, serum calcium, serum magnesium, RBC and HB is decreased in the trauma stress group, and there is significant difference between the stress group and the control group. (P<0.05).
     There are not statistical differences apparently between the two groups on the levels of other parameters.
     Conclusion
     1. Stress could cause the changes of biochemical and rout parameters in blood. This alteration may be related to all aspects of neuroendocrine system.
     2. Hepatic function and renal function may be controlled by the neuroendocrine system.
     3. The parameters of biochemistry and routine in blood may be defined as the significant markers. Mainly include: Blood glucose, CRP,AL,ALP, TBA, urine acid, serum calcium, serum magnesium, WBC and absolute value of neutrophil.
引文
1.陈主初,病理生理学,第1版,北京,人民卫生出版社,2005:22-23.
    2.郭金龙,应激医学研究进展,实用医药杂志,2003.2,20(2):151-152.
    3.王丽颖杨蕴萍创伤后应激障碍的研究进展(一)国外医学精神病学分册,2004,31(1):32-35.
    4.华金宝,邱来春,张志永,C反应蛋白与颅脑外伤的相关性研究,浙江创伤外科,2008.2,13(1):82-83.
    5.张建,石汉平,王深明,创伤应激后糖代谢的神经内分泌调节及血糖升高的处理,临床外科杂志,2005.12,13(12):781-783.
    6. Bolger GB.Molecular biology of cyclic aotide PhosPhod iesterases t a diverse family of regulalory enzymes-specific cyclic nucle2.Cel1 Signal, 1994, 6 (8) :851~859
    7.柯文波,应激状态对肝脏代谢的影响,实用肝脏病杂志,2006.4, 9(2):107-109.
    8. J Shaw JH.Wolfe RR.An integrated analysis of glucose,at.Protein metadolism inseverely traumatized Patients J J.AnnSurg.1989,209(1):63-72.
    9.安友仲,祝学光,杜如昱,创伤后早期神经内分泌改变与应激性高血糖,中国临床营养杂志,1998.6(2):55-58.
    10. J Elan J,Laurel A.Michael D.TheimPact of hyPerglycemia on Patients with sev -ere brain iniury.Trauma.2005, 59(1):47-50.
    11.王全楚,中德林,刘文德,创伤后应激性肝损伤发病情况调查分析,实用医药杂志,2006, 23(1):58-59.
    12. Nakatani T, Kobayashi K. Surgical stress and organ dysfunction: liver. Journal of Japan Surgical Society. 1996, 97(9):752-758.
    13.杨玉林,贺志安,临床肝病实验诊断学,中国中医药出版社,2007.9,10-11.
    14.王鸿利,实验诊断学,第1版,北京,人民卫生出版社,2006:261-262.
    15.王跃明,血清总胆汁酸在肝病诊断中的临床应用,临床和实验医学杂志,2008.2,7(2):93.
    16.西部医学编辑部,常用肝功能指标的临床意义,2005.7,17(4):331.
    17.朱一堂,李福坤,孙艳,王景阳,成年男性血清碱性磷酸酶活力降低的主要临意义,河北北方学院学报:医学版,2006. 23(4) :59-60.
    18.周新,涂植光,临床生物化学和生物化学检验,第3版,北京,人民卫生出版社,2003,6,22-23.
    19. LI Hong-hua, ZHAO Ting-bao, LI Zhi—liang.Changes of serum urea and creatini-ne concentrations in rats with lipopolys accharide and heat Co- exposure. J Sou -th Med Universe,2008,28(1):87-89.
    20.周宁,王国宝,祝峰,何海明,118例血清尿酸浓度降低患者临床病因分析,临床检验杂志,2005,23(5):397.
    21.扬钢,内分泌生理与病理生理学,第1版,天津,天津科学技术版,1996.2,322-338.
    22.邵美贞,镁的基础与临床,第1版,成都,四川科技出版社,2006.6,3-4.
    23.许文荣,临床基础检验学,第3版,北京,人民卫生出版社,2006.2.
    24.郝江,雷鸣,张音等,多发伤早期血小板计数变化及其对预后的影响,中国危重病急救医学,2003.10,15(10):615-616
    25. Fittschen B, Schultz KH, et al,Changes of immunogical parameters in healthy sub -jects under examination stress. International Journal of Neuroscience 1990,51: 241-242.
    26. Gocebel MU,Mills PJ.Acute Psychological stress and exercise and changes in Per -ipheral leukocyte adhesion molecule expression and density .Paychosomatic Me -dicine 2000, 62:664-670.
    1.钱令嘉,应激与应激医学,疾病控制杂志,2003.10,7-5:393-396
    2.陈主初,病理生理学,第1版,北京,人民卫生出版社,2005:22-23.
    3.郭金龙,应激医学研究进展,实用医药杂志,2003.2,20(2):151-152.
    4.张建,石汉平,王深明,创伤应激后糖代谢的神经内分泌调节及血糖升高的处理,临床外科杂志,2005.12,13(12):781-783.
    5.扬钢,内分泌生理与病理生理学,第1版,天津,天津科学技术版,1996.2,322-338.
    6.Shaw JH.Wolfe RR.An integrated analysis of glucose,at.Protein metabolism in severely traumatized patients [J].Ann Surg.1989,209(1):63-72.
    7.安友仲,祝学光,杜如昱.创伤后早期神经内分泌改变与应激性高血糖.中国临床营养杂志,1998.6(2):55-58.
    8.Snoechx LH .Cornelussen RN .Van Nieu Wenhoven FA.Heat shock proteins and cardiovascular pathophysiollgy [J].Physiol Rev. 2001. 81(4):461—497.
    9.Kozawa O. Matsuno H. Niwa M.Alphα.β-crystallin a low molecular?weight heart shock protein acts as a regulator of platet function [J].Cell Stress Chaperones. 20 01. 6(1):21—28.
    10.Lin KM.Lin B.Lian Y.Combined and individual mitochondrial HSP60 and HSP10 expression in cardiac myocytes protects mitochondrial function and prevents apo -ptotic cell deaths induced by simulated ischemia?reoxygenation [J]. Circula -tion .2001.103(13):1787—1792.
    11.Yaokobi T.Shoshany Y.Levkovitz S.Long—term effect of low energy laser irradi -ation on infarction and reperfusion injury in the rat heart[J].J Appl physiol. 2001. 90(6):2411—2419.
    12.Suzuki K .Sawa Y .Kagisaki K .Reduction in myocardial apoptosis associated with overexpression of heat shock protein 70 [J].Basic Res Cardiol. 2000 .95(5)397—403.
    13.Zhou X. Zhai XL. Ashraf M. Direct evidence that initial oxidative stress triffered by preconditioning contributes to second window of protection by endogenous antioxidant enzyme in myocytes [J] .Circulation. 1996. 93:1177—1184.
    14.Leger JP. Smith FM.Currie RW .Confocal microscopic localization of constitutive and heat shock—induced proteins HSP70 and HSP27 in the rat heart [J]. Circul -ation . 2000. 102(14):1703—1709.
    15.华金宝,邱来春,张志永,C反应蛋白与颅脑外伤的相关性研究,浙江创伤外科,2008.2,13(1):82-83.
    16.周新,涂植光,临床生物化学和生物化学检验,第3版,北京,人民卫生出版社,2003,6,22-23.
    17. Bolger GB.Molecular biology of cyclic AMP otide phosphodi-esterases:a diverse family of regulatory enzymes-specific cyclic nucle2.Cel1Signal,1994,6 (8) :851~859
    18.杨玉林,贺志安,临床肝病实验诊断学,中国中医药出版社,2007.9,10-11.
    19.文波,应激状态对肝脏代谢的影响,实用肝脏病杂志,2006.4, 9(2):107-109.
    20.Nakatani T. Kobayashi K. Surgical stress and organ dysfunction: liver. Journal of Japan Surgical Society. 1996, 97(9):752-758.
    21.朱一堂,李福坤,孙艳,王景阳,成年男性血清碱性磷酸酶活力降低的主要临意义,河北北方学院学报:医学版,2006. 23(4) :59-60.
    22.西部医学编辑部,常用肝功能指标的临床意义,2005.7,17(4):331.
    23.王跃明,血清总胆汁酸在肝病诊断中的临床应用,临床和实验医学杂志,2008.2,7(2):93.
    24.王鸿利,实验诊断学,第1版,北京,人民卫生出版社,2006:261-262
    25.周宁,王国宝,祝峰,何海明,1 18例血清尿酸浓度降低患者临床病因分析,临床检验杂志,2005,,23(5):397.
    26.邵美贞,镁的基础与临床,第1版,成都,四川科技出版社,2006.6,3-4.
    27.许文荣,临床基础检验学,第3版,北京,人民卫生出版社, 2006.2,.
    28.Fittschen B.Schultz KH,et al.Changes of immunological Parameters in healthy su -bjects under examination stress. International Journal of Neuroscience 1990, 51:241-242.
    29.Goebel MU.Mills PJ.Acute Psychological stress and exercise and changes in peripheral leukocyte adhesion molecule expression and density .Psychosomatic Medicine 2000, 62:664-670.

© 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