Model of the effect of the vestibular system on blood pressure during sleep]

A structural model of the effect of vestibular system on blood pressure during sleep is proposed. This model reflects joint action of the otolyth system and semicircular canal system, vestibular nuclei, vasomotor centre, vagus nuclei and of the central control mechanism of the state awakeness -- sleep. Anatomic and physiological prerequisites involved in the model are expressed by chains with transmission functions, signal generators, summators etc.     

Altered frequency characteristic of central vasomotor control in SHR

Previous work from our laboratory has demonstrated that the very low-frequency (VLF: 0-0.25 Hz) and low-frequency (LF: 0.25-0.8 Hz) power of arterial pressure variability (APV) are related to vasomotor reactivity in response to control signals from the rostral ventrolateral medulla (RVLM) via the sympathetic system in the rat. The present study evaluated the differences in the dynamic property of central vasomotor control between spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Experiments were carried out in 10- to 12-wk-old rats that were anesthetized with continuous infusion of pentobarbital sodium, paralyzed with pancuronium, and maintained on mechanical ventilation. We found that SHR exhibited significantly higher arterial pressure (AP), heart rate (HR), and VLF, LF, and high-frequency (0.8-2.4 Hz) power of APV than WKY under resting state. Broad-band electrical stimulation of the RVLM elicited parallel APV in the VLF and LF ranges in both rat strains. The evoked APV and transfer magnitude of the APV to stimulus spike rate variability (RVLM-AP magnitude) were significantly higher in SHR, especially in the LF range. The response frequency of central vasomotor control, represented by the high-cut frequency of RVLM-AP magnitude, was also extended in SHR. The disparity in RVLM-AP transfer magnitude between SHR and WKY became virtually absent after combined alpha- and beta-adrenoceptor blockade by phentolamine and propranolol. These results suggest that the dynamic control of RVLM on AP reactivity is enhanced in SHR, in which the adrenergic system may play a major role.     

Organ blood flow and vessels of microcirculatory bed in fish

Information on density of fish capillary network and its permeability, peculiarities of geometry, morphology, and ultrastructure of vessels of microcirculation bed—arterioles, venules, capillaries—is presented. A great attention is paid to vasomotor reactions and their participation in redistribution of blood. Nervous and humoral mechanisms of control of tone of the vessel smooth muscle wall and voluminous blood flow are considered. Effects of environmental factors on processes of microcirculation in fish are discussed.     

Mechanism of ethanol-induced vasodilation

The mechanism by which ethanol ingestion causes dermal vasodilation is unclear, but it may result from a direct action on central vascular control mechanisms. Forearm blood flow and peripheral skin temperatures were examined in five quadriplegics (lesions above T7) and five control subjects, before and after the ingestion of ethanol (0.75 ml/kg body wt). The lack of vasomotor efferent function was confirmed in the quadriplegics by the absence of vasodilation in response to radiant heating of the torso. There were no significant changes in peripheral temperatures or forearm blood flow after ethanol in the quadriplegics. The control subjects had a significant increase in forearm blood flow (1.12 +/- 0.2 ml.min-1.100 ml-1) and skin temperature (finger 2.4 +/- 0.4 degrees C, toe 3.4 +/- 0.3 degrees C) after ethanol. These data suggest that ethanol may induce peripheral vasodilation by modulation of central vasomotor control mechanisms.     

Role of nitric oxide in the mechanisms of formation of reflex vasomotor responses

This review focuses on modem data concerning the role of nitric oxide (NO) in the mechanisms of vasomotor regulation. On the background of the literature data and own experimental results, we have discussed some questions of NO integration into transmission of impulses in central and autonomic nervous system under condition of realization of cardiogenic and sinocarotid pressor and depressor reflexes, reflectory vasomotor responses formation under acute myocardial ischemia. According to literature and own functional and morphological data we suggest species differences in NO participations in mechanisms of reflex self--regulation of circulation.     

Raynaud's phenomenon and thermal entrainment: an objective test.

A new objective test for diagnosing Raynaud''s phenomenon was assessed in practice. The test is based on entrainment of the thermal vasomotor control system and entails non-invasive measurement of blood-flow responses in one hand while alternating thermal stimuli are applied to the contralateral hand. A significant (p less than 0.001) abnormality of vasomotor control was found in patients with Raynaud''s phenomenon compared with normal subjects. When applied clinically this test is diagnostic and indicates the severity of the disease and the effect of treatment.     

Cellular and humoral immunodepression in vultures feeding upon medicated livestock carrion

Veterinary pharmaceuticals contained in dead livestock may be ingested by avian scavengers and negatively affect their health and consequently their population dynamics and conservation. We evaluated the potential role of antibiotics as immunodepressors using multiple parameters measuring the condition of the cellular and humoral immune system in griffon (Gyps fulvus), cinereous (Aegypius monachus) and Egyptian vultures (Neophron percnopterus). We confirmed the presence of circulating antimicrobial residues, especially quinolones, in nestlings of the three vulture species breeding in central Spain. Individuals ingesting antibiotics showed clearly depressed cellular and humoral immune systems compared with nestlings from the control areas, which did not ingest antibiotics. Within central Spain, we found that individuals with circulating antibiotics showed depressed cellular (especially CD4⁺and CD8⁺T-lymphocyte subsets) and humoral (especially acellular APV complement and IL8-like) immune systems compared with nestlings without circulating antibiotics. This suggests that ingestion of antibiotics together with food may depress the immune system of developing nestlings, temporarily reducing their resistance to opportunistic pathogens, which require experimental confirmation. Medicated livestock carrion should be considered inadequate food for vultures due to their detrimental consequences on health derived from the ingestion and potential effects of the veterinary drugs contained in them and for this reason rejected as a management tool in conservation programmes.     

Coronavirus infection of the central nervous system: host-virus stand-off

Several viruses infect the mammalian central nervous system (CNS), some with devastating consequences, others resulting in chronic or persistent infections associated with little or no overt pathology. Coronavirus infection of the murine CNS illustrates the contributions of both the innate immune response and specific host effector mechanisms that control virus replication in distinct CNS cell types. Despite T-cell-mediated control of acute virus infection, host regulatory mechanisms, probably designed to protect CNS integrity, contribute to the failure to eliminate virus. Distinct from cytolytic effector mechanisms expressed during acute infection, non-lytic humoral immunity prevails in suppressing infectious virus during persistence.     

Effect of β Adrenoreceptor Blocker Propranolol during Reflex Renal Dystrophy Induced by Sciatic Nerve Cutting

We present the data on the functional status of the mineralocorticoid receptor system in the rat kidney in the course of renal reflex dystrophy induced by sciatic nerve cutting against the background of both renal denervation and injections of propranolol, a -adrenoreceptor blocker. According to the state of renal mineralocorticoid receptors, the simultaneous block of both neural and humoral pathological stimuli coming to the kidney after the nerve injury prevented cytochemical changes in the organ more effectively than the block of neural transmission alone. We propose that both the central neural transmission and humoral mechanisms control the activity of the molecular structures responsible for aldosterone reception in the cells of renal tubules.     

The role of endogenous bioregulators in formation of cardiogenic reflex effects on circulation

The possible role of endogenous endothelium-derived bioactive substances in organization of cardiogenic depressor reflexes under cardiac receptor stimulation (by veratrine and bradykinin) was investigated in acute experiments on anesthetized rats. The results have shown that endothelium-derived bioactive substances take part in forming of the cardiogenic depressor reflex humoral components of nervous response or nervous modulators. These data contribute to understanding of the role of endogenous endothelium-derived bioactive substances (prostacyclin) and different NOS isoforms in mechanisms of depressor reflex development and species differences in their involvement in reflex vasomotor reactions.     

促肾上腺皮质激素释放激素及去甲肾上腺素对高原鼠兔体液免疫的抑制作用

采用第三脑室注入CRF 及N E 的方法观察对高原鼠兔(Ochotona curzoniae) 体液免疫的影响。结果表明: 第三脑室注入CRF 1 Lg 可抑制抗体生成, 比对照下降29.2%(P<0.01) , 而在第三脑室注入CRF 受体阻断剂α-helical CRF2 (9-41) 50 Lg 后再注入CRF 1 Lg 则可取消CRF 对抗体生成的抑制作用; 第三脑室注入5 nM NE, 与对照相比, 抗体水平下降38.85%(P < 0.01) , 而使用62OHDA 损毁脑内交感神经系统则使抗体水平升高24.31% (P <0.01)。这些结果表明, 高原鼠兔中枢CRF 升高对体液免疫有抑制作用, 中枢交感神经系统对体液免疫也具有紧张性抑制作用。     

Effect of sodium hydroxybutyrate on cerebral circulation and regional vasomotor reflexes

In experiments on cats it was found using electromagnetic and resistographic methods that sodium hydroxybutyrate (100 mg/kg) considerably increases cerebral circulation. The drug also potentiates the blood flow to the brain during formation of pressor reflexes of the arterial pressure. The blood flow increase is also observed in the system of femoral arteries while in the intestinal artery, on the contrary, there is a reduction in the blood flow increase during vasomotor reflexes. The reflex changes of the resistance in regional vessels are also different: the inhibition of pressor reflexes in the cerebral vessels along with their facilitation in the intestinal and femoral arteries and the potentiation of the reflex dilatatory phase in the limb vessels are seen. Different sensitivity to the drug of synaptic formations in the central links of various regional vasomotor reflexes is likely to underlie the difference described.     

Pathway specific expression of neuropeptides and autonomic control of the vasculature

In this article, we review the immunohistochemical evidence for the pathway-specific expression of co-existing neuropeptides in autonomic vasomotor neurons, and examine the functional significance of these expression patterns for the autonomic regulation of the vasculature. Most final motor neurons in autonomic vasomotor pathways contain neuropeptides in addition to non-peptide co-transmitters such as catecholamines, acetylcholine and nitric oxide. Neuropeptides also occur in preganglionic vasomotor neurons. The precise combinations of neuropeptides expressed by neurons in vasomotor pathways vary with species, vascular bed, and the level within the vascular bed. This applies to both vasoconstrictor and vasodilator pathways. There is a similar degree of variation in the expression of neuropeptide receptors in the vasculature. Consequently, the contributions of different peptides to autonomic vasomotor control are closely matched to the functional requirements of specific vascular beds. This arrangement allows for a high degree of precision in vascular control in normal conditions and has the potential for considerable plasticity under pathophysiological conditions.     

B-lymphocyte requirement for vaccine-mediated protection from Theiler's murine encephalomyelitis virus-induced central nervous system disease.

The role of humoral immunity in the protection of vaccinated SJL/J mice from central nervous system disease induced by the DA strain (DAV) of Theiler's murine encephalomyelitis virus was investigated in B-cell-deficient mice. Mice were depleted of B cells by treatment with a mouse monoclonal antibody specific for immunoglobulin M. DAV-vaccinated, B-cell-deficient mice failed to clear viral infection and were no longer protected from Theiler's murine encephalomyelitis virus-mediated central nervous system disease. CD4+ T cells are required in this model of protection to provide help for the development of an antiviral antibody response in the central nervous system.     

High‐resolution definition of humoral immune response correlates of effective immunity against HIV

Defining correlates of immunity by comprehensively interrogating the extensive biological diversity in naturally or experimentally protected subjects may provide insights critical for guiding the development of effective vaccines and antibody‐based therapies. We report advances in a humoral immunoprofiling approach and its application to elucidate hallmarks of effective HIV‐1 viral control. Systematic serological analysis for a cohort of HIV‐infected subjects with varying viral control was conducted using both a high‐resolution, high‐throughput biophysical antibody profiling approach, providing unbiased dissection of the humoral response, along with functional antibody assays, characterizing antibody‐directed effector functions such as complement fixation and phagocytosis that are central to protective immunity. Profiles of subjects with varying viral control were computationally analyzed and modeled in order to deconvolute relationships among IgG Fab properties, Fc characteristics, and effector functions and to identify humoral correlates of potent antiviral antibody‐directed effector activity and effective viral suppression. The resulting models reveal multifaceted and coordinated contributions of polyclonal antibodies to diverse antiviral responses, and suggest key biophysical features predictive of viral control.     

Central actions of angiotensin in cardiovascular control: multiple roles for a single peptide.

Angiotensin II (ANG II) acts peripherally as a hormone, with actions on the vasculature, adrenals, and kidney. In addition, certain actions of ANG II in the central nervous system are directed toward cardiovascular control and fluid volume homeostasis. Dense binding sites for ANG II are found at circumventricular organs, which apparently have the ability to relay information to cardiovascular centers via neural circuitry. Microinjection of ANG II into the subfornical organ (SFO) or area postrema (AP) produces site-specific increases in blood pressure. In addition, electrophysiological studies demonstrate profound effects of ANG II, acting at the SFO, on activity of neurohypophysial neurons and release of oxytocin and vasopressin, which can be antagonized by ANG II blockers or attenuated by SFO lesions. Evidence from microinjection, electrophysiological, and lesion studies indicate a complex interaction between central sites involved in mechanisms of cardiovascular control: the SFO, AP, organum vasculosum of the lamina terminalis, and paraventricular and supraoptic nuclei of the hypothalamus. Not only is ANG II a humoral messenger in this central scenario, but evidence suggests it acts as a neurotransmitter or neuroendocrine substance within specific CNS pathways, suggesting multiple roles for this peptide in central cardiovascular control.     

Is neurotensin in the brain involved in thermoregulation of the monkey?

Cannulae for intracerebroventricular (ICV) infusion were implanted stereotaxically in monkeys (Macaca fasicularis) maintained post-operatively in a primate restraint chair. During each experiment, a series of physiological measures was recorded simultaneously on a polygraph which included colonic temperature, vasomotor tone, heart rate, respiratory rate, and basal metabolism as reflected by O₂ uptake. The ICV infusion in a volume of 0.5 ml of neurotensin (NT) in doses ranging from 3–150 μg produced neither a statistically significant nor consistent change in body temperature or vasomotor response. Although the highest dose of 450 μg NT infused ICV caused an immediate bradycardia and a concomitant decline in metabolic and respiratory rates, an average decline in core temperature of 0.6°C and the accompanying cutaneous vasodilation often had a latency as long as 1.0 hr. In contrast to the typical hypothermia in this species following an ICV infusion of catecholamines, implicated in the central pathways underlying thermoregulation, NT failed to elicit a coordinated set of physiological responses for heat dissipation in the monkey. Therefore, it is unlikely that this tridecapeptide plays a role in the central mechanisms mediating the control of body temperature of this primate species.     

Central nervous system and mechanisms of hypertension

There are several mechanisms by which the central nervous system participates in the neural and humoral alterations associated with various forms of experimental hypertension. Structures in forebrain with multiple integrative roles in neuroendocrine control of the circulation are involved. Tissue surrounding the anteroventral region of the third cerebral ventricle (AV3V region) is involved physiologically in thirst, sodium homeostasis, osmoreception, secretion of vasopressin and natriuretic factor and sympathetic discharge to blood vessels. Destruction of this tissue prevents or reverses many forms of hypertension. In genetically based spontaneous hypertension, limbic structures such as the central nucleus of the amygdala rather than the AV3V region are the necessary neuroanatomic substrate. Recent evidence suggests that a circumventricular organ in brain stem, the area postrema, is also involved in the mediation of several forms of experimental hypertension. In renin- and nonrenin-dependent forms of renal hypertension, two major factors activate central mechanisms. First, direct central actions of angiotensin, acting through receptors in the subfornical organ and organum vasculosum of the lamina terminalis, increase sympathetic discharge and secretion of vasopressin through mechanisms integrated at the level of the AV3V region. Second, sensory systems originating in the kidney can activate increased sympathetic discharge through complex projection pathways involving forebrain systems. Mineralocorticoid hypertension appears to involve enhanced secretion of vasopressin and central vasopressinergic mechanisms also dependent on the AV3V region. Reciprocal connections between key central areas involved in control of arterial pressure provide the neuroanatomical basis for central nervous system participation in hypertension.     

Sodium reabsorption and the aldosterone receptors in the cells of the kidney tubules in a dynamic disorder of the trophic function of the nervous system]

The results are presented of investigations on determining the functional state of mineralocorticoid receptor apparatus in rat kidney at diverse stages of the reflex renal dystrophy per se and that against the background of renal denervation along with propranolol injections produced at different terms following the disturbance of nervous system trophic function. It was shown that simultaneous blockade of neuroconductory and humoral pathways of pathological stimulus transmission from central end of cut ischiatic nerve to the kidney prevents the development of trophic disturbances in the organ as tested by the state of mineralocorticoid receptors, to a more extent than the blockade of neuroconductory pathway only. The activity of molecular structures which determine the mineralocorticoid reception in cells of renal tubules seems to be controlled both by central neuroconductory and humoral mechanisms.