Mechanism of effect of sympathetic nervous system on skin receptors

While researching the mechanism underlying the effect of the sympathetic nervous system on the operation of skin receptors, we demonstrated that a tremendous role in this process is played by smooth muscles, whose condition also mediates the sympathetic effect on receptors. The increase in the activity of the sympathetic nerve fibers results in an increase in the tonus of the smooth muscles which in turn alters the mechanical condition of the tissues surrounding the receptors. It was established that the change in the tonus of the smooth muscles in the skin itself affects the reaction of the receptors that is evoked by mechanical stimulation. The change in the tonus of the smooth muscles of the vessels affects the response of receptors caused by cooling of the skin.Nizhegorod Medical Institute, Russian Federation Ministry of Health. Translated from Neirofiziologiya, Vol. 24, No. 5, pp. 552–558, September–October, 1992.     

Participation of alpha and beta adrenoreceptors in facilitating and inhibiting the action of the sympathetic nervous system in parasympathetic bradycardia

Electrical stimulation of the distal vagal cervical end in urethane chloralose anesthetized cats caused bradycardia that could be both enhanced and inhibited during sympathetic activation. Sympathetic activation was induced by electrical stimulation of the sympathetic outflow of the spinal cord at the level of Th 1-Th 3 in pitched cats or by an intravenous injection of tyramine. It has been proved pharmacologically that alpha-adrenoceptors are involved in potentiation. The inhibitory influences are realized via both alpha- and beta-adrenoceptors.     

Selective quantification of the cardiac sympathetic and parasympathetic nervous systems by multisignal analysis of cardiorespiratory variability

Heart rate (HR) power spectral indexes are limited as measures of the cardiac autonomic nervous systems (CANS) in that they neither offer an effective marker of the beta-sympathetic nervous system (SNS) due to its overlap with the parasympathetic nervous system (PNS) in the low-frequency (LF) band nor afford specific measures of the CANS due to input contributions to HR [e.g., arterial blood pressure (ABP) and instantaneous lung volume (ILV)]. We derived new PNS and SNS indexes by multisignal analysis of cardiorespiratory variability. The basic idea was to identify the autonomically mediated transfer functions relating fluctuations in ILV to HR (ILV-->HR) and fluctuations in ABP to HR (ABP-->HR) so as to eliminate the input contributions to HR and then separate each estimated transfer function in the time domain into PNS and SNS indexes using physiological knowledge. We evaluated these indexes with respect to selective pharmacological autonomic nervous blockade in 14 humans. Our results showed that the PNS index derived from the ABP-->HR transfer function was correctly decreased after vagal and double (vagal + beta-sympathetic) blockade (P < 0.01) and did not change after beta-sympathetic blockade, whereas the SNS index derived from the same transfer function was correctly reduced after beta-sympathetic blockade in the standing posture and double blockade (P < 0.05) and remained the same after vagal blockade. However, this SNS index did not significantly decrease after beta-sympathetic blockade in the supine posture. Overall, these predictions were better than those provided by the traditional high-frequency (HF) power, LF-to-HF ratio, and normalized LF power of HR variability.     

Bioelectrical analysis of the regulatory interaction of sympathetic and parasympathetic nervous influences on the heart rhythm]

The changes of chronotropic effect on the isolated sinus node of the frog heart were studied during the separate and simultaneous stimulation of the sympathetic and intracardiac reflex parasympathetic pathways. Intracellular activity of the pacemaker cells was recorded. The separate stimulation of the intracardiac reflex system resulted in bradycardia (in winter) or tachycardia (in summer). Stimulation of sympathetic chain supervening the activation of the intracardiac pathways induced an intensification of both the parasympathetic bradycardia and tachycardia; these effects were cholinergic in nature. The recording of the intracellular pacemaker activity showed the existence of the complicated interaction between the sympathetic and parasympathetic pulse-mediator actions on the heart pacemaker both on the prepulase process and on the membrane polarization and other action potential parameters. Possible mechanisms of this interaction are discussed.     

Role of the parasympathetic nervous system in airway hyperresponsiveness after ozone inhalation

Airway hyperresponsiveness develops in dogs after ozone inhalation. This study examined the role of the parasympathetic nervous system in ozone-induced airway hyperresponsiveness in dogs. Dose-response curves to acetylcholine (n = 8) and histamine (n = 4) were measured before and after exposure to ozone (3 ppm for 30 min). The provocative concentration of each agonist was measured on two randomly assigned days separated by at least 1 wk. On one day a control experiment was performed, and on the other day the dogs were pretreated with the ganglionic blocker hexamethonium bromide in doses that block ganglionic transmission. The acetylcholine provocative concentration decreased on the control day from 5.5 mg/ml (%SE 1.8) before ozone to 0.5 mg/ml (%SE 2.0) after ozone (P less than 0.0001). After pretreatment with hexamethonium the acetylcholine provocative concentration decreased from 9.0 mg/ml (%SE 1.8) before ozone to 1.0 mg/ml (%SE 2.0) after ozone (P = 0.002). The results were similar when histamine was used as the agonist. Therefore, ganglionic blockade does not prevent airway hyperresponsiveness after ozone inhalation, and a parasympathetic reflex mechanism is not responsible for airway hyperresponsiveness after ozone inhalation in dogs.