Showing papers on "Autonomic nervous system published in 1980"

Pathology of Autonomic Neuropathy in Diabetes Mellitus

Abstract: Pathologic changes in the autonomic nervous system were studied postmortem in five cases of insulin-dependent diabetes of early onset. All had had clinical evidence of peripheral sensorimotor neuropathy and developed disturbances of autonomic function that included postural hypotension, diarrhoea, bladder dysfunction, impotence (in the men), and signs of cardiac denervation. In coeliac and other sympathetic ganglia there were many distended ('giant') or vacuolated neurons as well as enlarged club-shaped neural processes. The vagus nerve and sympathetic trunks showed severe loss of myelinated fibres. Smooth muscle in many viscera showed a hitherto undescribed focal hyaline degeneration. There were inflammatory changes in the autonomic ganglia in all cases and in or around bundles of unmyelinated nerve fibres in many. These findings suggest that there may be several different pathogenetic mechanisms involved in the development of autonomic neuropathy in diabetes.

Hemodynamic and myocardial consequences of scorpion venom.

Abstract: The hemodynamic effects of scorpion venom (Leiurus quinquestriatus) and the mechanism of heart failure were investigated in two groups of anesthetized spontaneously breathing dogs The effects of different adrenergic and cholinergic blocking agents on the venom-induced hemodynamic changes were also evaluated In one group the venom was given before autonomic nervous system blocking agents and in a second group propranolol, atropine, phentolamine and hexamethonium alone or in different combinations were given before the venom Complete autonomic nervous system blockade was induced in two animals to evaluate a possible direct myocardial effect of venom The venom, a powerful arrhythmogenic agent stimulating the autonomic sympathetic nervous system and adrenals, induced dramatic hemodynamic increases in left ventricular systolic and diastolic pressures, pulmonary and systemic arterial pressures and left ventricular contractility The hemodynamic data show clearly for the first time that pulmonary edema in severe scorpion envenomation is cardiac in origin, thus emphasizing the importance of the abnormal left ventricular hemodynamics Heart failure is most probably the result of the interaction of several mechanisms that include a catecholamine-induced decrease in left ventricular compliance and increased impedance to left ventricular emptying and cardiac arrhythmias, all of which may impede left ventricular filling The combination of propranolol and phentolamine was the most effective blocking agent in reversing the venom-induced hemodynamic changes However, atropine was effective only when the venom-induced cholinergic effects dominated the clinical picture

Functional changes in autonomic nervous responses with ageing.

Abstract: The effects of ageing on autonomic nervous responses have been investigated in 29 young adults, 64 healthy elderly in the age range 66 to 86 years, and 20 elderly in-patients with hypothermia, instability of bladder function or marked orthostatic hypotension. In the healthy elderly group, the beat-to-beat variation in response to postural change was significantly diminished, the vasoconstrictor response to cooling reduced and baroreflex sensitivity during lower-body negative pressure was decreased compared with young adults. Patients with an atronic bladder, determined by urodynamic tests, showed an even more marked decrease in baroreflex sensitivity. The multisystem nature of these autonomic disturbances suggests that physiological impairment may occur in autonomic neural pathways with ageing.

A nonadrenergic vagal inhibitory pathway to feline airways

Abstract: In cats anesthetized with chloralose-pentobarbital and artificially ventilated, electrical stimulation of the caudal end of the cut cervical vagus nerve has a biphasic effect on the bronchoconstriction induced by an intravenous infusion of serotonin. The response consists of a brief augmentation of bronchoconstriction followed by relatively prolonged bronchodilation. After muscarinic receptor blockade with atropine, vagal stimulation causes only bronchodilation. Vagally mediated bronchodilation is not affected by beta adrenergic blockade with propranolol, alpha adrenergic blockade with phenoxybenzamine, or adrenergic neuronal blockade with guanethidine, but is abolished by autonomic ganglionic blockade with hexamethonium. These findings support the conclusion that a nonadrenergic inhibitory nervous system is present in the pulmonary airways of the cat and that the system is supplied by preganglionic fibers in the cervical vagus nerves.

Inhibition and facilitation in parasympathetic ganglia of the urinary bladder.

Abstract: Neurons in vesical parasympathetic ganglia receive excitatory and inhibitory inputs from both divisions of the autonomic nervous system. Sacral parasympathetic pathways (cholinergic) provide the major excitatory input to these ganglia via activation of nicotinic receptors. Parasympathetic pathways also activate muscarinic inhibitory and excitatory receptors, which may exert a modulatory influence on transmission. Cholinergic transmission is relatively inefficient when preganglionic nerves are stimulated at low frequencies (< 1 Hz). However, excitatory postsynaptic potentials (EPSPs) and postganglionic firing markedly increase during repetitive stimulation at frequencies of 1-10 Hz. It is concluded that enhanced transmitter release accounts for the temporal facilitation and that vesical ganglia function as "high pass filters" that amplify the parasympathetic excitatory input to the detrusor muscle during micturition. Transmission in vesical ganglia is also sensitive to adrenergic inhibitory and facilitatory synaptic mechanisms elicited by efferent pathways in the hypogastric nerves. The effects of exogenous norepinephrine indicate that adrenergic inhibition is mediated by alpha receptors and reflects primarily a presynaptic depression of transmitter release although postsynaptic adrenergic hyperpolarizing and depolarizing effects have also been noted. Adrenergic facilitation is mediated by beta receptors as well as unidentified receptors. Norepinephrine also can inhibit or excite spontaneously active neurons in vesical ganglia. The existence of inhibitory and facilitatory synaptic mechanisms in vesical ganglia provides the basis for a complex ganglionic modulation of the central autonomic outflow to the bladder.

In Vivo Demonstration of Nonadrenergic Inhibitory Innervation of the Guinea Pig Trachea

Abstract: To determine if electrical stimulation of autonomic nerves could excite nonadrenergic inhibitory motor pathways in the guinea pig respiratory system in vivo, we studied the effects of electrical stimulation of the cervical vagi and sympathetic nerve trunks on pressure changes (P(p)) within an isolated, fluid-filled cervical tracheal segment which reflected changes in trachealis muscle tone. We preserved the innervation and circulation of the segment as evidenced by a rise in P(p) with vagus nerve stimulation and a fall in P(p) with intravenous isoproterenol. In five atropine-treated animals, stimulation of the cut vagi or sympathetic nerve trunks resulted in a mean fall in P(p) of 7.9 and 8.2 cm H(2)O, respectively. Treatment with propranolol attenuated the response to sympathetic stimulation but not vagal stimulation. To determine if these relaxation responses were mediated by an adrenergic or nonadrenergic mechanism, we studied an additional five animals that had been treated with 6-hydroxydopamine to destroy adrenergic nerve endings. In 6-hydroxydopamine, atropine, and propranolol-treated animals, sympathetic nerve stimulation decreased P(p) only 0.65 cm H(2)O, confirming the elimination of adrenergic nerve influences, whereas vagus nerve stimulation decreased P(p) 17.7 cm H(2)O. After sectioning the recurrent laryngeal nerves, the mean decrease in P(p) during vagus nerve stimulation was only 3.2 cm H(2)O. These findings demonstrate the presence of nonadrenergic inhibitory nerves in the guinea pig trachea in vivo. They further show that nonadrenergic inhibitory nerve effects are elicited during electrical stimulation of the vagus nerves and that interruption of the recurrent laryngeal nerves diminishes the magnitude of these effects.

Abnormal adrenergic and cholinergic sensitivity in cystic fibrosis.

Abstract: THE organ systems most clearly affected by cystic fibrosis are regulated in part by the autonomic nervous system. Abnormal autonomic regulation may contribute to the clinical spectrum of cystic fibrosis.1 , 2 Previous studies have suggested that alpha-adrenergic regulation may be abnormal in the pupils,3 , 4 that beta-adrenergic responses are abnormal in leukocytes,5 and that responses to cholinergic agents may be disordered in the submaxillary gland6 and bronchial smooth muscle.7 , 8 Thus, abnormalities in all three components of the autonomic nervous system may coexist in cystic fibrosis. One possible explanation for these observations is altered responsiveness of the end organs. To assess this possibility, . . .

Presynaptic Receptors in the Autonomic Nervous System

Abstract: This chapter is primarily concerned with the actions of α- and β-adrenoceptor agonists and antagonists on peripheral autonomic nerves. Such drugs may produce effects on these nerves unrelated to their action on α- and β-receptors. For example, many α antagonists block the neuronal uptake of catecholamines (Hertting et al., 1961 b; Iversen, 1965; Gillespie and Kirpekar, 1965), block extraneuronal uptake (Eisenfeld et al., 1967; Avakian and Gillespie, 1968; Cubeddu et al., 1974c) and block uptake into adrenergic storage granules (Euler and Lishajko, 1968). Some β-antagonists such as propranolol are powerful local anaesthetics (Morales-Aquilera and Vaughan- Williams, 1965) and even α-agonists in high enough concentration will act in this way (Starke, 1972 a). α-Antagonists such as phenoxybenzamine can release noradrenaline from adrenergic nerves if the dose is high enough (Axelrod et al., 1962; Cubeddu et al., 1974c), an action dealt with elsewhere in this volume (Westfall, 1977).

Pulse transit time in the analysis of autonomic nervous system effects on the cardiovascular system.

Abstract: The purpose of this study was the development of a simple method for assessing autonomic nervous system (ANS) effects on the cardiovascular system. Pulse transit time (PTT) is the interval between ventricular electrical activity and the peripheral appearance of the pulse (here measured by ear densitography). Six normal subjects were studied with six drugs which either enhanced or blocked activity of one of the three major divisions of the ANS: parasympathetic, beta-sympathetic, alpha-sympathetic. Data analysis revealed characteristic patterns of change in PTT and heart rate (HR) which permitted differentiation of five of the six drugs' effects. Vagal enhancement (edrophonium) and alpha-sympathetic enhancement (phenylephrine)—which reflexly also increases vagal tone to the heart—could not be distinguished from one another unless blood pressure also was monitored. Monitoring of PTT and HR offers a simple, non-invasive method which can be used on-line to evaluate ANS effects on the cardiovascular system.

Role of the autonomic nervous system in the mediation of LHA electrical stimulation-induced effects on insulinemia and glycemia

Abstract: The short-term effects of bilateral electrical stimulation of the lateral component of the lateral hypothalamic/medial forebrain bundle area (LHA) on peripheral plasma levels of glucose (G), immunoreactive insulin (IRI) and glucagon (IRG) were measured in food-derived, anesthetized rats in the presence of continuous low i.v. glucose infusion. In normal rats LHA stimulation induced a rapid but moderate rise in IRI in the presence of a simultaneous rapid rise in G. At the end of the 5 min stimulation period the glucose-induced IRI response was clearly attenuated. In rats receiving a continuous phentolamine (i.v.) infusion, the rapid IRI response was much larger in spite of only marginal rises of G. These findings suggest that electrical LHA stimulation activates two opposing mechanisms on IRI secretion, an excitatory component which is masked in normal animal by a sympathetic alpha-adrenergic inhibitory component. In an attempt to define the mediating pathway of this LHA stimulation-induced IRI excitatory component, both the parasympathetic and sympathetic divisions of the autonomic nervous system were pharmacologically and surgically manipulated, all in the presence of phentolamine infusion. Neither bilateral subdiaphragmatic vagotomy, atropine, propranolol infusion, nor spinal cord transection at T1 were able to block the IRI response. The findings are consistent with a humoral mediation of this IRI stimulatory response and support the existence of a lateral hypothalamic or hypophyseal factor which is released by LHA stimulation. The implications and physiological role of the LHA in the neural control of insulin secretion and ingestive behavior are discussed.

Cardiac arrhythmias accompanying acute compression of the spinal cord

Abstract: This study was undertaken to determine the cardiovascular response to compression of the spinal cord and to determine the autonomic mechanisms involved. The electrocardiogram and arterial blood pressure were recorded in anesthetized monkeys during inflation of a balloon catheter in the epidural space of the mid-thoracic region. Acute spinal cord compression resulted in a wide variety of severe cardiac arrhythmias and acute hypertension. The arrhythmias were found to result from hyperactivity of both the sympathetic and parasympathetic divisions of the autonomic nervous system.

Autonomic control of cardiovascular reflexes in narcolepsy.

Abstract: Six male patients with narcolepsy for several years, were studied without and with amphetamine in order to evaluate possible abnormalities in autonomic control of the cardiovascular system. Studies were made of (1) heart rate and blood flow in the resting forearm during contralateral isometric handgrip, (2) respiratory sinus arrhythmia and (3) heart rate response to the Valsalva manoeuvre. The patients had a slow heart rate, a reduced forearm blood flow increase on handgrip, and a subnormal sinus arrhythmia. Only two out of the six patients had an abnormal Valsalva ratio. Amphetamine did not alter the response to handgrip but increased the sinus arrhythmia in three patients and the Valsalva ratio in two. It is concluded that narcolepsy is accompanied by reduced vegetative reactivity in the cardiovascular system. Since this applies to functions mediated by both the sympathetic and parasympathetic systems, and since some parasympathetically-mediated functions are affected while others are not, the functional disturbance found probably is of central origin.

Alteration of the penile corpora in patients with erectile impotence

Abstract: We measured the content of the two principal neurotransmitters of the autonomic nervous system from the erectile tissue of four men with normal erection and 38 men impotent as a result of injury or disease. In the former the norepinephrine content was 812 +/- 82.6 (SE) pg per mg of wet weight; In the latter, statistically significant reductions of norepinephrine were found with the greatest decrease occurring with insulin-dependent diabetes mellitus. Neither choline acetyltransferase activity nor morphologic alterations of the nerve fibers of erectile tissue were observed in either group. Our findings suggest that the sympathetic nervous system is an integral component of human erection and that a functional alteration of the corporal nerve fibers occurs with several diseases associated with impotence.

Overdrive suppression in the transplanted heart: effect of the autonomic nervous system on human sinus node recovery.

Abstract: To assess the influence of the autonomic nervous system upon the recovery of the normal human sinus node, the responses to overdrive pacing at multiple cycle lengths of the denervated donor heart sinus nodes of 18 human cardiac transplant recipients were compared to the responses of those 18 patients' innervated, remnant atria and of 20 control subjects with normal sinus node function. The mean average spontaneous sinus cycle length of the donor atria (643 ± 78 msec [SD]) was significantly shorter than that for either the innervated recipient (822 ± 171 msec) or the control atria (840 ± 204 msec). The longest sinus node recovery time occurred after overdrive pacing at cycle lengths of 400 msec or less in 94% of the donor atria, but in only 28% of the recipient atria (p < 0.01) and 10% of the control atria (p < 0.0001). Secondary postpacing cycles were longer than the initial postpacing pause after at least one pacing intervention in only 6% of the donor, but in 78% of the recipient (p < 0.01) and 45% of the control atria (p < 0.01). Curves describing the relationship between the corrected sinus node recovery time and the cycle length of overdrive pacing were smooth and predictable in 72% of the donor atria, but in only 17% of the recipient (p < 0.01) and 20% of the control atria (p < 0.01). In transplant patients pacing was performed for both 60- and 15-second overdrive periods; recovery phenomena were qualitatively and quantitatively the same for the two durations of pacing. We conclude that the cardiac autonomic nervous system has considerable influence on the postpacing recovery phenomenon of the normal human sinus node. This may account, in part, for the insensitivity of the sinus node recovery time in detecting sinus node dysfunction.

Autonomic effects on the human cardiac conduction system. Evaluation by intracardiac electrocardiography and programmed stimulation techniques.

Abstract: After right heart catheterisation in 20 subjects, aged 30 to 82 years, the techniques of intracardiac electrocardiography and programmed stimulation were used to determine variables of normal function of the sinuatrial node, atrioventricular node, and intraventricular conduction system. Specific attention was paid to autonomic influences on these variables. These were assessed by comparison of determinations made before and after cardiac autonomic block induced by intravenous atropine, 0 03 mg/kg, and propranolol, 0.15 mg/kg. Sympathetic and larger depressant vagal effects on sinuatrial node function (sinus cycle length and sinus node recovery time after overdrive atrial pacing) were demonstrated. Autonomic effects on atrioventricular node conduction (AH interval and Wenckebach threshold to incremental right atrial pacing) were small, of similar magnitude (approximately 20% change), and opposing. Only significant vagal effects in increasing the effective and functional refractory periods of the atrioventricular node (pacing at 100 bpm) were demonstrated (approximately 15 and 12% change, respectively). The atrial effective refractory period, duration ofthe His bundle electrogram, and the HV interval were unchanged by either drug. Effects on refractory periods of the intraventricular conduction system could not be assessed because exact determinations were limited by refractoriness of the atrioventricular node. The QT interval with pacing at 100 bpm decreased significantly after atropine but was unchanged after propranolol.

Effects of pharmacological autonomic blockade upon cardiac rate and blood pressure conditioned and unconditioned responses in Macaca mulatta.

Abstract: Heart rate, systolic and diastolic blood pressures were recorded during classical delay conditioning of rhesus macaque monkeys. When portions of the autonomic nervous system were selectively blocked by pharmacological agents, it appeared that the initial increases in heart rate and blood pressures in response to the conditioned stimulus were the result of increased sympathetic activity and a concomitant decrease in parasympathetic activity. Towards the end of the conditioned stimulus, an increase in parasympathetic activity was indicated. Blockade of the autonomic system which produced total elimination of the conditioned cardiac rate response and substantial reduction or elimination of the conditioned blood pressure response, was not necessarily or always accompanied by a corresponding elimination of the respective unconditioned responses. Such a finding suggests a different underlying neural mediation of these conditioned and unconditioned responses.

Carotid dP/dt as a psychophysiological index of sympathetic myocardial effects: some considerations.

Abstract: Heart rate (HR) is modulated by both branches of the autonomic nervous system. Therefore, the neural regulation of a specific change in HR cannot be deduced from HR changes per se. For example, HR deceleration cannot be interpreted as being due to sympathetic nervous system withdrawal and/or parasympathetic nervous system activation. It is quite possible that sympathetic activation may be dominated by parasympathetic antagonism. To determine neurogenic influences on the heart, one group of researchers have focused on measuring contractility aspects of ventricular function since it has been demonstrated that the ventricles are sympathetically dominated. This paper assesses the validity of contractility-based dP/dt measures as indices of ventricular function, and thus of sympathetic activity, being especially concerned with the noninvasive carotid dP/dt measure which is of particular significance to psychophysiologists. The validation examination consists of an exploration into the underlying physiology of dP/dt measures as well as a critical appraisal of empirical psychophysiological findings related to dP/dt. Other important parameters related to psychophysiological measures, such as obtrusiveness and quantification, are also discussed. The conclusion is that carotid dP/dt has not been adequately validated for use by psychophysiologists and until such basic research is carried out, this psychophysiological index of sympathetic activity cannot seriously be considered a measure of sympathetic, betaadrenergic, or even ventricular function.

Cardiovascular response to static exercise during selective autonomic blockade in the conscious cat.

Abstract: Selective autonomic blockade with propranolol, atropine, and combined atropine and propranolol was used to elucidate the role of the autonomic nervous system in the cardiovascular responses that occur during voluntary static exercise in conscious cats. Seven animals were operantly conditioned to hold a bar against a fixed resistance for a constant time of 15 seconds and were then placed on an exercise regimen which consisted of small weekly increments in resistance. With a resistance of 100 g. heart rate (HR) increased by 7%. With exercise at a resistance of 200 g, HR (10%), left ventricle systolic pressure (LVSP, 16%), and LV max dp/dt (18%) increased, and significant changes in these parameters persisted throughout the remainder of the training period. beta-Adrenergic receptor blockade with propranolol abolished the increase in LV max dp/dt, whereas HR and LVSP increased. After atropine, the increase in HR was abolished at the early training stages, whereas LVSP and LV max dp/dt increased. Administration of atropine and propranolol blocked the increase in HR and LV max dp/dt responses, whereas LVSP increased. In this study, the increased HR in response to exercise was mediated primarily by the parasympathetic nervous system, whereas the increases in LV max dp/dt were mediated by the sympathetic nervous system. Furthermore, the bradycardia accompanying chronic performance of isometric exercise resulted from both an increase in vagal tone and a decrease in sympathetic tone.