交感神经系统与肺动脉高压的研究进展

肺动脉高压是一组不同病因导致的表现为肺动脉压升高、右心衰竭等特点的难治性疾病,交感神经在其发生发展中起到了作用,干预交感神经有望成为治疗肺动脉高压的新思路,深入研究交感神经系统在肺动脉高压的作用及相关机制具有重要意义。     

干预交感神经治疗肺动脉高压的研究进展

肺动脉高压(PAH)是以肺动脉平滑肌细胞增生和肺中小动脉重构为主要特征,导致肺血管阻力进行性增加,最终引起右心室肥厚和右心衰竭的一种致死性疾病。越来越多的研究显示,交感神经在PAH患者中的交感活性增强,且PAH患者的生存率和预后与交感神经活性密切相关。交感神经系统的激活在肺动脉重塑中发挥重要作用。目前干预交感神经系统治疗PAH的手段包括α/β受体阻滞剂、血管紧张素转换酶(ACE)抑制剂、血管紧张素1型受体(AT1R)抑制剂、醛固酮受体拮抗剂、ACE2激动剂、肺动脉去神经支配、肾交感消融和交感神经节阻滞等,均显示出一定的心脏和代谢保护作用,改善了心肺血流动力学。本文将对干预交感神经系统治疗PAH的相关基础及研究进展进行综述。     

交感神经系统在血管性疾病发生发展中的研究进展

交感神经系统通过释放各种交感神经递质直接参与血管正常生理功能的调节,对维持血管稳态具有重要作用.然而病理条件下交感神经系统的改变会影响血管张力以及血管的反应性等,从而导致高血压、动脉粥样硬化和肺动脉高压等血管性疾病.本文主要综述交感神经系统在相关血管性疾病的发生发展中的作用.     

心脏交感神经重构与心律失常的关系

心脏内广泛分布着交感神经并受其支配,交感神经在调节心率、心脏传导、心肌收缩和舒张等方面发挥了重要作用。近年研究发现,在很多心脏疾病中,交感神经的分布、密度、功能都发生了不同程度的改变。即我们所述的交感神经重构。心律失常在临床很常见,长期以来对心律失常的电生理机制的研究比较多,而近几年很多学者研究发现在心脏疾病中伴有的心脏交感神经重构与心律失常的发生有着密切的关联。心脏交感神经重构与心肌组织重构、电重构的相互影响可能是心律失常发生的基础。对交感神经重构进行药物与非药物干预可能是控制心律失常发生的一个新的治疗途径。     

肾动脉消融治疗慢性心力衰竭研究进展

慢性心力衰竭是一种复杂的临床症状群,是多种心血管疾病的共同转归。交感神经持续过度激活是其发生及发展的重要机制,多项临床及动物实验研究均表明,肾脏神经在交感神经活动中起着促进和传递的作用。2009年,Krum教授首次尝试利用导管靶向消融肾动脉周围的交感神经,从而降低全身过度激活的交感活性,达到治疗顽固性高血压的目的。这项新的治疗策略在有效地控制血压的同时还能有效降低心脏、肾脏以及肌肉组织等多个器官系统的交感神经活性,并能调节水盐代谢,改善心室重构和心脏功能,减轻机体高交感神经活性所导致的多器官损害。虽然其中具体的机制尚未明了,但我们有理由相信肾动脉消融在治疗高血压、慢性心力衰竭、代谢综合征等交感神经慢性过度激活的疾病有广阔的应用前景。     

干预心脏外在自主神经对室性心律失常影响的研究进展

研究显示,自主神经调节在室性心律失常的发生、发展中起重要作用,抑制交感神经活性或增加迷走神经活性均可抑制室性心律失常的发生。干预心脏外在自主神经如迷走神经、脊髓神经、肾交感神经、左星状神经节、颈动脉窦压力感受器、正中神经等可调节自主神经张力,为室性心律失常的治疗提供了新思路。     

老年人心力衰竭的病理生理机制探索新动向

心力衰竭（简称心衰）是老年人群中最常见的心血管疾病之一。本文综述了老年人心衰病理生理机制的特点;评价了交感神经过度激活、能量代谢重构在心衰中的作用及肾脏去神经术或曲美他嗪、辅酶Q10等药物治疗措施的疗效;同时介绍了肺动脉高压、心室一动脉偶联僵硬、系统性炎症状态等机制在射血分数保留心衰发生发展中的作用。     

去肾交感神经术对治疗慢性心力衰竭的作用

慢性心力衰竭(简称心衰)为各种心脏疾病的严重和终末阶段,是危害人类健康的最主要疾患之一。交感神经系统的激活对心肌病理性重构和心竭发生发展起着至关重要的作用,交感神经系统激活所致的去甲肾上腺素释放与心衰的发病率和死亡率密切相关,影响心衰的预后。近年研究证实,去肾交感神经术能够特异性地阻断肾脏传入和传出交感神经活动从而降低全身交感神经活性和减少去甲肾上腺素溢出,它不仅能够降低血压,还能减轻心肌肥厚,改善心功能等,从而为心衰的非药物治疗提供了一种新的方式。     

高血压与肾交感神经活性的关系再评价

<正>高血压是一种常见的慢性疾病,常并发多种疾病而严重影响患者的生活质量,且增加心血管疾病患者的死亡风险,顽固性高血压的治疗至今仍是一个难题[1]。我们就高血压与肾交感神经活性的关系及治疗新技术做一综述。1高血压与肾交感神经的关系交感神经过度兴奋常常导致血压上升,而高血压患者也往往合并交感神经活性增加,尤其是肾交感神经活性增加。     

低氧诱导因子-1在低氧性肺动脉高压中的研究进展

低氧性肺动脉高压(HPH)是由缺氧引起的肺动脉压力进行性升高的肺血管疾病。低氧诱导因子-1(HIF-1)是维持细胞氧稳态的核心转录因子,可促进细胞糖代谢模式的转变、调节细胞膜表面离子通道活性、调节肺血管收缩及舒张因子活性等,在HPH的发生和发展中具有重要作用。现对HIF-1及其下游信号分子在HPH发生和发展中的作用机制进行综述,有助于为HPH的治疗提供新的理论依据和治疗靶点。     

肾交感神经消融治疗高血压及其研究进展

肾交感神经的过度激活可能是高血压的产生和维持的关键因素,肾交感神经消融属选择性的去交感神经化治疗,为高血压的治疗提供了新途径,本文对肾交感神经消融治疗高血压的安全性、有效性及其适应症的进一步拓展作一综述。     

Sympathetic nervous system activation and β‐adrenoceptor blockade in right heart failure

Right heart failure may develop from pulmonary arterial hypertension or various forms of congenital heart disease. Right ventricular adaptation to the increased afterload is the most important prognostic factor in pulmonary hypertension and congenital heart disease, which share important pathophysiological mechanisms, despite having different aetiologies. There is substantial evidence of increased sympathetic nervous system activation in right heart failure related to both pulmonary hypertension and congenital heart disease. It is unknown to which degree this activation is an adaptive response, a maladaptive response, or if it mainly reflects disease progression. Several experimental studies and clinical trials have been conducted to answer these questions. Here, we review the existing knowledge on sympathetic nervous system activation and the effects of β‐adrenoceptor blockade in experimental and clinical right heart failure. This review identifies important gaps in our understanding of the right ventricle and discusses the potential of β‐blockers in the treatment of right heart failure.     

交感神经兴奋在慢性间歇性低氧引起高血压发生过程中的作用

交感神经活性增强在阻塞性睡眠呼吸暂停引起的高血压及其他心血管疾病发生过程中起到重要作用.阻塞性睡眠呼吸暂停(obstructive sleep apnea,OSA)最为明显的特征就是夜间反复的间歇 性低氧,这种间歇性低氧状态对于交感神经激活及血压升高显得尤为重要.以下就OSA相关性间歇性低氧引起的交感神经系统激活以及其...     

SYMPATHETIC NERVOUS SYSTEM,DIABETES, AND HYPERTENSION

Hypertension is twice as frequent in diabetic patients than in the general population. Its prevalence is higher in Type 2 than in Type 1 diabetes: in the former, the onset of hypertension often precedes the diagnosis of diabetes, whereas, in the latter it is strictly related to the presence of nephropathy. Sympathetic nerve overactivity is crucial in the pathogenesis of hypertension in diabetes. It can be related to the activation of the renin-angiotensin-aldosterone (RAA) system in Type 1 diabetic patients with chronic renal failure, or to a condition of insulin resistance/hyperinsulinemia in Type 2 patients with the metabolic syndrome. In patients with early autonomic neuropathy, vagal impairment can lead to a relative predominance of sympathetic activity in the sympatho-vagal balance. In these patients, the onset of hypertension is frequently preceded by reduced nocturnal dipping. Sympathetic overactivity stimulates RAA activity, promotes sodium reabsorption, and increases heart rate, stroke volume and peripheral vascular resistance, thus inducing hypertension and increasing cardiovascular risk. A number of drugs acting either directly or indirectly on sympathetic activity are available for the treatment of hypertension in diabetic subjects. Opinions on the potential advantages of the metabolic profile of some of these drugs are as yet conflicting.     

Cardiovascular risk and adrenergic overdrive in the metabolic syndrome

AimsThis paper will review the role of the sympathetic nervous system in the pathogenesis of the metabolic syndrome as well as its importance as target of non-pharmacologic and pharmacologic treatment.Data synthesisSeveral indices of adrenergic drive, such as plasma norepinephrine, norepinephrine spillover from adrenergic nerve terminals and efferent postganglionic muscle sympathetic nerve traffic, have all shown an increase in the different conditions clustering in metabolic syndrome, such as obesity, hypertension and insulin resistance state. This increase: 1) appears to be potentiated in the metabolic syndrome; and 2) contributes to a large extent at the cardiovascular structural and functional alterations typical of the disease. Based on this evidence, non-pharmacologic life-style interventions as well as drug treatment procedures used in the therapeutic approach to the metabolic syndrome should be aimed at exerting not only favourable haemodynamic and metabolic effects but also pronounced sympathoinhibition.ConclusionThe data reviewed in this paper strongly support the relevance of the sympathetic nervous system in the pathogenesis of the metabolic syndrome and the importance of the sympathomodulation as a specific aim of therapeutic intervention.     

交感神经系统在肺动脉高压发生发展过程中的作用

肺动脉高压（pulmonary arterial hypertension,PAH）是各种原因所致的一种慢性肺血管性疾病,主要表现为肺动脉重构和肺血管阻力进行性增加,最后导致右心室功能衰竭和死亡,预后极差。PAH时交感神经表现为过度激活,交感激活后可以通过多种机制参与肺动脉重构及加重右心室功能紊乱。干预交感神经可以改善PAH的预后,其原因与改善PAH的右心室功能和肺动脉重构密切相关,但是不良反应也较多,交感神经系统参与PAH发生发展的确切机制尚不完全知道,仍需进一步研究。     

Renal sympathetic nervous system and the effects of denervation on renal arteries

Resistant hypertension is associated with chronic activation of the sympathetic nervous system resulting in various comorbidities. The prevalence of resistant hypertension is often under estimated due to various reasons. Activation of sympathetic nervous system at the renal-as well as systemic-level contributes to the increased level of catecholamines and resulting increase in the blood pressure. This increased activity was demonstrated by increased muscle sympathetic nerve activity and renal and total body noradrenaline spillover. Apart from the hypertension, it is hypothesized to be associated with insulin resistance, congestive heart failure and obstructive sleep apnea. Renal denervation is a novel procedure where the sympathetic afferent and efferent activity is reduced by various techniques and has been used successfully to treat drug-resistant hypertension improvement of various metabolic derangements.Renal denervation has the unique advantage of offering the denervation at the renal level, thus mitigating the systemic side effects. Renal denervation can be done by various techniques including radiofrequency ablation, ultrasound guided ablation and chemical ablation. Various trials evaluated the role of renal denervation in the management of resistant hypertension and have found promising results. More studies are underway to evaluate the role of renal denervation in patients presenting with resistant hypertension in different scenarios. Appropriate patient selection might be the key in determining the effectiveness of the procedure.     

Recording sympathetic nerve activity from the skin

Sympathetic tone is important in cardiac arrhythmogenesis; however, methods to estimate sympathetic tone are either invasive or require proper sinus node function that may be abnormal in disease states. Because of the direct and extensive connections among various nerve structures, it is possible for the sympathetic nerves in the various structures to activate simultaneously. Therefore, we hypothesized that nerve activity can be recorded from the skin and it can be used to estimate the cardiac sympathetic tone. Preclinical studies in canines demonstrated that nerve activity is detectable using conventional ECG electrodes and can be used to estimate cardiac sympathetic tone. Subsequent clinical studies further supported this concept. In addition to studying the autonomic mechanisms of cardiac arrhythmia, these new methods may have broad application in studying both cardiac and non-cardiac diseases.     

Hypertensive subjects with type-2 diabetes,the sympathetic nervous system,and treatment implications

Central obesity is closely linked to hypertension and type-2 diabetes (DM2) in young/middle-age. In the elderly, systolic hypertension is a reflection of aging/stiff arteries. Diastolic (± systolic) hypertension in young/middle-age is accompanied by increased sympathetic nerve activity, particularly in the presence of the metabolic syndrome or DM2. High beta-receptor density (Bmax) and cyclic AMP (cAMP) levels in human lymphoctes, independent of blood pressure, are associated with a high risk of myocardial infarction (not stroke-risk, which is dependent on blood pressure). This has treatment implications in the young/middle-aged hypertensive subject. Antihypertensive agents that increase sympathetic nerve activity e.g. dihydropyridine calcium blockers, angiotensin receptor blockers, and thiazide-type diuretics, do not reduce (and may increase) the risk of myocardial infarction. Beta-1 blockade, effective in reversing and stabilising coronary atheromataous plaque, and with possible anti-tumor properties, is superior to ACE-inhibition, and is the treatment of choice in young/middle-aged hypertension with DM2.