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。     

Baroreceptor reflex and arterial rigidity in adolescents

The heart rate (HR) variability and pulse wave delay (PWD) in the major arteries of schoolchildren were studied. The function of ordinary coherence of the HR and PWD was used, which reflects the linear relationship between the two processes in the heart and vessels. The high tone of the sympathetic part of the autonomic nervous system (ANS) in schoolchildren causes an increase in heart performance and decreases the shift in the phase of association between HR and PWD, which leads to the appearance of a new characteristic of the system, arterial rigidity. The results of the physiological activation of the sympathetic part of ANS during passive orthostasis and pharmacological trials with blockers of ANS receptors in schoolchildren with heart arrhythmia at rest are presented.     

Baroreceptor reflex and arterial rigidity in schoolchildren

In this work there is shown a variability of heart rate and time delay of pulse wave of main arteries in schoolchildren.There is used the function of ordinary coherence of HR and DPW (time delay of pulse wave). This function reflects the rate of statistical linear relation of two processes in heart and blood vessels. A high tone of sympathetic part of vegetative nervous activity in schoolchildren increases CO (cardeiac out), shortens the hard connection phase of HR and DPW and results in a new system characteristic--arterial rigidity. There are presented results of passive orthostatic test and pharmacological tests on activation of sympathetic part of vegetative nervous activity in schoolchildren with heart rate problems.     

GABA-ergic influence on the crossed extensor reflex

Intraventricular administration of muscimol (25–100 ng) and intravenously applied aminooxyacetic acid (2.5–10 mg/kg) depressed the crossed extensor reflex response in a dose-dependent manner. The inhibitory effects of both drugs were clearly antagonized by a subconvulsive dose of bicuculline. A very small dose of bicuculline (10–40 μg/kg, i.v.) produced a dose-related enhancement of the crossed extensor reflex response without any sign of convulsion. These results suggest that the crossed extensor reflex response is very sensitive to GABAergic drugs and central GABAergic mechanisms play a role in the modulation of the crossed extensor reflex response.     

Role of reflex gain and reflex delay in spinal stability--a dynamic simulation

The goal of this study was to investigate the role of reflex and reflex time delay in muscle recruitment and spinal stability. A dynamic biomechanical model of the musculoskeletal spine with reflex response was implemented to investigate the relationship between reflex gain, co-contraction, and stability in the spine. The first aim of the study was to investigate how reflex gain affected co-contraction predicted in the model. It was found that reflexes allowed the model to stabilize with less antagonistic co-contraction and hence lower metabolic power than when limited to intrinsic stiffness alone. In fact, without reflexes there was no feasible recruitment pattern that could maintain spinal stability when the torso was loaded with 200N external load. Reflex delay is manifest in the paraspinal muscles and represents the time from a perturbation to the onset of reflex activation. The second aim of the study was to investigate the relationship between reflex delay and the maximum tolerable reflex gain. The maximum acceptable upper bound on reflex gain decreased logarithmically with reflex delay. Thus, increased reflex delay and reduced reflex gain requires greater antagonistic co-contraction to maintain spinal stability. Results of this study may help understanding of how patients with retarded reflex delay utilize reflex for stability, and may explain why some patients preferentially recruit more intrinsic stiffness than healthy subjects.     

Splenic reflex modulation of central cardiovascular regulatory pathways

The splenorenal reflex induces changes in mean arterial pressure (MAP) and renal function. We hypothesized that, in addition to spinal pathways previously identified, these effects are also mediated through central pathways. We investigated the effect of elevated splenic venous pressure on central neural activation in intact, renal-denervated, and renal + splenic-denervated rats. Fos-labeled neurons were quantified in the nucleus of the tractus solitarius (NTS), paraventricular nucleus (PVN), supraoptic nucleus (SON), and subfornical organ (SFO) after 1-h partial splenic vein occlusion (SVO) in conscious rats bearing balloon occluders around the splenic vein, telemetric pressure transducers in the gastric vein (splenic venous pressure), and abdominal aorta catheters (MAP). SVO stimulated Fos expression in the PVN and SON, but not NTS or SFO of intact rats. Renal denervation abolished this response in the parvocellular PVN, while renal + splenic denervation abolished activation in the magnocellular PVN and the SON. In renal-denervated animals, SVO depressed Fos expression in the NTS and increased expression in the SFO, responses that were abolished by renal + splenic denervation. In intact rats, SVO also induced a fall in right atrial pressure, an increase in renal afferent nerve activity, and an increase in MAP. We conclude that elevated splenic venous pressure does induce hypothalamic activation and that this is mediated through both splenic and renal afferent nerves. However, in the absence of renal afferent input, SVO depressed NTS activation, probably as a result of the accompanying fall in cardiac preload and reduced afferent signaling from the cardiopulmonary receptors.     

Cyclophosphamide induces NR2B phosphorylation-dependent facilitation on spinal reflex potentiation

It is well-established that cyclophosphamide (CYP) can sensitize the pelvic afferent nerve arising from the urinary bladder and therefore induce suprapubic pain. To test the possibility that CYP might mediate the development of visceral hypereflexia/hyperalgesia by facilitating spinal activity-dependent neural plasticity, we compared the pelvic-urethra reflex activity and spinal N-methyl-d-aspartate receptor NR2B subunit (NR2B) phosphorylation in rats treated with vehicle solution and CYP. Compared with vehicle solution, when accompanied by upregulation of phosphorylated NR2B expression in the lumbosacral (L(6)-S(2)) dorsal horn, CYP increased the evoked spikes in spinal reflex potentiation induced by repetitive stimulation (1 stimulation/1 s). Moreover, intraperitoneal pretreatments with N(G)-nitro-l-arginine methyl ester and roscovitine, nitric oxide synthase and cyclin-dependent protein kinase 5 (Cdk5) antagonists, respectively, overwrote CYP-enhanced reflex potentiation and NR2B phosphorylation. When compared with the untreated group, the treatment with small-interfering RNA of NR2B, which decreased the expression of NR2B expression, abolished CYP-dependent reflex facilitation and spinal NR2B phosphorylation. These results suggested that CYP might facilitate spinal reflex potentiation mediated by N-methyl-d-aspartate receptors and participate in the development of visceral hypereflexia/hyperalgesia through nitric oxide- and Cdk5-dependent NR2B phosphorylation at the lumbosacral dorsal horn.     

A large-scale model of some spinal reflex circuits

This paper reports the development of a large-scale model of some spinal reflex circuitry, useful for studying the dynamic interactions among neuronal populations during simple behaviors. The included populations and properties of the neurons and terminals were derived from the literature, mainly on cat spinal cord. The model was conceived as a symmetrical controller of a pair of antagonistic muscles, within the behavioral domain of the stretch and Golgi-tendon-organ reflexes, and was scaled to include realistic numbers of motoneurons. Inputs to the model were fiber populations providing random synaptic drive to some of the populations and sensory stimuli appropriate for the reflexes. The resulting model contained roughly 2300 neurons in six pairs of populations. The total number of connections in the model was about 600 000, and individual postsynaptic potentials were small (0.1–0.6 mV). Model responses were calibrated by examination of their ability to reproduce known aspects of the reflexes. Published algorithms were used to construct the environment, which is easily expandable, in terms of membrane channels, neuronal geometry, and synaptic properties. The system was built to combine a system-level perspective of spinal circuitry with the single-unit perspective common in electrophysiological investigation. It provides a computational tool for system-level investigations of spinal cord similar to the tools available at the level of membrane currents. Received: 16 May 1997 / Accepted in revised form: 2 October 1997     

Wiping reflex in the intact and spinal frogs

Studying the rostral wiping reflex, RWR, in intact grass frogs allowed us to identify two of its forms: flexor and extensor reflexes (FWR and EWR, respectively). Reflex fields of FWR and EWR considerably overlap; when the common zones are stimulated, both reflex forms can be observed. Mixed forms of the reflex are also possible. The probability of initiation of a certain RWR form depends on the stimulus position. Both FWR and EWR are preserved after spinalization, but their receptive fields are somewhat displaced. The hindlimb movement was divided into three phases: positioning (P), lowering, or orientation (L), and brushing aside (BA). In the intact frog, each phase is of approximately similar duration. The reflex phases and their temporal relations are preserved after spinalization. Total movement duration became longer in spinal animals, as compared with that in intact ones; in addition, this duration began to depend on the stimulus position. In the intact frogs, the position of a working limb shows the linear dependence on the stimulus localization; this dependence is preserved after spinalization. Our results allow us to conclude that the central generator of wiping reflex includes several subsystems determining the reflex form in a probabilistic manner.Neirofiziologiya/Neurophysiology, Vol. 27, No. 4, pp. 278–287, July–August, 1995.     

Baroreceptor reflex modulation by circulating angiotensin II is mediated by AT1 receptors in the nucleus tractus solitarius

Circulating ANG II modulates the baroreceptor reflex control of heart rate (HR), at least partly via activation of ANG II type 1 (AT1) receptors on neurons in the area postrema. In this study, we tested the hypothesis that the effects of circulating ANG II on the baroreflex also depend on AT1 receptors within the nucleus tractus solitarius (NTS). In confirmation of previous studies in other species, increases in arterial pressure induced by intravenous infusion of ANG II had little effect on HR in urethane-anesthetized rats, in contrast to the marked bradycardia evoked by equipressor infusion of phenylephrine. In the presence of a continuous background infusion of ANG II, the baroreflex control of HR was shifted to higher levels of HR but had little effect on the baroreflex control of renal sympathetic activity. The modulatory effects of circulating ANG II on the cardiac baroreflex were significantly reduced by microinjection of candesartan, an AT1 receptor antagonist, into the area postrema and virtually abolished by microinjections of candesartan into the medial NTS. After acute ablation of the area postrema, a background infusion of ANG II still caused an upward shift of the cardiac baroreflex curve, which was reversed by subsequent microinjection of candesartan into the medial NTS. The results indicate that AT1 receptors in the medial NTS play a critical role in modulation of the cardiac baroreflex by circulating ANG II via mechanisms that are at least partly independent of AT1 receptors in the area postrema.