刺激肾神经传入纤维的降压反应与颈动脉窦压力感受性反射的相互作用

在麻醉兔,研究了刺激肾神经传入纤维与颈动脉窦压力感受性反射在减压反射中的相互作用。电刺激肾神经传入纤维引起平均动脉压(MAP)下降,下降程度在一定范围有赖于刺激频率。当颈动脉窦被隔离和主动脉神经切断后,随着颈动脉窦内压逐渐升高,刺激肾神经传入纤维引起的减压反应不断减弱。在45至135mmHg 之间的7个颈动脉窦内压(ISP)水平,刺激肾神经传入纤维,并画出刺激前和刺激时的 ISP-MAP 关系曲线。在颈动脉窦内压为75至105mmHg 之间,刺激肾神经传入纤维显著降低 ISP-MAP 关系曲线的斜率和对ISP 的平均动脉压反应范围。这些结果提示:(1)颈动脉窦压力感受器的传入冲动可调制刺激肾神经传入纤维的降压反应,在一定范围内与颈动脉窦内压呈反比;(2)刺激肾神经传入纤维明显减弱颈动脉窦的压力感受性反射。     

颈动脉内注入腺苷对呼吸,血压和肾交感神经活动的影响

在33只麻醉家兔,观察了颈动脉内注入腺苷所诱发的平均动脉压、心率,呼吸和肾交感神经活动的变化。结果如下:(1)颈动脉内注入腺苷后,平均动脉压呈剂量依赖性下降;呼吸加快,深度变化不明显,剪断窦神经后注入腺苷,仍引起平均动脉压下降,而呼吸变化消失。(2)隔离的颈动脉窦灌流液内加入腺苷后,平均动脉压下降,心率减慢;颈动脉体(CB)失活后反应消失。(3)将腺苷灌注到颈动脉窦区后,平均动脉压下降,肾交感神经传出放电活动增加,CB 失活或剪断窦神经后,反应消失。由此提示:腺苷可作为兴奋 CB 的一种物质,引起平均动脉压降低,心率减慢,呼吸加强和肾交感神经放电活动增加。     

刺激家兔肾内感受器和肾传入神经的血流动力学效应

在39只麻醉家兔观察刺激肾脏机械和化学感受器以及电刺激肾传入神经的血流动力学效应。增加输尿管压8—22mmHg 及经输尿管向肾盂内逆向灌注 NaCl(1.0 mol/L)及 KCl(0.15mol/L)溶液时,引起平均动脉压(MAP)和心率(HR)下降;切断双侧缓冲神经后,MAP 降低更为显著。电刺激肾传入神经时,HR 减慢,MAP、肠系膜动脉和后肢动脉灌流压降低,左心室收缩压及其微分值下降,心输出量(CO)和总外周阻力(TPR)减小;切断双侧窦神经和减压神经后,除 HK、CO 和 TPR 外,其余各血流动力学指标的减弱更为显著。由此提示,动脉压力感受器反射对肾传入神经激活的心血管效应有缓冲作用。     

刺激家兔颈交感神经对颈动脉窦反射的影响

在36只麻醉家兔观察了电刺激颈交感神经(CSN)对颈动脉窦压力感受器(CSB)活动的影响。所得结果如下:(1)电刺激 CSN 可使夹闭颈动脉引起的加压反射消失或倒转,△BP 从刺激前的 39.5±3.6mmHg 变为刺激时的-0.31±5.4mmHg(P<0.001)。(2)在电刺激CSN 时,静注新福林所诱发的颈动脉窦压力感受器-心率反射增强,表现为反射性心率减慢较刺激前更为明显。(3)在以50—200mmHg 的压力充胀两侧颈动脉窦的条件下,刺激 CSN 引起窦内压与平均动脉压的关系曲线下移,与刺激前曲线相比有明显差异(P<0.01)。(4)切断 CSN 后,动脉血压有所升高,提示 CSN 对 CSB 活动有紧张性调节作用。以上结果比较明确地表明家兔 CSN 对 CSB 活动有调节作用。此作用可能是 CSN 作用于窦壁平滑肌而间接引起的。     

刺激家兔腹部迷走神经外周端引起的降压作用

本文对电刺激家兔腹部的迷走神经外周端所引起的降压反应进行了研究。在121只家兔中的实验结果表明:电刺激腹部迷走神经外周端可引起动脉压、小肠和后肢的灌流压同时降低,而心率则无明显变化。这一降压反应发生时,小肠静脉血中的组织胺含量较刺激前明显升高,然后恢复;将小剂量的组织胺 H_1受体阻断剂扑尔敏、非乃根和 H_2受体阻断剂甲氰咪胍(Cimetidine)分别注入肠系膜上动脉均能减弱刺激腹部迷走神经外周端引起的动脉压和小肠灌流压的降低。心得安能削弱此降压反应,而阿托品无效;切断两侧内脏大神经能显著削弱刺激腹部迷走神经外周端引起的降压反应。此残余的降压反应在注入抗组织胺剂后完全消失。由此推论,刺激家兔腹部迷走神经外周端引起的降压反应是通过中枢和外周两方面因素的作用,使血管舒张,外周阻力降低而实现的。     

房水平单向活瓣式补片对老年先天性心脏病合并重度肺动脉高压 的临床效果分析

目的:探究房水平单向活瓣式补片对老年先天性心脏病伴重度肺动脉高压患者的作用疗效。方法:选取我院心血管科收治的先天性心脏病伴重度肺动脉高压患者80例,随机分为对照组和实验组。对照组40例,予以常规基础药物治疗(波生坦);实验组,在基础药物治疗两个疗程后,采用房水平单向活瓣式补片进行手术治疗。比较两组患者治疗前后的肺动脉压(PAP)、体动脉压(SAP)、肺动脉压/体动脉压(PAP/SAP)、动脉血氧分压(Pa O2)、二氧化碳分压(Pa CO2)及吸氧浓度、右室收缩末期内径变化情况。结果:治疗后,与对照组比较,实验组肺动脉压下降幅度较大(P0.05);与治疗前比较,实验组肺动脉压与体动脉压的比值显著下降,且优于对照组(P0.05);治疗后,实验组动脉血氧分压、二氧化碳分压以及吸氧浓度显著优于对照组(P0.05);治疗后,实验组患者右室收缩末期内径显著小于对照组(P0.05);随访结果:实验组死亡1例、术后活瓣坏死2例、其余37例病情均转好且无复发情况;对照组死亡4例、出现各项并发症16例、剩余20例病情转好。结论:房水平单向活瓣式补片法可有效改善患者的肺动脉压、体动脉压、动脉血氧分压、二氧化碳分压及吸氧浓度、右室收缩末期内径及6 min步行距离,对老年先天性心脏病伴重度肺动脉高压患者疗效显著。     

双套管水柱法监测家兔平均动脉压

目的探讨双套管水柱的构成,用双套管水柱法测定家兔的平均动脉压,观察静脉麻醉对家兔血压的影响。方法双套管水柱的组成和使用,并在局麻或全麻下,用双套管水柱法及RM6000多导生理记录仪有创连续监测家兔平均动脉压,用T检验分析两种方法所测数据。结果静脉麻醉后家兔的平均动脉压从术前（149.88±1.77）cmH2O（局麻清醒安静状态下）下降到（127.60±4.09）cmH2O,有显著差异（P〈0.05）。双套管水柱法及RM6000多导生理记录仪测得结果间无显著性差异（P〉0.05）。结论用双套管水柱法可准确地、动态地监测麻醉家兔平均动脉压。静脉麻醉对家兔血压有明显的影响。     

老年男性原发性高血压患者脉压与颈动脉狭窄的相关分析

目的：探讨老年男性原发性高血压（EH）患者脉压（PP）与动脉粥样硬化性颈动脉狭窄（CS）的关系。方法：对入选的157例伴有颈动脉粥样硬化的老年男性EH患者行颈动脉超声检查,并收集行颈动脉超声检查前1年内的多次血压水平及临床资料,根据颈动脉狭窄程度分为：CS〈50％组（n=66）及CS≥50％组（n=91）,并进一步将颈动脉狭窄程度分级（I—V级）,分析颈动脉狭窄的危险因素及与脉压的相关性。结果：①CS≥50％组收缩压（SBP）及PP显著高于CS〈50％组,而舒张压（DBP）显著低于CS〈50％组（P〈0．05）,CS≥50％组的独立危险因素是外周动脉疾病（OR：4．543,95％CI：1．415．14．590）及脉压（OR：1．096,95％CI：1．038．1．157）;②CS分级与PP（r=0．402,P〈0．01）及血浆纤维蛋白原（FIB）（r=0．200,P〈0．05）呈正相关,经校正年龄、体重指数（BMI）、SBP、DBP、总胆固醇（TO）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-c）、低密度脂蛋白胆固醇（LDL-c）、D-二聚体（D-dimer）、血尿酸（UA）、空腹血糖（FBG）、氨基酸末端脑利钠肽前体（NT-proBNP）、总胆红素（TBIL）及直接胆红素（DBIL）等危险因素后,CS分级仍与PP及FIB有关。结论：老年男性原发性高血压患者脉压与颈动脉狭窄有关,治疗高血压的同时应当尽量减小脉压。     

孤束核组胺受体参与大鼠脑室注射组胺对颈动脉窦反射的抑制

目的:探讨孤束核(NTS)组胺(HA)受体在脑室注射(ICV) HA对颈动脉窦压力感受性反射(CBR)影响中的作用.方法:分离麻醉大鼠的双侧颈动脉窦区,将不同窦内压(ISP)与其对应的平均动脉压(MAP)值进行Logistic五参数曲线拟合,求得ISP-MAP关系曲线及其特征参数,观察ICV HA以及预先在NTS微量注射HA受体拮抗剂对CBR的作用.结果:ICV HA (100 ng)导致ISP-MAP关系曲线显著上移,ISP和增益关系曲线中部明显下移,反射参数中阈压、饱和压和最大增益时的窦内压值增大,MAP反射变动范围及反射最大增益减小.预先向NTS内注射H1或H2受体拮抗剂氯苯吡胺(CHL,0.5 μg)或西咪替丁(CIM,1.5 μg),均可明显减弱HA的上述效应,CIM的这种减弱作用不如CHL的显著.结论:脑室给HA使CBR产生快速重调定,反射敏感性下降,NTS的H1和H2受体尤以H1受体在ICV HA抑制CBR的机制中发挥重要作用,下丘脑-NTS的HA能通路可能是HA调节CBR的下行通路之一.     

刺激家兔腓深神经对颈动脉体化学感受性升压反射的调整作用

在麻醉、制动和人工通气的79只家兔上观察到,由颈动脉内注射氰化钠(NaCN)引起的颈动脉体化学感受性升压和肾交感放电增强反应(简称颈动脉体反应),在刺激腓深神经模拟电针“足三里”穴位时发生明显改变。此种改变与腓深神经刺激前颈动脉体反应的强度有关。在吸入气中加入CO_2或切断双侧颈迷走神经以提高心血管中枢活动水平时,颈动脉体反应增强,此时刺激腓深神经可使此反应减弱(P<0.01)。在迷走神经完整、增加潮气量使血液CO_2分压降低,使颈动脉体反应减弱时,刺激腓深神经可使颈动脉体反应增强(P<0.01)。上述结果表明,刺激腓深神经,对颈动脉体化学感受性心血管反应具有调整作用,这种作用与心血管中枢反应性密切相关。而后者又受到迷走神经传入冲动、PaCO_2水平和麻醉深度调制。     

Exercise training and the arterial baroreflex

To test the hypothesis that endurance training would attenuate the carotid sinus baroreflex in rats, studies were undertaken with 25 nontrained (NT) and 22 trained (T) male Sprague-Dawley rats that were exercised for 11-14 wk. Maximal O2 consumption was significantly increased 10% after training. The left carotid sinus region was functionally isolated in anesthetized animals. Subsequently, static carotid sinus pressure was raised in 20-Torr increments from 95 Torr until a maximal response in systemic arterial pressure and regional blood flows was recorded. Compared with the NT group, baroreflex control of blood pressure and calculated regional resistance of the T animals was less responsive to changes in carotid sinus pressure. Resting blood pressure, heart rate, and changes in peripheral blood flow velocity were similar for the two groups. Peripheral sensitivity to phenylephrine-HCl and hexamethonium bromide were also similar in the T and NT groups. It was concluded that the arterial baroreflex control of blood pressure was attenuated by exercise training. These findings support the concept that the trained individual is at disadvantage during hypotensive episodes and that endurance training will attenuate the sympathetic component of the arterial baroreflex.     

Unloading arterial baroreceptors causes neurogenic hypertension

We developed a new model to examine the role of arterial baroreceptors in the long-term control of mean arterial pressure (MAP) in dogs. Baroreceptors in the aortic arch and one carotid sinus were denervated, and catheters were implanted in the descending aorta and common carotid arteries. MAP and carotid sinus pressure (CSP) averaged 104 +/- 2 and 102 +/- 2 mmHg (means +/- 1 SE), respectively, during a 5-day control period. Baroreceptor unloading was induced by ligation of the common carotid artery proximal to the innervated sinus (n = 6 dogs). MAP and CSP averaged 127 +/- 7 and 100 +/- 3 mmHg, respectively, during the 7-day period of baroreceptor unloading. MAP was significantly elevated (P < 0.01) compared to control, but CSP was unchanged. Heart rate and plasma renin activity increased significantly in response to baroreceptor unloading. Removal of the ligature to restore normal flow through the carotid resulted in normalization of all variables. Ligation of the carotid below a denervated sinus (n = 4) caused a significant decrease in CSP but no systemic hypertension. These results indicate that chronic unloading of carotid baroreceptors can produce neurogenic hypertension and provide strong evidence that arterial baroreceptors are involved in the long-term control of blood pressure.     

The influence of carotid sinus pressure on plasma atrial natriuretic peptide in anaesthetized rabbits

The effect of changes in carotid sinus perfusion pressure on plasma immunoreactive atrial natriuretic peptide (IR-ANP) was examined in anaesthetized rabbits, and the role of arterial pressure in mediating the changes in IR-ANP was assessed. Plasma IR-ANP was significantly greater (101.7 +/- 24.3 pg ml-1) when carotid sinus pressure was 60 mmHg than when it was 160 mmHg (27.1 +/- 8.6 pg ml-1). Mean arterial pressure (MAP) was significantly greater when carotid sinus pressure was controlled at 60 mmHg compared to when it was 160 mmHg, but right atrial pressure (RAP) was not significantly different at the two carotid sinus pressures. The administration of hexamethonium attenuated the changes in MAP and heart rate (HR) which occurred in response to alterations in carotid sinus pressure, and abolished the change in plasma IR-ANP. The results suggest that an inverse relationship exists between carotid sinus pressure and plasma IR-ANP, and that the release of ANP in response to a reduction of carotid sinus pressure is mediated by the associated haemodynamic changes.     

Influence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbits.

Substance P (SP) is abundant in the carotid sinus nerve (CSN) and has been implicated in baro- and chemoreceptor reflexes. We examined the effect of SP on blood pressure, heart rate, phrenic nerve activity, hindlimb perfusion pressure, and cardiac contractile strength in urethane-anesthetized rabbits with bilaterally cut cervical sympathetic, vagus, and aortic depressor nerves. Retrograde simultaneous injection of SP (0.5-2.7 micrograms/kg in 0.2-0.3 ml saline) into both carotid sinus areas via the internal carotid arteries decreased blood pressure (by 56%), heart rate (by 13%), cardiac contractility (by 25%) and phrenic nerve activity (by 77%). The effect on hindlimb perfusion pressure was variable. There was both a reflex effect and direct hindlimb vasodilation. In another group of rabbits, the carotid sinus areas were vascularly isolated and perfused with SP (0.19 micrograms/min dissolved in Locke's solution) or Locke's solution alone for 5 min. While carotid sinus perfusion pressure was maintained in the range of 80-120 mmHg, mean arterial blood pressure, heart rate, and unit activity from the CSN were recorded. SP increased the activity of 11 of 18 baroreceptor fibers and inhibited all of 20 chemoreceptor fibers. SP decreased mean arterial blood pressure and heart rate, but the changes were less than those obtained with injection of SP into nonisolated carotid sinus arteries because systemic effects of SP, which in some cases counteracted the reflex effects, were eliminated.     

Effect of gamma-aminobutyric acid and phenibut on the central links of the vascular reflexes with chemo- and mechanoreceptors of the aorto-carotid zone]

Experiments were conducted on decerebrated cats. A depressive effect of gamma-aminobutyruc acid (GABA)--100--200 mg/kg and its phenyl derivative phenibut--20 mg/kg--on depressive reactions of the systemic arterial pressure and on the inhibition of spontaneous bioelectrical activity in the renal nerve occurring in stimulation of the mechanoreceptors of the carotid sinus and of the sinus and depressor nerve afferents (having a mechanoreceptor modality) was demonstrated. Pressor reactions of the systemic arterial pressure and evoked bioelectrical activity were enhanced in the renal nerve in stimulation of chemoreceptors of the carotid sinus following administration of the same GABA and phenibut doses. The data obtained are interpreted from the aspect of a deprimating action of GABA and phenibut in the area of the paramedian reticular nuclei of the medulla oblongata.     

Fluid structure interaction with contact surface methodology for evaluation of endovascular carotid implants for drug-resistant hypertension treatment

Drug-resistant hypertensive patients may be treated by mechanical stimulation of stretch-sensitive baroreceptors located in the sinus of carotid arteries. To evaluate the efficacy of endovascular devices to stretch the carotid sinus such that the induced strain might trigger baroreceptors to increase action potential firing rate and thereby reduce systemic blood pressure, numerical simulations were conducted of devices deployed in subject-specific carotid models. Two models were chosen--a typical physiologic carotid and a diminutive atypical physiologic model representing a clinically worst case scenario--to evaluate the effects of device deployment in normal and extreme cases, respectively. Based on the anatomical dimensions of the carotids, two different device sizes were chosen out of five total device sizes available. A fluid structure interaction (FSI) simulation methodology with contact surface between the device and the arterial wall was implemented for resolving the stresses and strains induced by device deployment. Results indicate that device deployment in the carotid sinus of the physiologic model induces an increase of 2.5% and 7.5% in circumferential and longitudinal wall stretch, respectively, and a maximum of 54% increase in von Mises arterial stress at the sinus wall baroreceptor region. The second device, deployed in the diminutive carotid model, induces an increase of 6% in both circumferential and longitudinal stretch and a 50% maximum increase in von Mises stress at the sinus wall baroreceptor region. Device deployment has a minimal effect on blood-flow patterns, indicating that it does not adversely affect carotid bifurcation hemodynamics in the physiologic model. In the smaller carotid model, deployment of the device lowers wall shear stress at sinus by 16% while accelerating flow entering the external carotid artery branch. Our FSI simulations of carotid arteries with deployed device show that the device induces localized increase in wall stretch at the sinus, suggesting that this will activate baroreceptors and subsequently may control hypertension in drug-resistant hypertensive patients, with no consequential deleterious effects on the carotid sinus hemodynamics.     

Plasma vasopressin response to haemorrhage in the anaesthetized rabbit

In chloralose-urethane anaesthetized rabbits the acute circulatory and plasma vasopressin (pAVP) responses to moderate haemorrhage of 6 mL/kg body weight (10% blood volume) were followed after serial section of the aortic, vagus, and carotid sinus nerves. With all nerves intact, haemorrhage resulted in significant increases in pAVP, accompanied by decreases in systemic arterial pressure and right atrial pressure. With subsequent section of each afferent nerve, pAVP still increased in response to haemorrhage regardless of the order of nerve section. These results suggest that, in the anaesthetized rabbit, there is a further component of the pAVP response to haemorrhage, in addition to those carried in the aortic, vagus, and carotid sinus nerves.     

Head Turning-Induced Hypotension in Elderly People

Carotid sinus hypersensitivity has a high prevalence in the elderly and is a possible cause of falls. In carotid sinus hypersensitivity, external triggers cause sudden reductions in blood pressure, leading to dizziness or syncope, resulting in falls. Turning of the head is considered an important example of such an external trigger in everyday life, wherein rotation of the neck is thought to manipulate the hypersensitive carotid sinus. However, direct evidence for this is lacking. The aim of this study was to investigate the effects of head turning in elderly with carotid sinus hypersensitivity. We performed a prospective, observational study in 105 elderly patients who visited a geriatric falls clinic in a university teaching hospital and in 25 community dwelling healthy elderly subjects. Continuous measurements of blood pressure and heart rate (Finapres) were performed before, during, and after head turning. Head turning-induced hypotension was defined as a drop in systolic blood pressure of at least 20 mmHg during head turning. Carotid sinus hypersensitivity was examined with carotid sinus massage. We also tested for two other common geriatric hypotensive syndromes, orthostatic hypotension and post prandial hypotension, using active standing and a meal test. All three hypotensive syndromes were defined using consensus definitions. Head turning resulted in hypotension in 39% of patients (mean systolic blood pressure drop 36 mm Hg) and in 44% of the healthy elderly, irrespective of the direction of the head movement. Carotid sinus hypersensitivity was associated with head-turning induced hypotension (OR= 3.5, 95% CI= 1.48 to 8.35). We conclude that head turning is indeed an important cause of sudden drops in blood pressure in elderly with carotid sinus hypersensitivity.     

Baroreceptor influence on a spinal cardiovascular reflex

A stretch of the walls of the thoracic aorta, performed in vagotomized cats without obstructing aortic flow, induces increases in heart rate, myocardial contractility, and arterial pressure. These reflex responses are still present after high spinal section. Cats under chloralose-urethane anesthesia were vagotomized and one carotid sinus was isolated and perfused with arterial blood at constant flow. The contralateral carotid sinus nerve and both aortic nerves were sectioned. A stretch of the walls of the thoracic aorta between the 7th and 10th intercostal arteries induced a reflex increase in mean arterial pressure 29 +/- 2 mmHg (mean +/- SE). Stepwise increases of carotid sinus pressure (CSP) or electrical stimulation of the carotid sinus nerve induced stepwise decreases of this reflex response. At maximal baroreceptor stimulation (CSP 212 +/- 9 mmHg) the reflex response to aortic stretch was reduced by 42%. These experiments show that this spinal cardiovascular reflex is at least partially under the inhibitory control of the baroreceptor input.     

Baroreflex responsiveness is maintained during isometric exercise in humans

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) "anticipation" of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.