清醒大鼠室旁核微量注射心房钠尿肽对压力感受性反射敏感性的影响

心房钠尿肽(atriaI natriuretic peptide,ANP)作为一种神经递质或调质可能参与心血管活动的中枢调节。本实验在清醒大鼠室旁核(paraventricular nucleus,PVN)注射ANP,探讨其对压力感受性反射敏感性的影响,并通过侧脑室注射血管升压素受体Ⅰ阻断剂OPC-21268,观察ANP对压力感受性反射敏感性的调节是否与中枢血管升压素有关。实验中观察到,在PVN内微量注射ANP(6、60 ng/0.2μl)可明显提高压力感受性反射敏感性(P<0.05),侧脑室预先注射OPC-21268 (0,45 μg/3 μl)后,ANP对压力感受性反射敏感性的增强作用明显减弱(P<0.05)。静脉注射ANP(60 ng/0.04 ml)不影响压力感受性反射敏感性。上述结果提示,心房钠尿肽对压力感受性反射活动起易化作用,心房钠尿肽的这种中枢作用可能部分通过中枢血管升压素介导。     

心力衰竭状态下的动脉压力感受器反射

心力衰竭是以心脏泵血功能降低（心输出量减少）为始动因素的临床综合征。心输出量降低首先引起动脉压力感受性反射失负荷,进而通过迷走-交感机制加快心率;同时,支配血管床的交感传出活动增强,进而增加总外周阻力。本文主要论述在心力衰竭状态下压力感受性反射在循环功能异常调控中的作用机制。本综述及我们近年的研究表明：（1）在心力衰竭状态下压力感受性反射功能明显减弱;（2）中枢血管紧张素Ⅱ和活性氧在压力感受性反射功能失调中发挥关键作用;（3）心交感传入刺激和化学感受性反射能抑制压力感受性反射;（4）适当的运动可以部分纠正异常的心血管反射活动。     

家兔主动脉神经高阈压力感受反射快速重调中枢过程的机能特征

实验在37只乌拉坦麻醉家兔中进行,切断双侧主动脉神经(AN)、窦神经及迷走神经。以模拟高值保持压的条件刺激(0.5ms,10Hz,4—6V,5min)给予切断的 AN 中枢段,借以诱导高阈压力感受反射快速重调的中枢过程,旨在观察中枢重调过程对压力感受反射的影响。实验表明:(1)该中枢过程显著衰减由 AN A-纤维和 c-纤维混合传入所激发的压力感受反射降压效应(-45.5%,P<0.01,n=10)及肾交感神经活动抑制效应(-10.6%,P<0.05,n=11),(2)对选择兴奋 A-纤维激发的压力感受反射,仅衰减其降压效应(-32.1%,P<0.05,n=7),而不影响其肾交感神经活动抑制效应(2.4%,P>0.05,n=7),结果进一步证实:快速重调中枢过程对压力感受反射的衰减性影响和传入纤维成分的依赖关系,主要衰减诱导该中枢过程的同类纤维激发的压力感受反射。     

老年人中枢交感神经紧张性增加对心血管系统的影响

随着年龄的增加,中枢交感神经的紧张性增加,这会引起心血管系统的结构和功能有所改变,如四肢血流量减少、动脉血压调节发生改变、压力反射作用减弱、动脉管腔增厚以及心血管系统对肾上腺素受体的刺激反应性降低等。这些改变可能是在机体衰老过程中维持自身生理功能和机体稳态的重要代偿因素,同时也是促发老年人心血管疾病和代谢性疾病的危险因素。因此,研究老年人群交感神经的慢性紧张性增加对心血管系统的影响对进一步改善和提高老年人生活质量,治疗老年人疾病有着很大的意义。     

中枢血管紧张素对心血管活动调节作用

血管紧张素(Ang)广泛存在于中枢神经系统和外周组织中,对心血管活动和交感神经活动起重要调节作用。本文介绍了孤束核(NTS)、延髓头端腹侧区(RVLM)、延髓尾端腹侧区(CVLM)和室旁核(PVN)内Ang对心血管活动的影响,Ang对动脉压力感受性反射(ABR)和心交感传入反射(CSAR)的调节作用,肾素-血管紧张素系统的基因敲除研究,以及Ang与高血压和慢性心力衰竭的关系。     

家兔主动脉神经低阈压力感受反射快速重调中枢过程的特征

40只家兔,乌拉坦静脉麻醉。切断双侧主动脉神经(AN)、窦神经及迷走神经。以选择兴奋 AN 有髓传人纤维的条件刺激(0.02ms,50Hz,4—6V,5min)给予切断的 AN 中枢段,模拟导致低阈压力感受反射快速重调的保持压背景,借以诱导快速重调的中枢过程。实验表明:该中枢过程使 AN 有髓纤维传入所激发的压力感受反射降压效应衰减41.82%(P<0.01),肾交感神经活动抑制效应衰减19.31%(P相似文献   

延髓头端腹外侧区神经元电活动与心血管活动相干性的研究

本文分析了大鼠延头端腹外侧区（ＲＶＬＭ）神经元单位活动与心血管活动的相干性,观察了ＲＶＬＭ区神经元电 对电刺激中脑防御反应区的诱发反应,以及对压力感受性反射的反应,并用ＦＦＴ对ＲＶＬＭ区神经元自发单位放电和血压波进行频域的相干性分析,以判断是具有心节律。还分析了ＲＶＬＭ区单位放电变异性与心率变异性的相干性。结果显示：ＲＶＬＭ区大多数神经元对电刺激中脑防御反应区呈兴奋反应（６７％）,７０％神经元放电     

中枢神经系统对血压的调节

一、引言中枢神经系统对血压的调节是生理学中一个比较老的题目。上一世纪后期,生理学家开始用刺激躯体传入神经的方法观察血压反射,用逐段切断脑干的方法研究心血管中枢的定位,至今已经一百多年。然而,随着研究技术的不断更新和发展,人们对心血管中枢和各种心血管反射的认识也不断深入和更新。关于心血管神经元的生理特征及其在中枢的所在部位,至今仍是许多生理学家热中于研究的课题。中枢神经系统活动异常和原发性高血压发病的关系,得到了普遍的承认。各种中枢神经递质和调节肽在血压调节和高血压形成中的作用,也受到了广泛的重视。本文仅就心血管中枢、若干心血管反射,以及神经系统与高血压发病的关系等几个问题的研究情况作一概述。二、延髓血管运动中枢的定位     

大鼠延髓腹面尾端加压区与头端加压区心血管效应的差异

雄性Ｗｉｓｔａｒ大鼠５６只,乌拉坦麻醉,双侧脑区微量注射谷氨酸钠,观察延髓腹面尾端加压区（ｃＶＭＰ）与头端加压区（ｒＶＭＰ）心血管效应的差异。结果表明：ｃＶＭＰ的升压效应弱于ｒＶＭＰ,不伴随明显的心率效应,ｒＶＭＰ升压效应强于ｃＶＭＰ兼有明显的心率增加。在谷氨酸钠兴奋作用下,ｒＶＭＰ抑制动脉压力感受反射,而ｃＶＭＰ易化该反射。提示两者对心血管功能的影响具有不同的神经途径和机能意义。     

增食因子对心血管活动的中枢调节

增食因子是一种下丘脑神经肽,最初被认为是一种食欲调节因子。现有的研究表明,增食因子可作用于中枢神经系统的不同位点,以多种方式调节交感神经传出,影响心血管活动。增食因子基因敲除小鼠表现为基础血压降低和防御反应减退。本文综述增食因子对心血管活动中枢调节的研究进展。     

A Biofeedback System of Baroreceptor Cardiac Reflex Sensitivity

The evidence presently available suggests that the parasympathetic nervous system and sympathetic-parasympathetic interactions could play a role in the pathophysiology of cardiovascular disorders and, specifically, in hypertension. A loss of sensitivity of the baroreceptor reflex is one of the fundamental mechanisms underlying the deficits found in parasympathetic cardiac control. The baroreceptor reflex is a basic mechanism for the regulation of blood pressure, a powerful source of vagal afferent input to the central nervous system, and one of the most important physiological mechanisms affecting efferent cardiac vagal activity. This paper describes a computerized system for the on-line analysis of the baroreceptor cardiac reflex function using the noninvasive spontaneous sequence method in the time domain. The system provides feedback of the baroreceptor reflex sensitivity (the change in heart period per unit change in systolic blood pressure) differentially both when the systolic blood pressure is increasing and when it is decreasing. The accuracy of the described system has been tested against the conventional off-line procedure. None of the parameters supplied by the analysis show a significant difference between the on-line and off-line methods. These results confirm the accuracy of the on-line system to analyze baroreceptor cardiac reflex function.     

Central cardiovascular actions of vasopressin in the rat

Arginine vasopressin (AVP) containing neurones and pathways have been localized in various cardiovascular control centers of the central nervous system in rats. AVP influences cardiovascular regulation when injected into various areas of the central nervous system. The blood pressure increases in response to central AVP injections were shown to be initiated by stimulation of central V1-AVP receptors and mediated by stimulation of sympathetic outflow to the periphery. On the other hand, AVP has also been shown to attenuate the pressor responses to electrical stimulation of the mesencephalic reticular formation when injected into the brain ventricular system. In addition, AVP can participate in cardiovascular regulation by modulating baroreceptor reflex sensitivity. We have shown that in rats peripheral (hormonal) AVP can sensitize the heart rate component of the baroreceptor reflex by acting on V2-AVP receptors accessible from the blood, while at the same time central (neuronal) AVP can attenuate the baroreceptor reflex through brain V1-AVP receptors that cannot be reached from the blood. Binding and functional studies favour the existence of V1-AVP receptors in the central nervous system, whereas evidence for central V2-AVP receptors is still scarce. The role of AVP in hypertension remains controversial, but recent evidence suggests that a discordance between the various central and peripheral cardiovascular actions of AVP, rather than its hormonal vasopressor effects, may contribute to the pathogenesis of hypertension.     

Glutamate and GABA in the medial amygdala induce selective central sympathetic/parasympathetic cardiovascular responses

Glutamate and γ-aminobutyric acid (GABA) participate in central cardiovascular control, and are found in the rat posterodorsal medial amygdala (MePD), an area of the forebrain that modulates emotional/social behaviors. Here we tested whether these neurotransmitters in the MePD could change the basal activity, chemoreflex, and baroreflex cardiovascular responses in awake rats. Power spectral analysis and symbolic analysis were used to evaluate these responses. Microinjections of saline, glutamate (2 μg), or GABA (61 ng or 100 μg; n = 5-7 rats per group) did not affect basal parameters or chemoreflex responses. However, baroreflex responses showed marked changes. Glutamate increased power spectral and symbolic sympathetic indexes related to both cardiac and vascular modulations (P < 0.05). In turn, the displacement of the baroreflex half-maximal heart rate (HR) response was associated with a GABA (61 ng) mediated decrease in the upper plateau (P < 0.05). Administration of GABA (61 ng, but not 100 μg) also increased HR variability (P < 0.05), in association with parasympathetic activation. These data add novel evidence that the MePD can promote selective responses in the central regulation of the cardiovascular system, i.e., glutamate in the MePD evoked activation of a central sympathetic reflex adjustment, whereas GABA activated a central parasympathetic one.     

Nervous mechanisms in the regulation of blood sugar

The aim of this paper is to precise the involvement of the nervous system in blood glucose regulation. The relevant mechanisms, triggered by blood glucose changes (increase or decrease of glycemia), intervene through the control of pancreatic and surrenal hormone release on the one hand, and hepatic glucose synthesis on the other hand. The part of various efferents and afferents, sensory endings and central "glucosensitive" neurons was analyzed in different situations. 1) Hyperglycemia increases the activation of the pancreatic parasympathetic fibres and decreases that of the surrenal sympathetic fibres. Hypoglycemia elicits reverse effects in the two types of efferents. 2) Hyperglycemia produces an activation in hepatic efferent vagal fibres and thus an acceleration of glycogen synthesis. Reversely, hypoglycemia stimulates both the hepatic sympathetic efferents and the glucose release by the liver. 3) The gustative receptors and the gastro-intestinal glucoreceptors are stimulated by glucose, which produces an insulin release. 4) The various kinds of afferents modify the efferent control of blood glucose level, through the "glucosensitive" central neurons located in hypothalamic and medullary regions.     

Phase Synchronization of Hemodynamic Variables at Rest and after Deep Breathing Measured during the Course of Pregnancy

Background

The autonomic nervous system plays a central role in the functioning of systems critical for the homeostasis maintenance. However, its role in the cardiovascular adaptation to pregnancy-related demands is poorly understood. We explored the maternal cardiovascular systems throughout pregnancy to quantify pregnancy-related autonomic nervous system adaptations.

Methodology

Continuous monitoring of heart rate (R-R interval; derived from the 3-lead electrocardiography), blood pressure, and thoracic impedance was carried out in thirty-six women at six time-points throughout pregnancy. In order to quantify in addition to the longitudinal effects on baseline levels throughout gestation the immediate adaptive heart rate and blood pressure changes at each time point, a simple reflex test, deep breathing, was applied. Consequently, heart rate variability and blood pressure variability in the low (LF) and high (HF) frequency range, respiration and baroreceptor sensitivity were analyzed in resting conditions and after deep breathing. The adjustment of the rhythms of the R-R interval, blood pressure and respiration partitioned for the sympathetic and the parasympathetic branch of the autonomic nervous system were quantified by the phase synchronization index γ, which has been adopted from the analysis of weakly coupled chaotic oscillators.

Results

Heart rate and LF/HF ratio increased throughout pregnancy and these effects were accompanied by a continuous loss of baroreceptor sensitivity. The increases in heart rate and LF/HF ratio levels were associated with an increasing decline in the ability to flexibly respond to additional demands (i.e., diminished adaptive responses to deep breathing). The phase synchronization index γ showed that the observed effects could be explained by a decreased coupling of respiration and the cardiovascular system (HF components of heart rate and blood pressure).

Conclusions/Significance

The findings suggest that during the course of pregnancy the individual systems become increasingly independent to meet the increasing demands placed on the maternal cardiovascular and respiratory system.     

A neural set point for the long-term control of arterial pressure: beyond the arterial baroreceptor reflex

Arterial baroreceptor reflex control of renal sympathetic nerve activity (RSNA) has been proposed to play a role in long-term control of arterial pressure. The hypothesis that the "set point" of the acute RSNA baroreflex curve determines the long-term level of arterial pressure is presented and challenged. Contrary to the hypothesis, studies on the long-term effects of sinoaortic denervation (SAD) on arterial pressure and RSNA, as well as more recent studies of chronic baroreceptor "unloading" on arterial pressure, suggest that the basal levels of sympathetic nerve activity and arterial pressure are regulated independent of arterial baroreceptor input to the brainstem. Studies of the effect of SAD on the long-term salt sensitivity of arterial pressure are consistent with a short-term role, rather than a long-term role for the arterial baroreceptor reflex in regulation of arterial pressure during changes in dietary salt intake. Renal denervation studies suggest that renal nerves contribute to maintenance of the basal levels of arterial pressure. However, evidence that baroreflex control of the kidney plays a role in the maintenance of arterial pressure during changes in dietary salt intake is lacking. It is proposed that a "baroreflex-independent" sympathetic control system must exist for the long-term regulation of sympathetic nerve activity and arterial pressure. The concept of a central nervous system "set point" for long-term control of mean arterial pressure (CNS-MAP set point), and its involvement in the pathogenesis of hypertension, is discussed.     

Maturation of central autonomic control of the circulation

Postnatal maturation of central neural regulation of cardiovascular function is being examined in developing swine. Three major types of investigations have been undertaken: 1) alterations of inputs from visceral and somatic afferents, e.g., baroreceptor manipulation, stimulation of sciatic nerves; 2) stimulation of central vasoactive sites; 3) subjecting the animals to the stresses of hemorrhage, hypoxia, or hypercapnia. Our findings indicate that cardiovascular reflexes mature at different postnatal ages. For example, the J-receptor reflex had almost the adult pattern of response at birth, whereas the Bezold-Jarisch reflex had a markedly delayed postnatal maturation. Recordings of spontaneous discharge in a major efferent sympathetic supply, i.e., the greater splanchnic nerve, have indicated that neural innervation to the adrenal medulla and splanchnic vasculature is present at birth in piglets.     

Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses

Diet-induced obesity (DIO) attenuates the arterial cardiac baroreceptor reflex, but the mechanisms and sites of action are unknown. This study tested the hypothesis that DIO impairs central aortic baroreceptor pathways. Normal chow control (CON) and high-fat-chow obesity-resistant (OR) and obesity-prone (OP) rats were anesthetized (inactin, 120 mg/kg) and underwent sinoaortic denervation. The central end of the aortic depressor nerve (ADN) was electrically stimulated to generate frequency-dependent baroreflex curves (5-100 Hz) during selective activation of myelinated (A-fiber) or combined (A- and C-fiber) ADN baroreceptors. A mild stimulus (1 V) that activates only A-fiber ADN baroreceptors induced robust, frequency-dependent depressor and bradycardic responses in CON and OR rats, but these responses were completely abolished in OP rats. Maximal activation of A fibers (3 V) elicited frequency-dependent reflexes in all groups, but a dramatic deficit was still present in OP rats. Activation of all ADN baroreceptors (20 V) evoked even larger reflex responses. Depressor responses were nearly identical among groups, but OP rats still exhibited attenuated bradycardia. In separate groups of rats, the reduced heart rate (HR) response to maximal activation of ADN A fibers (3 V) persisted in OP rats following pharmacological blockade of β(1)-adrenergic or muscarinic receptors, suggesting deficits in both parasympathetic nervous system (PNS) and sympathetic nervous system (SNS) reflex pathways. However, the bradycardic responses to direct efferent vagal stimulation were similar among groups. Taken together, our data suggest that DIO severely impairs the central processing of myelinated aortic baroreceptor control of HR, including both PNS and SNS components.     

The variability characteristics of the arterial pressure in man and animals

The development of computer monitoring methods over haemodynamic parameters has made possible on objective quantitative estimation of blood pressure (BP) variability in humans and animals which can have both periodic and aperiodic feachers. The spectral analysis of spontaneous BP fluctuations reveals presence of several power peaks main of which, as well as in heart rate variability, reflect sympathetic and parasympathetic activity. Both in hypertensive patients and animal models of arterial hyper tension BP variability is higher, but its relationship with BP level is not realized in a simple causal scheme. Observations in prehypertensive period demonstrate an opportunity of dissociation between rates of BP level and variability increase. The pharmacological analysis permisses to suggest the sympathetic activation as the main cause of BP destabilization. Despite a leading role of baroreceptor reflex (BR) in damping of evoked BP fluctuations, its role in regulation of spontaneous variability seems to be ambiguous. The studies excluding episodes of locomotor and other activities from the curve analysis do not confirm a correlation between BP variability and BR gain. The spectral analysis of BP lability in animals with denervated mechanoreceptor zones has revealed BR effective control only of a low and superlow frequency areas (less than 0.07 Hz). The study of the regional blood flows in sinoartic denervated rats has concluded that the increase of their autonomy is the main reason of BP lability. The offset of BR efferent limb by ganglionic blocking agents or desympathization leads to analogical BP lability. Thus, BP variability seems to be a reflection of functional efficiency of BP stabilization mechanisms. Considering that on its origin, connections with other haemodynamic parameters, amplitude and frequency characteristics is a complex phenomenon, no one of mechanisms is an universal instrument of its regulation.