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。     

Static magnetic field effect on microcirculation,direct versus baroreflex-mediated approach

We compared in conscious rabbits, sedated using pentobarbital intravenous (i.v.) infusion (5 mg kg^{? 1} h^{? 1}), the effect of a static magnetic field (SMF), generated by Nd₂–Fe₁₄–B magnets, on microcirculation during its 40 min local exposure to the microvascular network in cutaneous tissue [20 sham exposure and 20 SMF (0.25 T) exposure runs] or to sinocarotid baroreceptors [14 sham exposure and 14 SMF (0.35 T) exposure runs]. Mean femoral artery blood pressure (BP), heart rate (HR), arterial baroreflex sensitivity (BRS), assessed from HR and BP responses to i.v. bolus of nitroprusside and phenylephrine, and microcirculatory blood flow, using microphotoelectric plethysmography (MPPG), were simultaneously monitored. SMF significantly increased microcirculation on a 17.8% in microvascular and on a 23.3% in baroreceptor exposure series. In baroreceptor exposure series, SMF significantly decreased BP, increased heart rate variability, BRS and sodium nitroprusside (NO-donor) i.v. bolus microcirculatory vasodilatory effect. These suggest augmentation of the arterial baroreflex capacity support NO-dependent vasodilation, by increased sensitivity of vessels to NO, to be a new physiological mechanism of BP buffering and microcirculatory control. A significant positive correlation was also found between increase in BRS and in MPPG (r = 0.66, p < 0.009), indicating baroreflex participation in the regulation of the microcirculation and its enhancement after SMF exposure. Both direct and baroreflex-mediated approaches demonstrate SMF significant vasodilatory effect with potential clinical implication in macro- and microcirculatory disorders.     

大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用

目的：揭示蓝斑（LC）的H1和H2受体在足底电击应激对颈动脉窦反射（CBR）重调定中的作用。方法：足底电击应激1周的SD大鼠,麻醉后孤离双侧颈动脉窦区,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、ISP-增益（Gain）关系曲线及反射特征参数,观察Lc微量注射选择性H1或H2,受体拮抗剂氯苯吡胺（CHL）或西咪替丁（CIM）对应激状态下CBR的影响。结果：应激导致ISP-MAP关系曲线显著全面上移（P〈0.05）,ISP-Gain关系曲线中部明显下移（P〈0.05）,反射参数中闪压、饱和压、调定点和最大增益时的ISP值增大（P〈0.05）,而MAP反射变动范围及反射最大增益减小（P〈0.05）;LC内注射CHL（0.5μg/μl）或CIM（1.5μg/μl）20min内均可明显减弱应激对CBR的上述改变（P〈0.05）,CIM的减弱效应不如CHL的显著（P〈0.05）;LC注射上述相同剂量的CHL或CIM对非应激大鼠的CBR无明显影响（P〉0.05）;LC内注射CHL或CIM均不能使应激的CBR水平完全恢复到相应的非应激对照水平。结论：应激引起CBR重调定,反射敏感性下降;部分机制可能是激活中枢纽胺能系统,LC的H1和H2受体尤为H1受体在应激对CBR的重调定机制中发挥重要作用,下丘脑-LC的组胺能通路可能是应激所致CBR重调定的下行通路之一;除此之外,应激作用中尚有其他因素的参与。     

内皮素对麻醉大鼠动脉压力感受器反射的调制作用

在27只隔离灌流颈动脉窦区的麻醉大鼠,观察了内皮素（ET-1）对动脉压力感受器反射的调制作用。结果如下：（1）在颈动脉窦区灌流1nmol／L的ET-1时,压力感受器机能曲线向左下方移位,曲线的最大斜率（PS）由0.40±0.02增至0.51±0.02kPa／kPa（P＜0.01）,压力感受器反射性血压下降幅度（RD）由5.66±0.23增至6.76±0.22kPa（P＜0.01）。由此提示,这一剂量的FT-1对压力感受器反射有易化作用。（2）用10nmol／L的ET-1灌流时,压力感受器机能曲线则向右上方移位,PS降至0.28±0.01kPa／kPa（P＜0.01）,RD降至4．16±0.19kPa（P＜0.01）;100nmol／L的ET-1可使压力感受器机能曲线向右上方移位更为明显,PS降至0.19±0.03kPa（P＜0.001）,RD进一步降至3.33±0.38kPa（P＜0.001）。这些结果表明,上述两种剂量的ET-1对压力感受器反射有抑制作用。（3）ETA受体选择性阻断剂BQ123（0.15μmol／L）可以阻断ET-1（10nmol／L）对压力感受器反射的抑制效应。（4）预先灌流KATP通道阻断剂格列苯脲（10μmol／L）,也可阻断ET-1的效应。综上所述,ET-1对压力感受器反射有双重效应,低剂量时有易化作用,而较高剂量时则有抑制作用,后一作用由ET-1型受体介导并有KATP通道的参与。     

90d模拟失重大鼠动脉压力反射反应性的改变

本工作研究了90d模拟失重大鼠动脉压力反射反应性的改变。即以血管活性药物变动平均动脉压(MAP),并同时记录反射性心率(HR)变化,采用非线性曲线拟合方法,定量评价清醒大鼠的动脉压力反射反应性的特征参数的改变。同时还利用受体阻断实验,观察迷走和交感神经成分在压力反射活动中的贡献。结果表明:模拟失重大鼠MAP-HR反应曲线向右上方移位,心率低限坪值升高,血压调节范围变窄,静态工作点升高。当心得安阻断β受体后,悬吊组大鼠压力感受性心率反射的平均增益及心率反应范围均高于对照组,提示模拟失重大鼠反射活动中迷走作用增强。     

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   

Geomagnetic field effect on cardiovascular regulation

The goal of the present research was try to explain the physiological mechanism for the influence of the geomagnetic field (GMF) disturbance, reflected by the indices of the geomagnetic activity (K, K(p), A(k), and A(p) indices), on cardiovascular regulation. One hundred forty three experimental runs (one daily) comprising 50 min hemodynamic monitoring sequences were carried out in rabbits sedated by pentobarbital infusion (5 mg/kg/h). We examined the arterial baroreflex effects on the short term blood pressure and heart rate (HR) variabilities reflected by the standard deviation (SD) of the average values of the mean femoral arterial blood pressure (MAP) and the HR. Baroreflex sensitivity (BRS) was estimated from blood pressure/HR response to intravenous (i.v.) bolus injections of vasoconstrictor (phenylephrine) and vasodilator (nitroprusside) drugs. We found a significant negative correlation of increasing GMF disturbance (K(p)) with BRS (P = 0.008), HR SD (P =0.022), and MAP SD (P = 0.002) signifying the involvement of the arterial baroreflex mechanism. The abrupt change in geomagnetic disturbance from low (K = 0) to high (K = 4-5) values was associated with a significant increase in MAP (83 +/- 5 vs. 99 +/- 5 mm Hg, P = 0.045) and myocardial oxygen consumption, measured by MAP and HR product (24100 +/- 1800 vs. 31000 +/- 2500 mm Hg. bpm, P = 0.034), comprising an additional cardiovascular risk. Most likely, GMF affects brainstem and higher neural cardiovascular regulatory centers modulating blood pressure and HR variabilities associated with the arterial baroreflex.     

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。     

The effects of specific respiratory rates on heart rate and heart rate variability

In this study respiratory rates of 3, 4, 6, 8, 10, 12, and 14 breaths per minute were employed to investigate the effects of these rates on heart rate variability (HRV). Data were collected 16 times at each respiratory rate on 3 female volunteers, and 12 times on 2 female volunteers. Although mean heart rates did not differ among these respiratory rates, respiratory-induced trough heart rates at 4 and 6 breaths per minute were significantly lower than those at 14 breaths per minute. Slower respiratory rates usually produced higher amplitudes of HRV than did faster respiratory rates. However, the highest amplitudes were at 4 breaths per minute. HRV amplitude decreased at 3 breaths per minute. The results are interpreted as reflecting the possible effects of the slow rate of acetylcholine metabolism and the effect of negative resonance at 3 cycles per minute.     

植物雌激素三羟异黄酮抑制麻醉大鼠颈动脉窦压力感受器反射

采用隔离灌流麻醉雄性大鼠颈动脉窦技术,观察了植物雌激素三羟异黄酮（genistein,GST）对颈动脉窦压力感受器反射的影响。其结果如下:（1）以GST（50μmol/L）隔离灌流颈动脉窦区时,压力感受器机能曲线向右上方移位,曲线最大斜率（peak slope,PS）由0.36±0.01降至0.23±0.01（P<0.001）;反射性血压下降幅度（reflex decrease,RD）由39.75±1.58降至27.00±0.60 mmHg（P<0.001）,阈压（TP）和饱和压（SP）分别从65.63±2.10和192.23±3.90升至82.05±1.95mmHg（P<0.001）和215.76±3.75mmHg（P<0.001）。其中RD、PS和TP呈明显的剂量依赖性;（2）用Ca2+通道激动剂Bay K 8644（500 nmol/L）预处理后,能取消GST（50 μmol/L）对压力感受器反射的抑制作用;（3）预先灌流NO合酶阻断剂（L-NAME,100μmol/L）,不能阻断GST（50μmol/L）对压力感受器反射的抑制效应。以上结果提示,GST可能通过阻断Ca2+通道途径而抑制大鼠颈动脉窦压力感受器反射,并非由血管内皮细胞释放NO所致。