多种血管病危险因素与血管病发病率之间关系与洛阳市医务工作者对代谢综合症知识调查研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的针对临床上常见的多种血管病危险因素共存在于同一个体,其复发率较高且损害较重的特点,对尚未出现血管疾病但是有血管病危险因素的个体进行前瞻性研究,了解其发病程度。并通过动物实验了解多因素存在使血管内膜的病损程度。进一步调查了洛阳市医务工作者关于代谢综合症知识的认识情况,为卫生行政部门制定预防血管病策略提供资料和依据。
     方法该研究分四部分组成。第一部分了解代谢综合症个体患脑卒中后的转归情况,取首次发生脑卒中的患者,给予相同的治疗和健康教育,分为合并代谢综合征组(A)和单纯脑卒中组(B),观察各自的中位生存时间和首次发病时与再发卒中时的神经功能缺损评分,两者进行统计学分析。第二部分评估中国人代谢综合症不同异常数目与血管疾病之间的关系。根据中华医学会糖尿病协会提出的代谢综合症诊断标准选定血压、血糖、甘油三脂、高密度脂蛋白及体重的异常指标作为我们的研究对象。以居住在洛阳的市民中进行了一项序列研究,选取样本334例,年龄36岁-75岁(男人183例,女人151例),根据不同的异常数目分组,共分为五组,观察两年,了解其在这两年中发生血管病的情况,并进行统计学处理。在这项研究中我们所提到的血管病包括冠心病、脑卒中和周围动脉疾病。第三部分动物实验。将相同动物进行随机分组,分别给予高脂喂养和高脂加果糖水喂养。其他生存条件相同,在实验开始时、六周和12周时禁食不禁水一夜,于次日清晨从尾静脉采血,送生化检测,取得各自的NO,ET-1,TC,HDL-C,LDL-C,FBS ,IN各项指标,并测血压,计算每个均值,进行统计学处理。试验结束时处死所有大鼠,观察两类不同大鼠的颈内动脉和椎基底动脉壁的结构和细胞结构。第四部分了解医务人员对代谢综合症的认识并做出分析。2005.10-2006.1在洛阳市医务人员4589人中发放问卷,包括代谢综合症的基本内容、危害、治疗及预防,每一项内容分若干小项,并将其量化,对结果按年龄、职业和受教育程度划分并进行X2分析。
     结果通过研究显示:第一部分单纯脑卒中组的中位生存时间为22个月,合并代谢综合症的脑卒中患者中为生存时间为13个月,两者相比统计量为28.9703,p<0.01有明显统计学意义。且他们的神经功能缺损评分,在首发时单纯脑卒中的患者为24.58±5.63,合并代谢综合症的患者为24.59±6.43,统计量为0.01,p值为0.9938,无明显差异。而再发卒中时,单纯脑卒中的患者为26.59±4.61,合并代谢综合症的患者为30.67±5.41,统计量为4.06,p<0.05,有明显差异。合并代谢综合征组的神经功能缺损明显高于单纯脑卒中组,有明显差异。第二部分在中国人群中代谢综合征中的异常指标数目与血管病之间有显著的相关性,且异常数目越多血管病发病率越高。所有数据采用x2检验以得到各组与血管疾病的发生在横断面上和前瞻性研究的不同,该研究使用Mantel-Haenzel断层x2检验分析得出血管疾病的发生率与血液中异常成分之间的相对危险度和各自的可信区间。所有分析采用SAS8 (version 1)统计软件处理。有一个异常成分的人群发生血管疾病的发生率定为1(即最低的患病率)各组的相对危险度:在2,3,4,5个异常成分的组中患冠心病的相对危险度依次为1.81, 2.65, 4.03, 4.10,患脑卒中的相对危险度依次为1.41, 2.23, 3.30, 3.85,患周围血管病的相对危险度依次为1.63, 1.62, 3.22, 5.34。我们可以得出患冠心病,脑卒中,周围血管病的发生率随着代谢综合症中异常成分的增多而升高。经过调整年龄,又得出单纯高血压与血管病之间的相对危险度为7.27(95% CI: 4.74 to 11.17),在正常血压和不正常血压之间该数值有显著意义统计量为92.5883,p<0.001。同理可以得出,高血糖,高密度脂蛋白降低,高甘油三脂及超重发生血管病得相对危险度依次为4.36 (95% CI: 2.92 to 6.49), 1.52 (95% CI: 1.05 to 2.21), 1.31(95% CI: 0.9 to 1.9), 2.73(95% CI: 1.86 to 4)除甘油三脂(其统计量为1.9893,p>0.05)外,在各自正常值和不正常值之间该数值有显著意义,各自的统计量及p值依次为:高血糖56.17,p<0.001高密度脂蛋白降低4.95,p<0.05,超重27.79,p<0.001。除甘油三脂不是血管病独立的危险因素外,其余各项,无论是哪项值的异常,均和血管病有直接相关性。从我们的研究中还可看出对于中国人群代谢综合症的各种异常因素中,高血压发生率最高,其次是糖尿病。第三部分在入选时NO,ET-1,TC,HDL-C,LDL-C,FBS ,IN指标均无差异,所有指标的p值均>0.05,在第6周时HDL和BP无差异p>0.05,而Tc、NO、ET、FBS、IN和LDL均有差异P<0.05,到第12周时,HDL、NO、ET和BP有差异P<0.05,Tc、LDL、FBS和IN有显著差异P<0.01。并经过重复方差分析结果显示,血压、血糖、胰岛素、甘油三脂、低密度脂蛋白这几项指标不仅存在组间的差异和时间点上的差异,并且组间和时间的交互效应也有差异,其P值均小于0.05。而高密度脂蛋白、NO、ET这三项指标时间点上有差异p小于0.05,组间和时间和组间的交互效应均无差异p大于0.05。从光镜图片可以看出MS组颈内动脉和基底动脉内膜不完整,平滑肌细胞排列紊乱,并可以看到大量脂滴浸润之平滑肌层。高血脂组颈内动脉内膜完整,平滑肌层细胞排列整齐,但是在平滑肌细胞之间可看到较少的脂滴。电镜下显示MS组大鼠的血管内皮细胞核已经完全变形,胞浆内有大量的脂滴,泡沫细胞已经形成。高脂血症组大鼠血管内皮细胞核变大、轮廓还没有完全破坏,胞浆内有脂滴。单纯高脂血症大鼠的血管结构和细胞结构损害较代谢综合症大鼠的血管结构和细胞结构损害轻,并且在有高血糖存在的情况下,血管病危险因素更加向血管病方向转化。第四部分调查得出,从年龄划分,年龄大于50岁的人群对各种知识的知道比率为36.15%,较同类比较的人群要大得多p<0.05具有统计学意义,而小于30岁的人群对各种知识的知晓率为30.73%,三十岁到五十岁的人群对各种知识的知晓率为27.00%。从学历划分,本科学历以上的人群对各种知识知道的比率为39.73%,在同分类中与其他相比有显著差异p<0.05,而高中和中专的人群对此知识知道比率为30.09%,而大专的人群对此知识知道比率为29.49%,从职业划分,医生对各种知识的认识知道比率为29.34%,护士对各种知识的认识知道比率为28.26%。而行政后勤人员对各项知识的认识程度较低,仅有14.77%。
     结论第一部分本研究旨在证明血管危险因素的多或少对血管病及生存质量的影响,我们的调查中单纯脑卒中患者危险因素相对减少,血管病的复发率较低,且中位生存时间也明显延长;由于危险因素的增加,对血管的影响相对增加,在代谢综合症组,脑卒中的复发率明显升高,中位生存时间也明显缩短,并且两者的神经功能评分在第一次入院时无明显差别,第二次复发时则有明显差别。由此提醒我们一定要提高对血液成分变化的认识,并加以干预。第二部分研究指出居住在城镇的中国居民患有代谢综合症不同异常因素增加了冠心病,脑卒中和周围血管病的发生率。对于中国人群代谢综合症的各种异常因素中,高血压发生率最高,其次是糖尿病。为了控制,认识并治疗代谢综合征,公共卫生事业应加大对高血压和糖尿病的防治,同时不可放松对其他异常因素的控制。这些措施将有助于减轻我国在血管病方面的社会医疗负担。第三部分该项试验选择了高血脂动物和高血脂合并高血糖动物,以观察两者血液成分和血管内皮结构的改变和不同,结果发现在高血糖存在时,高血脂的动物其血液成分更加向有害方面发展,血管内皮细胞的损害加重,因此我们推测,当多种血管病危险因素共同存在时,它们对血管的损害不仅仅是各自危害的叠加,这些因素是相互作用加速了损害。尽管我们还没有证明它们相互作用的具体数据化信息,但是其互相促进的模式已经存在。由此提醒我们,在相同条件下代谢综合症严重影响血管内皮的完整和功能,单纯的高脂血症对血管内皮的完整性和功能有影响,但是比起代谢综合症要小得多,这就提醒我们对代谢综合症要加强监护和治疗。第四部分调查分析得出医务工作者对代谢综合症认识处于较低级阶段,社会人群的认识可能更低,这就要求我们医务工作者行动起来,自己要及时更新知识,并积极对社会人员宣传教育,使代谢综合症的观念深入人心,从根本上减少心脑血管病的发生。
Objective: There are multipul risk factor of angionosis coexist in one body. It have the feature which can leads heighter relapse rate of vessel disease(VD) and more severe disadvantage then one which have only one risk factor of angionosis .Doing perspective study in some one who have one or more risk fector of VD but have not appear VD to understand the relation between them.Then studying the interaction of mutipul risk factor exist same one and the damage of endangium with animal experiment. Last we investigat to get the message about metabolic syndrome knowledge among medical worker.The aim is to provide some data to Medical Adminstrative Command for formulation preventing VD.
     Method : The study consists of four parts.Each part is listed as following. First To understand the tuneover condition in human who had metabolic syndrome and had not metabolic syndrome after having first stroke.We got the first stroke patients and divided into two groups, stroke addition metabolism syndrome (A )and simple stroke (B). Taking alike treatment and health education ,we get theire meso-lifetime and the score of neurologic impaiment at first stroke and relapse,and do statistic analyze. Second This study aimed to assess the number of abnormal components in the metabolic syndrome (MetS) and their association with cardiovascular diseases (CVD) in Chinese population. The information available about the abnormal components of the Metabolic Syndrome (MetS) was according to Chinese Diabetes Federation proposed the definition. We conducted a population-based succession study in an urban of Luoyang, based on the number of abnormal we divide five parts in a sampling of 334 participants who age is 36 to 75 years (183 men, 151 women) .To getting the relation between the relaps of VD and the abnormal factor , we observe this sample in two years. The CVD included in this study was diagnosed coronary heart disease (CHD), strokes, and peripheral arterial diseases (PAD).Third Getting 24 SD rats, we divide into two groups A and B randomization. Taking different feeding condition and identical life condition:height fat with water and height fat with diabetin water.Drown blood from the vena caudalis of rat who were fasted during the fore night then the blood sample were carried out biochemical analysis.The markers were total cholesterol(TC) , high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-C),fast blood sugar(FBS),insulin(IN),nitric oxide(NO), endothelium-1(ET-1) at the begin ,6 weeks and 12 weeks. Up to the end, killing all rats observes these structure of the two groups rat’s internal carotid and basilar artery and cellular structure.Fourth In 2005.12-2006.1,we distrubuted questionnaire to Luoyang medical worker in all 4589. It includes three parts: base concept, detriment,cure and precaution .Every part was dividatured some small parts and becomes quantization.We divided this result according to aged,occupation and educations .To anasis this result with x2。
     Results The studying show: First The meso-lifetime of merely stroke(A) is 22 months more longger then the meso-lifetime of strok with metbolic syndrom(B) is 13 months. A longger then B.Their statistics is 28.9703, p<0.01 They have obviously statistical significance.Their neurologic impairment score is A24.58±5.63 ,B24.59±6.43 at first falling ill. The score is alike .Their statistics is 0.001, p>0.05. They have not obviously statistical significance.But at second falling ill the score of A is 26.59±4.61,of B is 30.67±5.41.Their statistics is4.06, p<0.05. They have obviously statistical significance.Second There was a significant relationship between the number of abnormal components in the Metabolic Syndrome and Cardiovascular Diseases in Chinese Population. We found a significantly increased prevalence of CHD, Strokes and PAD with an increasing number of METS components. Data were managed using Chi-square test to examine differences in continuous and categorical variables respectively. Mantel-Haenzel demixing Chi-square test was used to study the relation between cardiovascular disease and abnormal component in blood calculate risk ratios (RRs) and their 95% confidence intervals (CI). All analyses were conducted using SAS8 (version 1). The incidence of CVD occurred in population with only one abnormal component was defined as one (the lowest prevalence in the group), in turn the relative risk in each group was deferred. This number could be gotten based on table 1: The RR of CHD in different group is 1.81, 2.65, 4.03, 4.10 for two or more, three or more, four or more and five or more individuals. The RR of Stroke in different group is 1.41, 2.23, 3.30, 3.85 for two or more, three or more, four or more and five or more individuals. The RR of PAD in different group is 1.63, 1.62, 3.22, 5.34 for two or more, three or more, four or more and five or more individuals. We found a significantly higher prevalence of CHD, Stroke and PAD with an increasing number of METS components. after adjusting age we can get that the RR of high blood pressure was 7.27 (95% CI: 4.74 to 11.17) and there was significant difference between the population with normal and abnormal blood pressure. So as the RRs of high fasting glucose, lower high-density lipoprotein, hypertriglyceridemia, and overweight were 4.36 (95% CI: 2.92 to 6.49), 1.52 (95% CI: 1.05 to 2.21), 1.31(95% CI: 0.9 to 1.9), and 2.73(95% CI: 1.86 to 4) respectively. Besides hypertriglyceridemia( statistics is 1.9893,p>0.05) the rest every one have significant difference between the population with normal and abnormal.Thire statistics of high fasting glouse, lower high-density lipoprotein and overweight were 56.17,p<0.001, 4.95,p<0.05,27.79,p<0.001 respectively. Exept hypertriglyceridemia is not standalone risk factore of VD, the rest every one have directly associativity with VD.Chinese population, hypertension is more prevalent than the other components of MetS. The increase in fasting blood glucose is listed on second seat. Third At simple hyperlipoidemia and high fasting glouse accompaniment with hyperlipoidemia,there have not different between two parts a begin.Thire p are up 0.05.At 6 week,HDL and BP have not different, p>0.05.But Tc、NO、ET、FBS、IN and LDL have different, P<0.05. At 12 week,every one have different, P<0.05 or P<0.01. From repeat analysis of variance we can find that high blood pressure, high fasting glouse , hypertriglyceridemia, high low-density lipoprotein and insulin have different at parts and parts (p<0.005), HDL-C, NO, ET-1 have different times(p<0.005), but they have not different at parts and times multiply parts.(p>0.005) From light microscope picture we can find that the endarterium of arteria carotis interna and arteria basilaris is not integrated,thire smooth muscle cells rank disorder,there are much lipid droplet infiltrate in smooth muscle at MS rat .and the endarterium of arteria carotis interna and arteria basilaris is integrated,thire smooth muscle cells rank order,there are small amounts lipid droplet in smooth muscle at hyperlipoidemia rat.From electron microscope we can find that The core of endothelial cell have had completely out of shape, there are much lipid droplet infiltrate in intracytoplasm whit MS rat, and The core of endothelial cell have had bigger but out line have had not fully ruinned, there are lipid droplet infiltrate in intracytoplasm whit hyperlipoidemia rat. The damage of the blood vessel texture and celluar structure with simple hyperlipoidemia rat is more lightly then MS rat. Hperlipoidemia accompaniment with high fasting glouse, the risk factor of VD convert more quickly to VD. Fourth From our investagation,according to age divided,>50 year,30-50 year,<30 year know every news of MS is 36.15%,27.00%,30.73% respectively; according to acadimic career divided,above bachelor's degree , between bachelor's degree and high school, below high school know every news of MS is 39.73%,29.49%,30.09% respectively. according to occupation divided, doctor ,nurse, administration and rear service know every news of MS is know every news of MS is 29.34%, 28.26%,14.77% respectively.
     Conclusion First This study is to prove the contribution of between the number of the risk factor in VD and the relapse of VD, the molar of survival.From our investigation we can find the number of VD risk factor is littler,the relapse of VD is lower and the meso-live time is longer.Becouse of MS part have more risk factor then simple stroke part,the meso-live time of MS part is shorter then simple stroke part meso-live time, and then their score of neurologic impairment is likely at first with stroke, but at relapse, score of neurologic impairment of MS part is highter then score of neurologic impairment of simple stroke part.They have significant deviation. It needs us to think highly of to the change of blood constituent and do some interfere in. Second Our data indicate that Chinese people living in urban regions with abnormal parameters of MetS have increased risks for CHD, stroke, and PAD. In Chinese population, hypertension is more prevalent than the other components of MetS. The increase in fasting blood glucose is listed on second seat. In order to prevent, recognize and treat MetS, we should develop effective public health strategies to control the hypertension and the increased fasting glucose and other abnormal parameters. Third This study selected hyperlipemia rat and hyperlipemia accompaniment whit high fasting glouse to observation thire different in blood vessle endothelium fomulative and blood consitituent. At the end ,we find that The damage of the blood vessel texture and celluar structure with simple hyperlipoidemia rat is more lightly then MS rat. Hperlipoidemia accompaniment with high fasting glouse, the risk factor of VD convert more quickly to VD.So we presume when there are many risk factor of VD to exist with one the damage of the blood vessel texture and celluar structure is not only every plus each other but they interact damage each other. In spite of we have not accurate date about they interact damage each other, but the mode of they interact damage each other have existed. It call attention to us do a lot of work in care and treat at MS. Fourth The study tells us the recognition about MS in medical worker is lesser. we suppose the recognition about MS in common crowd is least. The damage of MS is more and more severity, it need us learning new knowledge in time and education to public croed, making the concept of MS interiorize and downwards the incidence of VD from base.
引文
1. Reuen GM. Role of insulin resistance in human disease. Diabetes, 1988, 37( 12) :595- 607.
    2. Report of a WHO consultation: Definition, diagnosis and classification of Diabetes Mellitus and it scomplication[R]. WHO NCDNDS,1999,p31-33.
    3. Ninomya JK, L’Italien G, Crqui MH, et al. Association of the metabolic syndrome with his story of myocardial infraction and stroke in the third national health and nutrition examination survey.Circulation,2004,109:42-46.
    4. Klein BE, Klein R, LeeKE. Components of the metabolic syndrome and risk of cardiovascular disease and diabetes in beaver dam. Diabetes Care, 2002,25:1790-1794.
    5. Prakash CD. Metabolic syndrome and vascular disease is nature or naturele adding the new epidemic of cardiovascular disease? Circulation,2004,109:2-4.
    6. Kim KH, L ee K, Moon Ys, et al. A cysteine- rich adi-pose tissue- specific secretory factor inhibits adipocyte differentiation. J Biol Chem, 2001, 276( 6) :11252-11256.
    7. WANGGX, LIGR,WANGYD, et al. Characterization of neuronal cell death in normal and diabetic rats following experimental focal cerebral ischemia[J]. Life Sciences,2001,69:2801-2810.
    8. Fasshauer M, Klein J, Neumanns, et al. Tumor necro-sis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3- L1adipocytes.Biochem Biophys Res Commun, 2001, 288( 4) :1027-1031.
    1. Wu Z, Yao C, Zhao D, et al. Sino-MONICA project: a collaborative study on trends and determinants in cardiovascular diseases in China, part I: morbidity and mortality monitoring. Circulation 2001;103:462–8.
    2. Yao C, Wu Z, Wu Y. The changing pattern of cardiovascular diseases in China. World Health Stat Q 1993;46:113– 8.
    3. Bonow RO, Smaha LA, Smith SC Jr, et al. World Heart Day 2002. The international burden of cardiovascular disease: responding to the emerging global epidemic. Circulation.2002;106:1602–1605.
    4. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet.1997;349:1269–1276.
    5. Haffner SM, Valdez RA, Hazuda HP, Mitchell BD, Morales PA, Stern MP. Prospective analysis of the insulin-resistance syndrome (Syndrome X). Diabetes 1992;41:715–22.
    6. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001;24:683–9.
    7. Trevisan M, Liu J, Bahsas FB, Menotti A. Syndrome X and mortality: a population-based study. Risk Factor and Life Expectancy Research Group. Am J Epidemiol 1998;148:958–66.
    8. Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 2002;288:2709–16.
    9. National Institutes of Health. Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Executive Summary. NIH Publication No. 01-3670, 2001.
    10. IDF. The IDF Consensus Worldwide Definition of the Metabolic Syndrome. Available at:http://www.idf.org/home/index.cfm?_unode_1120071E-AACE-41D2-9FA0-BAB6E25BA072. Accessed April 14, 2005.
    11. Yao He, Bin Jiang, Prevalence of the metaboloc syndrome and its Relation to ChineseJournal of the American College of Cardiology Vol. 47, No. 8, 2006 ? 2006 by the American College of Cardiology Foundation ISSN 0735-1097/06/$32.00 Published by Elsevier Inc.
    12. WHO/MONICA-Project. Multinational Monitoring of Trends and Determinants in Cardiovascular Diseases (MONICA Project) and Manual of Operation. Geneva, Switzerland: World Health Organization, Cardiovascular Disease Unit, 1983. a Chinese population. Diabetes Res Clin Pract 2005,67:251–7.
    13. Newman AB, Siscovick DS, Manolio TA, et al. Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group. Circulation 1993,88:837– 45.
    14. Lakka HM, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E, Tuomilehto J, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 2002,288:2709–2716.
    15. Ridker PM, Buring JE, Cook NR, Rifai N. C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American women. Circulation 2003,107:391–397.
    16. Girman CJ, Rhodes T, Mercuri M, Pyorala K, Kjekshus J, Pedersen TR, et al. The metabolic syndrome and risk of major coronary events in the Scandinavian Simvastatin Survival Study (4S) and the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/ TexCAPS). Am J Cardiol 2004,93(2):136–41.
    17. Sattar N, Gaw A, Scherbakova O, Ford I, O’Reilly DS, Haffner SM, et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation 2003,108(4):414– 9.
    18. Gu D, Reynolds K, Wu X, et al. Prevalence of the metabolic syndrome and overweight among adults in China. Lancet 2005,365:1398– 405.
    1.顾苏兵,赖小标,华艳玲.高血压病、糖尿病、高脂血症与血管内皮的损害.中华动脉硬化杂志,1999,7,(3) :259.
    2. Vanhoutte PM. Endothelial dysfunction and atherosclerosis.[J]. Eur Heart J,1997,18(suppl E): E19-E29.
    3. Jonathan A. Role of Endothelial dysfunction in Coronary artery disease [J]. AMJ Cardiol, 1997,79(12B):29.
    4. Ghiadoni L, Virdis A, MagagnaA, etal. Effect of the angiotensin-II type receptor bloker candesartan on endothelial function in patients with essential hypertension [J]. Hypertension, 2000,35,(part 2):501-506.
    5. Noll G..Endothelium and high blood pressure. Intl Microcirc Clin Exp, 1997,17 (5)273-279.
    6. Shimokawa H. Endothelial dysfunction in hypertension . J Atheroscler Thromb1998, 4(3):118~127.
    7.方圻,王钟林,宁田海,等.血脂异常防治建议.中华心血管病杂志,1997,25:1692172.
    8.张明,霍海洋,李占全.甘油三脂/高密度脂蛋白胆固醇比值对冠心病的诊断价值的探讨.中华心血管病杂志,2000,28:33235.
    9.寺本民生.高脂血症的治疗和脑卒中的预防.日本医学介绍,2003, 24(12): 541-545.
    10.秦俭,陈运贞,等.高脂血症大鼠的血管和内皮功能.重庆医科大学学报,2002,27(2):127-130.
    11.廖志红,修玲玲,余斌杰.型糖尿病患者的血脂变化及其与冠心病的关系[J].中国动脉硬化杂志,1998,6(4):3252328.
    12.马晓云.维生素与糖尿病. [J]国外医学内分泌学分册, 1995, 15( 2) :75- 77.
    13.柴伟栋,陈家伟等.葡萄糖、胰岛素对血管内皮细胞功能的影响.中华微循环杂志,2003.7(4)204-208.
    14.郭瑜键,陈生弟.胰岛素抵抗与缺血性脑血管病.国外医学脑血管疾病分册,1998,6(1):28-31.
    15.罗义,郭南山,李光廉.冠状动脉病变程度与胰岛素敏感性的关系.中华心血管病杂志, 2000,28(6):273-276.
    16.胡兆霆,杨钧国,何勇.冠心病患者胰岛素抵抗与血载脂蛋白异常的关系.[J] .临床心血管杂志,2000,16(9):387-389.
    17.绍欣,牟建军,董平拴等.肥胖高血压患者血清游离脂肪酸与代谢紊乱.中华误诊学杂志, 2004,4(7):997-999.
    1. Reaven GM. Role of insulin resistance in human disease. Diabetes, 1988, 37( 12) :595- 607.
    2.绍欣,牟建军,董平拴等.肥胖高血压患者血清游离脂肪酸与代谢紊乱.中华误诊学杂志, 2004,4(7):997-999.
    3.梅爱农,张苏明.代谢综合症、胰岛素抵抗与糖尿病.中华神经科杂志, 2004,10,37(5):468-470.
    4. FordES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: fingds from the Third National Health and Nutrition Examination Survey[C]. JAMA,2002,287(3):356-359.
    5.吴元民,邵宝蓉,顾惠琳等.上海市华阳社区糖尿病高血压血脂紊乱及代谢综合征基线调查.上海医学,2001,24(4):195-199.
    6.李健斋,王抒,曾平.北京市职业人群代谢综合症患病率调查.基础医学与临床, 2004,12(2):217-222.
    7.常青,何耀,倪彬,等.老年人吸烟饮酒与脑卒中的流行病学研究.中国公共卫生, 2004, 20(5):550-551.
    8.刘建平,解瑞谦,程锦泉等.中国居民吸烟!饮酒等行为因素与脑卒中的关系.中国行为医学科学,2005, 14(7):613-616.
    9.张栓虎.我国居民吸烟与脑卒中关系的Meta-analysi .中国慢性疾病预防与控制,2000,8,4:156-157.
    10. Targher G, Alberiche M,Zenere MB, et al. Cigarette smoking and insulin resistance in patients with non insulin dependent diabetes mellitus [J]. J Clin Endocrinol Metab.1997,82:3619-3624.
    11. Nilsson PM, Lind L, Puare T, et al. Increased level of hemo-globin Alc, but not impaired insulin sensitivity, found in hypertensive and normotensive smokers [J]. Matabolism,1995,44:577-561.
    12. Eliasson B, AttnvallfS, The insulin resistance syndrome in smoker is related to smoking habits [J]. Arterioscler Thromb, 1994,14(12):1946-1950.
    13. Geriatrics.降低体重并减少食盐量能增强对血压的控制[J] .国外医学:老年医学分册, 1999, 20( 3) :140.
    14.张晓萍,赖小平,李丽萍,罗丽君. 138例高血压病病人生活方式干预效果观察.护理研究2005.1.19(1)下半月版(总第136期)131-132.
    1.孙继州,孙翠梅.卒中的遗传和炎症机制.国外医学脑血管病分册, 2004.2.12(2): 155-157.
    2.唐宇平,蔡定芳.急性脑出血损伤的病理生理学机制.国外医学脑血管病分册, 2005.1.13(1):11-15.
    3. Atword CS, Bowen RL, Smith MA, etal. Cerebrovascular requirement for sealant, anti-coagulant and remodeling molecules that allow for the maintenance of vascular integrity and blood supply. Brain Res Rev,2003,43:164-178.
    4. Mayer SA. Ultra-early hemostatic therapy for intracebral hemorrhage .N Engl J Med.2001.344:1450-1460.
    5.许宏伟,杨期东,刘晓英. MMP-2/9与脑出血后脑水中关系的探讨.中风与神经疾病杂志,2003.10(20):412-414.
    6.吴万福,胡长林.炎性因子在脑出血继发性损害中的作用.国外医学脑血管病分册, 2005.4,13(4):303-305.
    7.吴家幂,刘春梅,李君.脑出血后周围组织继发脑损伤炎性机制的研究.临床神经病学杂志, 2004, 7(4):278-279.
    8.李燕化,孙善全.大鼠出血性脑水肿水通道蛋白-4表达的研究.中华危重病急救医学,2003,15(9):538-541.
    9.郭建文,何迎春,陈少宏.复方中风醒脑口服液干预急性脑出血治疗时间窗的临床研究.中国脑血管杂志, 2005,6:255-259.
    10.Chu WJ, Wason GF, Pan JW, etal. Meuntz JM, Regional cerebral blood flow and magnetic resonance spectroscopic imaging findings in diaschisis from stroke. Stroke, 2002,33:1243-1248.
    11.王丽萍,郑广修.灯盏花素治疗急性脑出血的临床观察.中国脑血管杂志. 2004,10:445-447.
    12.张尉华,饶明俐.实验性脑出血血肿周围组织的细胞凋亡.中风与神经疾病杂志,2003,10(20):412-414.
    13. Landau E, Tirosh R, Pinson A, et al. Protection of thrombin receptor expression under hypoxia. J Biol Chen. 2000,275:2281-2287.
    14.Striggow F, Riek M, Breder J, etal, The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concertrations .W Proe Natl Acad Sci USA ,2000,97:2264-2269.
    15.姜亚军,常减.脑出血后脑组织内凝血酶受体的表达及其意义,中风与神经疾病杂志, 2004,21:100-102.
    16.张磊,梅元武,局部压低温治疗急性脑出血的临床研究,中国康复理论与实践,2004.1(10)53-54.
    17.葛朝阳,张旭东,梁德胜.尼莫地平对高血压脑出血患者血肿体积及周围水中带的影响.中国脑血管病杂志,2004.6255-257.
    1 Reaven GM. Role of insulin resistance in human disease. Diabetes, 1988,37(12): 595-6071031
    2.何嗣英,党静,洪佳伟等.胰岛素抵抗与高血压及脑卒中的关系分析.广东医学院学报,2005,8,23(4) :428-429.
    3 De Fromco RA. The triumvirate:beta-cell,muscle,liver.Acollusion responsible for N1DDM. Diabetes,1988,37:667-687.
    4李光伟,潘孝仁,Stephenlilliojas,等.检测人群胰岛素敏感性的一项新指数.中华内科杂志,1993,32:656-660.
    5 Report of a WHO consultation: Definition, diagnosis and classification of Diabetes Mellitus and it scomplication [R].WHO NCDNDS,1999,p31-33.Geneva.
    6 Ford ES, Giles WHD. Prevalence of the metabolic syndrome among US adults findings from the Third National Health and Nutrition Examination. Survey.JMA,2002,287:356-369.
    7.Helaine ER.Metabolic syndrome in American Indians. Diabetes care,2002,25(7):124-127.
    8.贾伟平.胰岛素抵抗与受体.第二军医大学学报,2003,24(5):528-529.
    9.王萍,刘丽伟,王虹.胰岛素抵抗与相关疾病及防治.中国误诊学杂志,2004,11(4):1796-1797.
    10.Kim KH,Lee K, Moon Ys, etal. Acysteine-richadi-Posetissue-specificsecretory factor inhibit sadipocyte differentiation. JBiolChem,2001,276(6):11252-11253.
    11.House knechet KL,Baile CA,Matter KL,etal. The Bidogy of leptin:areview. JAnimSci, 1998,76:1405.
    12.Shintoni M,OgawaY, NakaoK,etal. Insulin resis-tance, role of leptin and leptinreceptor. NipponKin-sho,2000,58:327.
    13 Moriya M,OkumuraT,TakahashiN,etal. Anin-Verse correlation between serum leptin levels and hemoglobin Alcinpatients with non-insulin dependent diabete smellitus.. Diabetes Res Clin Pract, 1999,43:187.
    14鲁谨,邹大进,张家庆.肿瘤坏死因子-A致胰岛素抵抗.中国病理生理杂志,1999,15:1146-1148.
    15 FasshauerM,KleinJ,Neumanns,etal.Tumornecro-Sis factor alphaisa negative regulator of resistingeneExpression and secretion in 3T 3-L1adipocytes.BiochemBiophysRes Commun,2001,288(4):1027-103.
    16Yang Ws,LeeWJ,FunahashiT,etal.Weight reduction in crease splasma levels of anadipose-derived antinflammatory protein adiponectin. Jclin Endocrinol Metab, 2002,87(4):1626.
    17 MatsuzawaY. Adipocyte function and insulin resistance. Nippon Rinsho,2000, 58(2):338-343.
    18OuchiN, KiharaS, AritaY, etal. Novel modulator for endothelia ladhesio molecules: adipocyte-derivedplas-maproteinadiponectin.Circulation,1999,100(25):2473-2476.
    19 RieussetJ,ChambrierC,BouzakriK,etal.Theex-pression of the P85 alphasubunit of phospatidylinositol 3-kinase is induced by activation of the peroxisome proliferator-activated rectp to rgamma in humanadipocytes.Dia2betdogia, 2001,44: 544-554.
    20 Henry M,Tergour D A, Alessi MC,etal.Metabolic Determinants are much more important than genetic Polymorphisms in determining thePAI-l activity andAntigen plasma concentrations a family study with part of the stanislas cohort. Arerioscler ThrombVascBiol,1998,18(1):84-91.
    21.柴伟栋,陈家伟等.葡萄糖、胰岛素对血管内皮细胞功能的影响.中华微循环杂志,2003.7(4)204-208.
    22朱旅云.胰岛素抵抗与糖尿病、高血压[J].医学综述,1998,4(9):496-498.
    23.杨秀真,邢云英,李永红.胰岛素抵抗与原发性高血压的关系探讨[J].中国误诊学杂志,2003,3(12):1824-1825.
    24. Haffner SM, FerranniniE, HazudaHP. Clustering of cardio vascular risk factors in confirm edprehypertensive individuals [J]. Hypertension, 1992,20(1):38-43.
    25.Haffner Sm,D Agostino RJr, MrkkanenL. Insulin Sensitivity in Subjects with type-2 diadetes [J].DiabetesCare,1999,22(4):562-568.
    26.张胜兰,王滨.胰岛素抵抗与冠心病[J].山东医药,2003,43(13):56.
    27.刘绪宏,游国雄,穆继珍.两种胰岛素抵抗的测定方法评估与脑梗塞及其病情的关系[J].第四军医大学学报,1999,20(2):184.
    29.高妍.胰岛素抵抗是心血管疾病的重要危险因素[J].中华内分代谢杂志,2000, 16(2):135-136.
    30.楚新梅,何秉贤.胰岛素抵抗和冠心病关系的再认识[J].中国循环杂志,2003, 18(4):317.
    31. Stern MP. Diabetes and cardiovascular disease: the“common soil”hypothesis [J]. Diabetea,1995, 44(4):369-394.