2型糖尿病患者自主神经功能与单纯性运动性高血压

目的 探讨2型糖尿病合并自主神经病变患者与单纯性运动性高血压的关系。方法 随机选取血压正常的2型糖尿病患者80例，按标准心血管自主神经功能试验（SCANFT）（以下简称神功试验）检查结果分为糖尿病自主神经病变（DAN）组（38例）和单纯性糖尿病（SDM）组（42例），与自主神经功能检查阴性的40例健康组作对比分析，并分析其静态血压，运动负荷后血压及动态血压变化。结果 三组静态血压无明显差异，DAN组运动负荷后的血压及运动性高血压发生率明显高于SDM组及对照组（均P＜0．01）。动态血压显示：糖尿病患者2h SBP,dSBP,nSBP均高于对照组（P＜0．01），而DAN组的24h DBP,dDBP,nDBP及心率较SDM组及对照组显著增高（P＜0．01），结论 自主神经功能异常的糖尿病患者，运动负荷后的血压明显升高，运动性高血压可作为糖尿病患者合并自主性神经病变的预测指标之一。     

心血管自主神经功能与高血压并2型糖尿病患者血压节律的相关性研究

目的分析心血管自主神经功能与高血压并2型糖尿病患者血压节律的相关性。方法选取2013年6月—2015年6月东营市河口区人民医院心内科收治的门诊高血压患者80例(高血压组)、高血压并2型糖尿病患者80例(高血压并2型糖尿病组)。比较两组患者动态血压监测指标[包括24 h收缩压(24 h SBP)、24 h舒张压(24h DBP)、昼间SBP(Dt-SBP)、昼间DBP(Dt-DBP)、夜间SBP(Nt-SBP)、夜间DBP(Nt-DBP)、昼夜SBP下降值(ΔSBP)、昼夜DBP下降值(ΔSBP)、杓型血压发生率]和标准心血管自主神经功能测试(SCAFT)指标[包括Valsalva动作反应指数、呼吸差、卧立位血压差、30∶15比值、SCAFT评分],采用Spearman秩相关分析SCAFT评分与高血压并2型糖尿病患者动态血压监测指标、糖化血红蛋白的相关性。结果两组患者24 h SBP、24 h DBP、Dt-SBP、Dt-DBP比较,差异无统计学意义(P>0.05);高血压并2型糖尿病组患者Nt-SBP、Nt-DBP高于高血压组,ΔSBP、ΔDBP及杓型血压发生率低于高血压组(P<0.05)。高血压并2型糖尿病组患者Valsalva动作反应指数、30∶15比值低于高血压组,呼吸差、卧立位血压差、SCAFT评分高于高血压组(P<0.05)。Spearman秩相关分析结果显示,SCAFT评分与高血压并2型糖尿病组患者Nt-SBP、Nt-DBP、糖化血红蛋白呈正相关(rs值分别为0.433、0.372、0.583,P<0.05),与ΔSBP、ΔDBP呈负相关(rs值分别为-0.315、-0.448,P<0.05)。结论心血管自主神经功能与高血压并2型糖尿病患者血压节律密切相关。     

自主神经功能与糖尿病患者左心室功能、心律失常的关系

目的 探讨糖尿病患者自主神经功能与部分心脏合并症之间的关系。方法 采用24小时动态心电图和血压同步监测102例糖尿病患者，左心室功能和结构参数用彩色多普勒超声心动图测定。结果 随SDNN（24小时内全部正常R－R间期的标准差）降低，糖尿病患者的舒张末期二尖瓣口血流频谱A峰与E峰峰值流速的比值（PVA／PVE）、室间隔厚度（IVSTd)、左心室后壁厚度（LVPWTd)、左心室重量指数（LVMI）均增加；二尖瓣前叶活动斜率（MEF）降低，IVSTd/LVPWTd则无变化；严重的心律失常如Lown‘s≥3级的室性心律失常及短阵房速、房颤的发生率也明显增加。上述变化与夜间血压的异常增高相伴随。结论 SDNN低的糖尿病患者心脏受累严重，并可能预示患者日后发生心源性猝死的危险性增加。     

心率变异评价新疆维吾尔族2型糖尿病患者的自主神经功能

目的　探讨新疆维吾尔族2型糖尿病(T2DM)患者自主神经病变与心率变异(HRV)及其他脏器受损的关系。　方法　选择确诊为 T2DM的 150 例维吾尔族住院患者,其中单纯糖尿病(SDM)组72例,合并心血管疾病的糖尿病(DC)组78例,病程 <5年组54例,5~10年组51例,>10年组45例。正常对照(NC)组为健康的维吾尔族人 60 名,全部进行 24 h动态心电图及 HRV分析。　结果　T2DM患者HRV均小于NC组(t'= 6.5366~9.5677, P<0.05 ),DC组的 HRV较 SDM组低(t=4.0791~8.9233,P<0.05 ),病程>5 年的两组患者所有正常 R R间期的标准差值均低于病程<5年组(t=7.5935~10.631,P<0.05 )。　结论　HRV是早期判断维吾尔族 T2DM患者自主神经病变最准确而又最敏感的方法,可能对是否合并心脏缺血性病变有提示作用。     

2型糖尿病患者高血压与糖尿病性神经病变的关系

目的 探讨2型糖尿病患者高血压与糖尿病性神经病变的关系。方法 利用心自主神经功能检测系统和神经电生理检测仪对107例（高血压组52例,非高血压组55例）2型糖尿病患者的心自主神经功能和肢体的末梢神经传导速度、皮肤痛温觉、振动沉进行测定,以判断心自主神经病变和末梢神经病变。结果 两组间末梢神经功能和心自主神经功能各指标除心的是距频谱分析的高频值外差异均无显著性（P＜0.05）。Logistic回归分析显示高血压与心自主神经病变显著相关（P＜0.01）,而与末梢神经病变无显著相关。结论 2型糖尿病患者高血压是心自主神经病变发病的危险因素,而与末梢神经病变无明显关系。     

2型糖尿病心血管自主神经功能检查的临床意义

目的:研究2型糖尿病患者心血管自主神经功能检查对无症状型冠心病的诊断价值。方法:在2型糖尿病患者中筛选出伴有心血管自主神经病变的患者52例为观察组,另选出不伴有心血管自主神经病变的患者58例作为对照组,两组患者均行平板运动试验。结果:观察组平板运动试验阳性率为55.8%,高于对照组平板运动试验阳性率34.5%,两组差异有显著性(P<0.05)。结论:2型糖尿病人心血管自主神经检查有助于提高其合并的冠心病的诊断率。     

高血压并发心衰患者自主神经功能的变化

目的探讨高血压并发心衰患者自主神经功能异常与心力衰竭的关系。方法选择高血压并发心衰患者63例与高血压心功能正常者63例,根据性别、年龄配对,运用动态心电图,结合心率变异指标,通过计算机处理数据,观察两组患者自主神经功能异常程度,评价自主神经功能及平衡情况。结果高血压并发心衰患者心率变异指标较高血压心功能正常者明显降低（P〈0．05或〈0．01）。结论高血压并发心力衰竭患者自主神经功能明显受损。     

高血压合并2型糖尿病患者的动脉弹性与内皮功能

目的探讨高血压合并2型糖尿病对动脉功能的影响。方法研究对象137例根据标准分为正常对照组、原发性高血压(EH)组、高血压合并2型糖尿病(EH 2DM)组,各组分别测定一氧化氮(NO)、一氧化氮合酶(NOS)、颈股脉搏波传导速度(cfPWV)及血流介导的血管舒张功能(FMD)和反应性充血(RH)。结果与对照组比较,EH 2DM组和EH组NO、FMD、RH值明显降低,cfPWV明显升高(P<0.01);与EH组比较,EH 2DM组的FMD、RH降低(P<0.05)。相关分析结果显示收缩压、舒张压、血糖、cfPWV与FMD负相关(r=-0.507,P=0.001;r=-0.404,P=0.001;r=-0.373,P=0.001;r=-0.270,P=0.001);NO与FMD正相关(r=0.256,P=0.002)。结论EH 2DM患者血管内皮功能和大动脉弹性进一步减退。     

高血压合并2型糖尿病患者的动脉弹性与内皮功能

目的 探讨高血压合并2型糖尿病对动脉功能的影响.方法 研究对象137例根据标准分为正常对照组、原发性高血压(EH)组、高血压合并2型糖尿病(EH 2DM)组,各组分别测定一氧化氮(NO)、一氧化氮合酶(NOS)、颈股脉搏波传导速度(cfPWV)及血流介导的血管舒张功能(FMD)和反应性充血(RH).结果 与对照组比较,EH 2DM组和EH组NO、FMD、RH值明显降低,cfPWV明显升高(P＜0.01);与EH组比较,EH 2DM组的FMD、RH降低(P＜0.05).相关分析结果显示收缩压、舒张压、血糖、cfPWV与FMD负相关(r=-0.507,P=0.001;r=-0.404,P=0.001;r=-0.373,P=0.001;r=-0.270,P=0.001);NO与FMD正相关(r=0.256,P=0.002).结论 EH 2DM患者血管内皮功能和大动脉弹性进一步减退.     

北京地区2型糖尿病患者糖尿病心脏自主神经病变现况调查

目的:调查北京地区2型糖尿病（T2DM）心脏自主神经病变（CAN）的患病率,探讨CAN的临床特点和发病危险因素。方法:本研究为多中心随机横断面研究。对2015年10月至2016年4月在北京市城区和郊区13家医院门诊就诊的T2DM患者,采用随机抽样的方法进行问卷调查、体格检查及实验室检查。根据心脏自主神经功能试验结果将患...     

Catecholamines and Diabetic Autonomic Neuropathy

In diabetic patients with autonomic neuropathy plasma noradrenaline concentration, used as an index of sympathetic nervous activity, is low. This decrease is, however, only found in patients with a long duration of diabetes with clinically severe autonomic neuropathy. This apparent insensitivity of plasma catecholamine measurements is not due to changes in the clearance of catecholamines in diabetic autonomic neuropathy. The physiological responses to infused adrenaline and to noradrenaline are enhanced, for noradrenaline mainly cardiovascular responses. Adrenoceptors (alpha and beta adrenoceptors) are not altered in circulating blood cells in diabetic autonomic neuropathy. Thus, a generalized up-regulation of adrenoceptors does not occur in diabetic autonomic neuropathy.     

Mortality in Diabetic Patients with Cardiovascular Autonomic Neuropathy

Cardiovascular autonomic diabetic neuropathy (CADN) may carry an increased risk of mortality. However, in previous studies the prognosis of patients with CADN seemed to be influenced by life-threatening macro- and microvascular complications which had already been present at the start of the study period. Between 1981 and 1983, 1015 diabetic patients have been examined for CADN (abnormal heart rate variation at rest and during deep respiration) at the Diabetes Research Institute, Düsseldorf. Thirty-five patients (28 with Type 1 diabetes, 7 with Type 2 diabetes) with CADN have been retrospectively recruited and reviewed 8 years later and compared with 35 patients without CADN who were matched for sex, age, and duration of diabetes. Exclusion criteria for entry into the study included severe micro- or macrovascular complications, such as proliferative retinopathy, proteinuria or symptomatic coronary artery disease. During the 8-year observation period, 8 patients with CADN and 1 patient without CADN died. The survival rate estimates steadily declined in patients with CADN over the whole period studied. The 8-year survival rate estimate in patients with CADN was 77 % compared with 97 % in those with normal autonomic function (p < 0.05). Deaths were mainly due to macrovascular diseases (n = 3) and sudden unexpected deaths (n = 3). One patient with CADN died after an episode of severe hypoglycaemia. Among the deceased patients, coefficient of variation of R-R intervals during deep breathing was significantly reduced when compared with those who survived (1.04 ± 0.5 % vs 1.87 ± 1.0 %; p < 0.05), and symptoms of autonomic neuropathy (orthostatic hypotension, gastroparesis, gustatory sweating) were more frequent (7/8 vs 10/27 patients). The mean QTc interval was not different between the groups. These results suggest a relatively poor prognosis of patients with CADN in the absence of clinically detectable micro- and macrovascular complications.     

QT Interval Length and Diabetic Autonomic Neuropathy

QT interval length was measured in ECG recordings from three groups of age-matched male subjects: 36 normal subjects, 41 diabetic patients without (DAN-ve), and 34 with (DAN+ve) autonomic neuropathy. ECG samples were selected from previously recorded 24-h ECGs on the basis of a clearly defined T wave and a steady RR interval over 2 min of around 750 ms (80 beats min^?1). There were no significant differences in RR interval between the groups. The two diabetic groups had slightly longer QT measurements (normal 365 ± 14 (±SD) ms, DAN-ve 373 ± 18 ms, DAN+ve 375 ± 23 ms, p = 0.05), and corrected QT (QTc) values (normal 423 ± 15 ms, DAN-ve 430 ± 20 ms, DAN+ve 435 ± 24 ms, p = 0.05). Ten diabetic patients fell above our defined upper limit of normal for QTc (>mean + 2SD). There was a significant correlation in the DAN-ve group between the QT indices and 24-h RR counts (QT r = ?0.38, p < 0.01; QTc r = ?0.40, p < 0.01). We conclude that there are some small alterations in QT interval length in the steady state in diabetic autonomic neuropathy. The changes appear to be due to autonomic impairment, rather than diabetes per se.     

Postural Hypotension in Diabetic Autonomic Neuropathy: a Review

Postural hypotension is uncommon in diabetes but can occur secondary to autonomic neuropathy. Symptoms are rare and include dizziness, weakness, blurred vision, tiredness, and loss of consciousness. The pathophysiology of postural hypotension is not clear, but changes in intravascular volume, heart rate, cardiac output, and splanchnic vascular resistance are similar in patients and controls. The main factors producing hypotension are a blunted catecholamine response to standing, and failure of lower limb vascular resistance to increase adequately. Treatment for symptomatic postural hypotension includes avoidance of dehydration, adequate salt intake, and fludrocortisone. Other treatments are reviewed but are less helpful. Patients with postural hypotension have intermittent symptoms over the years but rarely become severely disabled. They have a poorer prognosis than patients with symptomatic autonomic neuropathy without postural hypotension.     

通心络胶囊对糖尿病自主神经病变的影响

目的观察通心络胶囊联合甲钴胺片对糖尿病自主神经病变（DAN）患者的影响。方法48例DAN患者均予通心络胶囊4老V次口服,3次／d,甲钴胺片500μg／次口服,3次／d,共2个月。观察服药前后患者心率变异性（HRV）的变化,并记录患者症状的积分情况。结果通心络胶囊治疗后患者多汗、腹泻、便秘、排尿障碍、直立性低血压症状减轻或消失,5项症状的积分均较治疗前减少达50％以上,与治疗前比较差异有统计学意义（P〈0．05）;HRV各指标中低频范围内的功率（LF）降低（32．8±11．4）ms^2,LF／高频范围内的功率（HF）降低（1．8±0．6）ms^2,余指标均增高,差异有统计学意义（P〈0．01）,且未见明显不良反应。结论通心络胶囊联合甲钴胺片对糖尿病自主神经病变有改善交感、迷走神经平衡失调的作用,是治疗DAN安全、有效的药物。     

Autonomic and Peripheral Nerve Function in Early Diabetic Neuropathy

ABSTRACT. Sundkvist G, Lilja B, Rosén I, Agardh C-D (Departments of Internal Medicine and Clinical Physiology, Malmö General Hospital, and Departments of Clinical Neurophysiology and Internal Medicine, University Hospital, University of Lund, Lund, Sweden). Autonomic and peripheral nerve function in early diabetic neuropathy. Possible influence of a novel aldose reductase inhibitor on autonomic function. Acta Med Scand 1987; 221:445–53. Autonomic and peripheral nerve functions as well as the possible short-term effect of a novel aldose reductase inhibitor (ARI) on neuropathy were evaluated in 30 male type I diabetics (age 25–44 years, mean 34; duration of diabetes 10–20 years, mean 34) with neurographic signs of peripheral neuropathy (PN). Autonomic neuropathy (AN) was established by the heart rate reactions to deep breathing (E/I ratio = vagal function) and to tilt (acceleration index = sympathetic and vagal functions; the brake index = vagal function). Twenty-nine patients, 13 with AN, completed the study. Among neurographic variables, only sural nerve function tests correlated with autonomic functions. Patients with AN showed significantly lower mean sensory action potential amplitudes (SAPA) sural, indicating axonal losses, than patients without AN (3.58±0.79 μV vs. 7.34±1.12 μV; p<0.01). PN as measured by neurography did not improve during ARI treatment. On the other hand, vagal function (brake indices) improved (p<0.05) during ARI in AN patients.     

肥胖患者运动性高血压的临床研究

目的比较肥胖组与正常对照组运动负荷后的血压变化,探讨运动性高血压对肥胖患者高血压病早期诊断的临床意义.方法观察静态及次极量踏车运动试验后血压变化,两组进行对比分析,并行24小时动态血压检查.结果静态下两组血压无差异,运动后肥胖组血压超过标准者(42.86%)明显高于对照组(13.33%);动态血压分析显示肥胖组24小时及日间收缩压高于对照组,舒张压及夜间血压无显著差异.结论肥胖患者运动性高血压患病率明显高于对照组,提示运动性高血压对肥胖者高血压病的早期诊断有一定参考价值.     

The Splanchnic Circulation and Postural Hypotension in Diabetic Autonomic Neuropathy

Postural hypotension results from sympathetic failure to cause superior peripheral vasoconstriction. The importance of the splanchnic circulation was studied by measuring mesenteric artery blood flow with duplex Doppler scanning. Nine normal and 9 Type 1 diabetic controls were compared to 8 Type 1 patients with autonomic neuropathy whose pressure fell 40–113 mmHg (range) on tilting. Measurements were made supine and after vertical tilt, fasting without insulin and after a 550 kcal meal. Superior mesenteric artery diameter decreased on tilting in normal controls but not in diabetic control or neuropathy groups (supine vs tilted: controls. 6.3 ± 0.9 to 5 ± 0.9 mm, p = 0.004, diabetic controls: 6.0 ± 0.6 to 6.0 ± 1.0 mm, and neuropathy group: 6.4 ± 0.9 to 5.6 ± 0.9 mm), but proportional blood flow changes were similar in all subjects (controls: 407 ± 154 to 255 ± 67 ml min^?1 (-31%, p = 0.03), diabetic controls: 379 ± 140 to 306 ± 149 ml min^?1 (-8%, p = 0.28), neuropathy group: 639 ± 371 to 435 ± 142 ml min^?1 (-23%, p = 0.10). Postprandially supine superior mesenteric artery flow increased in all subjects but this did not affect the degree of systolic blood pressure drop on tilting (fasting vs postprandial blood flow: controls: 407 ± 154 to 775 ± 400 ml min^?1 (p = 0.04), diabetic controls: 379 ± 140 to 691 ± 262 ml min^?1 (p = 0.01), neuropathy group: 639 ± 371 to 943 ± 468 ml min^?1 (p < 0.06)). The similarity of superior mesenteric artery responses to tilting in the three groups, and the lack of exacerbation of postural hypotension in the presence of postprandial hyperaemia indicates that control of splanchnic blood flow is less important in the aetiology of diabetic autonomic postural hypotension than previously thought.