实验性心肌缺血时的某些内感受性反射

在29只麻醉开胸犬身上,观察了急性心肌抉血对某些内感受性反射的影响,主要结果如下:(1)在阻断左前降冠状动脉分支而致急性心肌缺血期间,颈总动脉闭塞性加压反射显著减弱;切断两侧颈部迷走神经后,这一反射减弱不再出现。(2)Valsalva 试验时所诱发的反射性血压增高(超射相),在心肌缺血期间也明显减弱。(3)在急性心肌缺血过程中,肾交感神经传出放电明显减少,由此表明血管运动中枢活动受到抑制。(4)与压力感受器反射不同,颈动脉内注射烟碱(8微克/公斤)所致的化学感受性加压反射在心肌缺血期间保持不变。(5)静脉内注射去甲肾上腺素(1微克/公斤)的加压效应,在心肌缺血前后无明显差异。根据以上结果,似可认为,心肌缺血通过激活心脏迷走神经传入纤维而抑制血管运动中枢的活动,而这种抑制效应可能在心源性休克发生机制中起重要作用。     

大鼠脑室注射P物质引起的血压升高与脑啡肽和β-内啡肽有关

给乌拉坦麻醉大鼠侧脑室注射P物质(SP)10μg 引起的升压效应,可被脑室注射纳洺酮15μg 部分阻断。将抗β-内啡肽抗血清、抗甲啡肽抗血清及抗亮啡肽抗血清各10μl 分别注入侧脑室预处理60min 后,再注入 SP,其升压效应明显减弱;而抗强啡肽抗血清则对其无影响。上述结果提示:大鼠脑室注射 SP 引起的升压效应,可能是通过释放β-内啡肽和脑啡肽实现的。     

暴露于高压氧时大鼠纹状体和下丘脑内L—Enk含量的变化

本研究目的在于探讨大鼠氧惊厥时,纹状体和下丘脑内亮-脑啡肽(L-Enk)含量的变化。实验中将32只雄性大鼠随机分为4组:常压空气组、高压常氧氮组、高压氧未惊厥组和高压氧惊厥组。用放射免疫法测定了纹状体和下丘脑内L-Enk含量。结果显示,在高压氧环境中暴露的大鼠纹状体和下丘脑内L-Enk含量明显高于常压空气组和高压常氧氮组;且增高到一定水平时发生惊厥。实验结果提示,动物惊厥与纹状体和下丘脑中L-Enk含量的增加呈正相关,而与高压氧环境及加减压方式无显著关系。     

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.     

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。     

刺激兔下丘脑诱发的防御反应和室性期前收缩

电刺激兔下丘脑近中线区可以引起血压升高、肢体血流量增多、内脏血流量减少、瞳孔扩大和呼吸急促、鼻翼扇动、四肢爬动等一系列类似于猫发生防御反应时的植物、躯体性反应,但其中肢体血流增多反应不能为阿托品所阻断。在出现上述反应的同时可出现心交感活动亢进、产生室性期前收缩等心律失常。摘除双侧星状神经节后,刺激下丘脑诱发的室性期前收缩(HVE)几乎消失,升压反应也减弱。在颈部切断双侧迷走神经可使 HVE 增多、升压反应增强,静脉注射阿托品(0.2mg/kg)不产生 HVE 增多和升压反应增强的效应。根据上述结果,可以认为兔下丘脑也存在着“防御反应区”,HVE 主要是兴奋了防御反应区造成心交感活动亢进所致。迷走神经对 HVE 有抑制作用,其效应可能与传入纤维的活动有关。     

内毒素休克家兔脑区、脑脊液、血浆中脑啡肽含量的改变及纳洛酮的抗休克作用

本工作在戊巴比妥钠麻醉的家兔上进行。采用夹闭肠系膜上动脉阻断血流方法建立内毒紫休克的实验模型。用放射免疫分析法测定了休克前后脑区、脑脊液及血浆中脑啡肽含量的变化,并观察了脑室或静脉注射纳洛酮的抗休克效应。结果如下:1.休克时,下丘脑、延脑、桥脑的亮脑啡肽含量显著升高,中脑无明显变化、丘脑、纹状体下降。脑脊液和血浆中亮脑啡肽明显增加。外周静脉血与肾静脉血中无显著差别。2.侧脑室或静脉注射纳洛酮,均可使休克动物的血压回升,延长存活时间。脑室注射的升压数值略大,维持升压时间也较长。实验结果提示:脑啡肽参与内毒素休克过程。断阿片样物质的作用,可能是治疗内毒素休克的一个途径。     

吗啡和内啡素对摄食活动的影响

人们早已发现,下丘脑控制摄食行为。近年来的研究结果表明,存在于中枢神经系统,特别是下丘脑的一些单胺和神经肽类,参与摄食活动的调节,内源性阿片样物质(e(?)dogenous opiate like substance),亦称内啡素(endorphins)便是其中的一种。一、脑内注射吗啡或内啡素可增加摄食β-内啡肽被发现不久,有人发现将它注入大鼠下丘脑的腹内侧核引起摄食增加,并持续1.5小时以上。后来,Tepperman等和Reid等又证明,向该部位注射吗啡(2.7～10.6nMol)也有同样的效应,注射后3小时最明显。Morley等向大鼠侧脑室内注射强啡肽(1～10μg),间隔20分钟后摄食增加;人工合成的脑啡肽类似物——2-丙氨酸甲硫脑啡肽(dalamet)亦有这种作用。在上述实验中,预先或同时中枢或外周给予纳洛酮,则可减弱     

兔肾性高血压时的动脉压力感受器反射

14只雄性家兔在双肾缩扎术后12周,经氨基甲酸乙酯静脉麻醉,分别在缓冲神经完整、切断两侧减压神经或切断两侧窦神经后静注新福林或硝普钠升降血压以改变动脉压力感受器活动,观察其心率、后肢血管阻力和肾交感神经活动的反射性变化,并与正常血压兔的反射效应相比较。主要结果如下:(1) 动物双肾动脉缩扎后12周,平均动脉血压(131±9mmHg)较正常动物血压(95±10mmHg)有显著升高(P<0.001);(2) 缓冲神经完整时,新福林和硝普钠升降血压诱发的心率反射性变化与正常血压动物相比显著减弱(P<0.001),而后肢血管阻力和肾交感神经活动的反射性调节无明显改变,表明肾性高血压动物的心率反射性调节与外周循环的反射性调节机能不相平行;而由股动脉内直接注射新福林或硝普钠时,股动脉灌流压的增减幅度与正常血压动物相比并无明显差异;(3) 切断两侧减压神经或切断两侧窦神经后,在正常动物仅使反射性心率调节作用减弱,而后肢血管阻力和肾交感神经活动的反射性调节无明显改变;但在高血压动物,除心率的反射性调节进一步减弱外,新福林和硝普钠升降血压时后肢血管阻力和肾交感神经活动的反射性调节效应也显著地减弱(P<0.001),提示肾性高血压时动脉压力感受器反射的潜在调节能力降低。由此似表明,肾性高血压时动脉压力感受器反射     

兔颈动脉窦和主动脉弓压力感受器反射效应的比较研究

对81只麻醉兔,在静脉注射新福林和硝普钠升降血压而改变动脉压力感受器活动的条件下,观察心率,后肢血管阻力和肾交感神经活动的反射性变化。主要结果如下:(1) 由新福林升高血压时,心率减慢、后肢血管阻力降低和肾交感神经活动抑制;硝普钠降低血压时引起相反效应。各指标的反射性变化有良好的可重复性。(2) 切断两侧减压神经或切断两侧窦神经后,静注新福林和硝普钠诱发的心率反射性变化均显著减弱(P<0.01);切断两侧减压神经较切断两侧窦神经后减弱得更为明显,其中对于新福林升压时的心率减慢反应差异显著(P<(0.05)。相反,对于新福林和硝普钠引起的后肢血管阻力反射性变化,与缓冲神经部分切断之前相比无明显差异;在对照肾交感神经活动已增高的基础上,硝普钠降压时肾交感神经活动的反射性兴奋效应降低,而新福林升压时的肾交感神经活动反射性抑制效应与神经切断前相比无明显差异。(3) 缓冲神经全部切断(SAD)后,新福林和硝普钠引起的平均动脉血压(MAP)变动幅度显著增大(P<0.05)。此时心率、后肢血管阻力和肾交感神经活动的反射调节效应均明显减弱(P<0.001)。(4) 进一步切断两侧迷走神经后,残留的反射效应即行消失。 以上结果表明,颈动脉窦和主动脉弓压力感受器传入以单纯相加的方式对心率进行反射性调节,以主     

The effect of afterload on the cardiodepressor reflex response to coronary artery occlusion in dogs

The acute hemodynamic responses to anterior and posterior wall ischemia were examined at different afterloads in 30 open-chest anaesthetized dogs. Regional and global left ventricular responses to acute ischemia were also measured before and following bilateral cervical vagotomy in 18 dogs. As the preocclusion afterload (mean aortic pressure) was progressively raised with intravenous methoxamine, a significant decrease in stroke volume occurred following circumflex artery occlusion, whereas no change in stroke volume occurred following occlusion of the left anterior descending artery. Bilateral cervical vagotomy completely inhibited the decrease in stroke volume during circumflex occlusion at high afterload. Vagotomy had no effect on the hemodynamic response to acute anterior wall ischemia. Reversible cold vagal block in paced hearts at high afterload unmasked compensatory inotropy in the nonischemic anterior myocardial segment during circumflex occlusion. Restoring vagal tone by rewarming attenuated the fractional shortening of the nonischemic segment. The results indicate that a relationship exists between myocardial wall tension and reflex cardioinhibition during acute posterior wall but not anterior wall ischemia in dogs.     

缓冲神经在电针抑制犬急性实验性高血压中的作用

在切除双侧窦神经与主动脉弓神经的慢性犬,血压很快回复至对照水平,但较易波动。在此种犬静脉匀速注射去甲肾上腺素造成高血压状态时,电针“足三里”不再有明显降压作用。在麻醉犬静脉勻速注射去甲肾上腺素时,肾交感冲动随血压上升而受到明显抑制,然后在16分钟内逐渐回升。血压上升时呼出气 CO_2百分比明显升高,伴随动脉血 CO_2分压升高而 O_2分压降低。在切除缓冲神经后再注射去甲肾上腺素时,肾交感冲动未见明显变化。在清醒犬静脉匀速注射去甲肾上腺素时,动脉血 O_2分压也有明显降低,而注射苯肾上腺素时,血 O_2分压很少改变。电针“足三里’对苯肾上腺素性高血压的降压作用不明显。且心得安可阻断电针对去甲肾上腺素性高血压的降压作用。此外,电针能抑制山梗菜碱所致的化学感受性升压反射,此种抑制作用可为静脉注射纳洛酮所阻断。结果表明,去甲肾上腺素除能收缩血管升高血压,增加压力感受性传入冲动外,还能刺激新陈代谢,改变血液气体成分而引起化学感受性升压反射。电针“足三里”主要因能抑制化学感受性反射而能降压,仅有压力感受性传入冲动的增多并不能使电针具有明显降压效应。     

Both central command and exercise pressor reflex reset carotid sinus baroreflex

In decerebrate unanesthetized cats, we determined whether either "central command," the exercise pressor reflex, or the muscle mechanoreceptor reflex reset the carotid baroreflex. Both carotid sinuses were vascularly isolated, and the carotid baroreceptors were stimulated with pulsatile pressure. Carotid baroreflex function curves were determined for aortic pressure, heart rate, and renal vascular conductance. Central command was evoked by electrical stimulation of the mesencephalic locomotor region (MLR) in cats that were paralyzed. The exercise pressor reflex was evoked by statically contracting the triceps surae muscles in cats that were not paralyzed. Likewise, the muscle mechanoreceptor reflex was evoked by stretching the calcaneal tendon in cats that were not paralyzed. We found that each of the three maneuvers shifted upward the linear relationship between carotid sinus pressure and aortic pressure and heart rate. Each of the maneuvers, however, had no effect on the slope of these baroreflex function curves. Our findings show that central command arising from the MLR as well as the exercise pressor reflex are capable of resetting the carotid baroreflex.     

刺激迷走神经向中端对大鼠不同脑区脑啡肽含量的影响

自从1975年(Hughes et al. 1975)发现脑啡肽以来,经多方面研究已认为脑啡肽可能是一种神经递质,它具有多种生理功能(范少光、汤健,1978)。据新近文献报道,脑啡肽与催产素及加压素三者具有共同存在的并存关系(Martin and Voigt。1981)。 已经证明,刺激迷走神经向中端,可引起脑内释放乙酰胆硷,从而促使神经垂体释放压加素和催产素,肾上腺释放肾上腺素(Chang, et al. 1937;1961,1964;吕运明等1965,1977;唐正荣1981)。但是,刺激迷走神经向中端,是否也能引起脑内脑啡肽的释放,迷走神经传入纤维与脑内脑啡肽能神经原之间,是否存有机能上的联系?关于这个     

颈动脉窦内压的变化速率对反射性降压效应的影响

在成年狗身上制备右侧孤离颈动脉窦,借助灌流装置用饱和氧的任氏液对其进行灌流。灌流压为搏动性的。通过改变每搏泵出量、灌流管道的阻力和弹性来调节灌流压及其变化速率。用多导生理记录仪同步记录股动脉血压、窦内灌流压及其变化速率。本文主要观察窦内压的变化速率对降压反射的影响。在8只狗身上共进行了93次实验。结果表明,在窦内压相同的情况下,灌流压的上升速率愈快,降压效应愈明显,而其下降速率则无显著作用。已有资料证明搏动性窦内压所引起的降压效应较非搏动性压力更为明显。由此可见,狗的颈动脉窦压力感受器不仅对搏动性压力而且对其上升的变化速率也很敏感。     

Microinjection of a cannabinoid receptor antagonist into the NTS increases baroreflex duration in dogs

Baroreceptor afferent fibers synapse in the nucleus tractus solitarius (NTS) of the medulla. Neuronal cannabinoid (CB)(1) receptors are expressed in the NTS and central administration of CB(1) receptor agonists affect blood pressure (BP) and heart rate. In addition, there is evidence that endocannabinoids are produced in the brain stem. This study examined whether changes in CB(1) receptor activity in the NTS modulated the baroreceptor reflex, contributing to changes seen in BP and heart rate. Baroreflexes were evoked in anesthetized dogs by pressure ramp stimulations of the isolated carotid sinus before and after microinjection of CB(1) receptor agonist WIN-55212-2 (1.25-1.50 pmol) or antagonist SR-141716 (2.5-3.0 pmol) into cardiovascular regions of the NTS. Microinjection of the SR-141716 did not affect baseline BP or baroreflex sensitivity. However, SR-141716 significantly prolonged the time needed to return to the baseline level of BP after the pressure ramp. Microinjection of WIN-55212-2 had no effect on the baroreflex. These data suggest that endocannabinoids can modulate the excitability of NTS neurons involved in the baroreceptor reflex, leading to modulation of baroreflex regulation.     

Differential localization of leu-enkephalin and hyperglycemic hormone in axon terminals of the sinus gland of the crabsCarcinus maenas,eriocheir sinensis,andUca pugilator

Summary Leu-enkephalin containing secretory granules were demonstrated in axon terminals of immunogoldlabeled electron-microscopic sections of the sinus gland of three brachyuran crustaceans. These granules have a diameter of 120+-15 nm and differ in electron density from those located in adjacent terminals containing hyperglycemic or molt-inhibiting hormone. These neurohormones do not show co-localization with leu-enkephalin. The cross-reactivity of leu-enkephalin antiserum with met-enkephalin is less than 1%. The sinus glands of the three species examined show no immunoreactivity for FMRF-amide. A modulatory activity of endogenous enkephalin by paracrine mechanisms is suggested.     

颈动脉窦区注入枸橼酸钠抑制家兔呼吸的机制

向颈总动脉头端注入枸橼酸钠能使大多数家兔发生呼气性呼吸暂停和呼吸频率变慢。此呼吸抑制效应可被地卡因麻醉颈动脉窦区所消除。切断窦神经不能阻断枸橼酸钠对呼吸的抑制。切断迷走神经窦支则使半数以上家兔的呼吸抑制减弱或消失,而在结状神经节上方切断迷走神经能阻断大多数家兔的呼吸抑制。结果提示,迷走神经窦支是颈动脉窦区感受器传入通路之一,向颈动脉窦区注入枸橼酸钠对呼吸的抑制主要是通过迷走神经传入引起的。     

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

Electrical stimulation (100 Hz, 1 ms, 150 microA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After alpha-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current-response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.     

Acute tolerance to the excitatory effect of enkephalin microinjections into hippocampus.

Microinjections of 1–20 μg of leu-enkephalin were done in the dorsal hippocampus of cats and rats in acute experiments. Long lasting epileptiform changes in the hippocampal EEG were produced. These changes were prevented by previous microinjections of naloxone at the same site. When repeated microinjections of the same dose of enkephalin which initially was epileptogenic were done a progressive loss of effectiveness of the drug was observed. Also, progressively higher doses of enkephalin were necessary to produce effects comparable to the effect of the initial injection. These results suggest that acute tolerance may develop to the epileptogenic effect of leu-enkephalin in hippocampus.