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Relatively few studies have examined the effects of nociception pe se on sympathetic nerve activity in awake healthy human subjects. Painful stimuli can produce differential responses from cutaneous and muscle postganglionic sympathetic neurones in the anaesthetised cat, and some animal and human studies suggest that nociceptive stimuli originating in different tissues may produce differential sympathetic effects- deep nociception causing vasodepressive and superficial nociception triggering an excitatory effect on cardiovascular state. It is important to understand how the sympathetic nervous system responds to nociception in healthy subjects in order to make more meaningful comparisons with the behaviour which occurs following damage to sympathetic pathways, e.g. nerve lesions (chronic regional pain syndromes) and spinal cord injury (autonomic dysreflexia (AD)). Additionally, it has been suggested that muscle spindles afferents may play a role in chronic pain, most notably the 'vicious cycle' of pain. While this has been investigated in animal studies, it has not been thoroughly investigated in healthy human subjects. Muscle spindle and sympathetic nerve activity from muscle and skin postganglionic neurones were directly recorded in healthy awake human subjects using microneurography; effector organ responses (blood pressure, heartrate, skin blood flow and sweat release) were recorded in both healthy and spinal cord injured subjects. Deep and superficial nociception was induced by intramuscular and subdermal injections of hypertonic saline given at unexpected times and in quasi-random order. Regardless of the origin of nociception (deep or superficial), general responses tended to be excitatory with increases seen in muscle and skin sympathetic nerve activity, heartrate, blood pressure and sweat release. A gender effect was noted regarding skin blood flow, with males largely showing decreases and females increases. No changes were noted in spindle firing rates and painful stimuli did not significantly increase effector organ responses in spinal cord injured subjects. Contrasting with previous studies, we did not see a differential sympathetic response or change in spindle firing rate to painful stimuli originating in different tissues. While it is believed that noxious stimuli trigger AD, we did not see exaggerated sympathetic responses in spinal cord injured subjects. More investigation is required regarding innocuous triggers of AD.

Relatively few studies have examined the effects of nociception pe se on sympathetic nerve activity in awake healthy human subjects. Painful stimuli can produce differential responses from cutaneous and muscle postganglionic sympathetic neurones in the anaesthetised cat, and some animal and human studies suggest that nociceptive stimuli originating in different tissues may produce differential sympathetic effects- deep nociception causing vasodepressive and superficial nociception triggering an excitatory effect on cardiovascular state. It is important to understand how the sympathetic nervous system responds to nociception in healthy subjects in order to make more meaningful comparisons with the behaviour which occurs following damage to sympathetic pathways, e.g. nerve lesions (chronic regional pain syndromes) and spinal cord injury (autonomic dysreflexia (AD)). Additionally, it has been suggested that muscle spindles afferents may play a role in chronic pain, most notably the 'vicious cycle' of pain. While this has been investigated in animal studies, it has not been thoroughly investigated in healthy human subjects. Muscle spindle and sympathetic nerve activity from muscle and skin postganglionic neurones were directly recorded in healthy awake human subjects using microneurography; effector organ responses (blood pressure, heartrate, skin blood flow and sweat release) were recorded in both healthy and spinal cord injured subjects. Deep and superficial nociception was induced by intramuscular and subdermal injections of hypertonic saline given at unexpected times and in quasi-random order. Regardless of the origin of nociception (deep or superficial), general responses tended to be excitatory with increases seen in muscle and skin sympathetic nerve activity, heartrate, blood pressure and sweat release. A gender effect was noted regarding skin blood flow, with males largely showing decreases and females increases. No changes were noted in spindle firing rates and painful stimuli did not significantly increase effector organ responses in spinal cord injured subjects. Contrasting with previous studies, we did not see a differential sympathetic response or change in spindle firing rate to painful stimuli originating in different tissues. While it is believed that noxious stimuli trigger AD, we did not see exaggerated sympathetic responses in spinal cord injured subjects. More investigation is required regarding innocuous triggers of AD.

INTRODUÇÃO: Frente às evidências de que a depressão associa-se a eventos cardíacos, morte súbita, desenvolvimento de coronariopatia, e maior mortalidade por causas cardiovasculares, torna-se muito importante estudar as possíveis causas das alterações cardiovasculares na depressão. Alterações de sistema nervoso autonômico (SNA) vêm sendo descritas em pacientes deprimidos. Os estudos sobre funcionamento do SNA têm utilizado a dosagem de catecolaminas séricas e urinárias e análise de VFC, que são avaliações indiretas do funcionamento do SNA. Avaliações diretas, como a microneurografia, aparentemente ainda não foram utilizadas no estudo do funcionamento do SNA em pacientes com depressão maior. MÉTODOS: Neste estudo o comportamento do sistema nervoso simpático em indivíduos deprimidos, em período basal e após teste de estresse mental, foi comparado com controles. Realizaram as avaliações: 19 pacientes com depressão maior e 15 controles, com 18 a 45 anos de idade. Indivíduos que apresentassem condições médicas e/ou uso de medicamentos que pudessem interferir com o comportamento do sistema nervoso autonômico não foram incluídos. A avaliação psiquiátrica incluiu a administração da Escala de avaliação para depressão de Montgomery e Asberg (MADRS) e Entrevista Clínica Estruturada para o DSM-IV - Transtornos do Eixo I - Versão 2.0 (SCID-I /P). Atividade nervosa simpática muscular (ANMS) foi medida pela microneurografia. Fluxo sangüíneo muscular (FSM) no antebraço foi medido pela técnica de peltismografia de oclusão venosa. A pressão arterial (PA) foi monitorizada de forma não invasiva por um manguito inflado automaticamente, e a freqüência cardíaca (FC) foi medida por eletrocardiograma. O registro basal foi realizado por 3 minutos, seguido de teste de cores, que foi realizado por 4 minutos. RESULTADOS: Os grupos de pacientes deprimidos e controles não diferiram significativamente em relação a idade, peso e índice de massa corpórea. Os grupos de pacientes deprimidos e controles não apresentaram diferenças significativas nos valores de ANSM, PA sistólica, PA diastólica, PA média, FC, FSM e condutância vascular no antebraço no período basal. Não houve diferença significativa na reatividade ao estresse mental entre os grupos. Houve correlação positiva e significativa (0,84; p=0,0001) entre os valores de MADRS e de ANSM média no período basal dos pacientes com depressão. Houve correlação positiva e significativa (0,70; p=0,01) entre os valores do item tensão da MADRS e de ANSM média no período basal dos pacientes com depressão. CONCLUSÕES: Não foram encontradas diferenças nas medidas basais de atividade simpática entre indivíduos deprimidos e controles. Também não foram encontradas diferenças na reatividade cardiovascular a teste de estresse mental entre os grupos. Houve uma correlação positiva e significativa entre sintomas depressivos e atividade nervosa simpática muscular (ANSM), medida por microneurografia. Houve também uma correlação positiva e significativa entre sintomas ansiosos e ANSM. / INTRODUCTION: It is well established that depression is associated with cardiac events, sudden death, higher cardiovascular mortality and higher incidence of coronary artery disease (CAD). A number of biological mechanisms linking depression and CAD have been identified, including dysregulation of autonomic nervous system (ANS). Studies with heart rate variability and catecholamines measures have been perfomed in depressed patients. Microneurography is a direct and efficient method to measure sympathetic nerve traffic in humans. To our knowledge, there is no previous study with microneurography in depressed patients. METHODS: ANS functioning, during rest and mental stress, in depressed patients was compared to controls. Nineteen depressed patients and 15 controls (18 to 45 years old) were involved in the study. Subjects with medical conditions and/or use of medications that could interfere on ANS were not included. Psychiatric evaluation included the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I/P, Version 2.0) and the Montgomery and Asberg Depression Rating Scale (MADRS). Muscle sympathetic nervous activity (MSNA) was directly measured from the peroneal nerve using microneurography. Forearm blood flow (FBF) was measured by venous occlusion pletysmography. Blood pressure (BP) was monitored noninvasively by an automatic BP cuff, and heart rate (HR) was measured by electrocardiogram. Baseline register was performed by 3 minutes and Stroop color word test was performed for 4 minutes. RESULTS: There was no difference in age, weight and body mass index between the two groups studied. No significant difference was found between groups in regard to systolic BP (SBP), diastolic BP (DBP), mean BP (MBP), HR, MSNA, FBF and forearm vascular conductance at baseline. All parameters significantly increased during mental stress in the two groups. The reactivity to mental stress showed no difference between groups. There was a significant positive correlation between MADRS total scores and mean baseline MSNA (0,84; p=0,0001) among depressed patients. There was also a significant positive correlation between MADRS tension scores and mean baseline MSNA (0,70; p=0,01) among depressed patients. CONCLUSIONS: There were no differences in baseline measures of sympathetic activity between depressed patients and controls. The reactivity to mental stress between the groups did not differ as well. There was a positive significant correlation between depressive symptoms and mean baseline MSNA. There was a positive significant correlation between anxiety symptoms and mean baseline MSNA.

Muscle spindles are complex sensory organs that have been strongly implicated in the control and perception of movements. Human muscle spindles in relaxed muscles behave as stretch receptors, responding to the length and velocity of their parent muscles. However, it has been unclear how they discharge during active movements since their discharges are also affected by fusimotor activity and extrafusal contractions. The vast majority of neurophysiological recordings of muscle afferents have been obtained under passive conditions, or active but behaviourally restricted conditions. These restrictions prevent predictions of human muscle afferent activity during purposeful multi-joint movements, naturally occurring during tasks such as hand shaping, grasping or key-pressing. An experimental protocol was therefore developed which allowed recordings of muscle receptor afferent activity using microneurography during unrestrained wrist and digit movements. Along with single afferent discharges, recordings were obtained of electromyographic activity of major forearm muscles and the kinematics of the wrist and digits. This approach allowed investigations of the factors shaping afferent discharge during everyday manual tasks, i.e., block-grasping and pressing sequences of keys, and during active sinusoidal joint movements. The afferents’ ability to encode information concerning the state of the muscle and joint kinematics during these tasks was also assessed. The responses of spindle afferents from load-bearing muscles were approximatelly 90 degrees more phase-advanced than expected on the length of their parent muscles. That is, the discharges of primary muscle spindle afferents were significantly affected by both velocity and acceleration, the discharges of secondary afferents by velocity, and neither afferent type was particularly affected by static muscle length. Accordingly, these afferents failed to encode length, encoded velocity well and acceleration poorly. The representation of muscle length and velocity was, however, significantly improved when the discharge activity of Golgi tendon afferents was taken into consideration along with muscle spindle activity. The discharge of primary afferents during both key-pressing and block-grasping was best correlated to the muscle velocities observed ~100-160 ms in the future. This predictive ability went beyond what could be expected from the spindles’ simultaneous sensitivity to velocity and acceleration, and could thus only be explained by implicating the fusimotor drive. In addition, evidence is presented that the fusimotor control of spindles was contingent on entire movement sequences during the key-pressing task. It is proposed that the phase relationship between the discharge rate of spindle afferents and the length of their parent muscles is load dependent. Moreover, muscle spindles seem to act as forward sensory models of their parent muscle, which makes sensorial feedback control possible despite neural delays.

The response patterns of human stretch receptors in the finger extensor muscles of the forearm were studied using the microneurography technique. Single-unit recordings were obtained from one-hundred and twenty-four afferents. A procedure was developed to classify the units in muscle spindle primary afferents, secondary afferents, and Golgi tendong organ afferents. The procedure allows an objective and reproducible classification on the basis of the afferents’ responses to a series of tests which individually are non-conclusive. It was demonstrated that maximal twitch contractions can be elicited in the finger extensor muscles of the forearm, without causing undue discomfort to the subjects, or hazarding the single-unit recording. The response of the units to this test allowed, in most cases but not always, a separation in muscle spindle and tendon organ afferents. Thus the test was not adequate for an unequivocal classification. Three discrete response parameters were extracted from ramp-and-hold stretches, viz. the presence or absence of an initial burst and a deceleration response, and prompt silencing at slow muscle shortening. The distributions of the parameters were significantly different among the three unit types. These parameters which were pair-wise independent constituted a set of considerable discriminative power. It was shown that human muscle spindles have about the same static position sensitivity to fractional muscle stretch as previously found in animals. Stretch sensitization was demonstrated by rapid, repeated stretches of the muscle which enhanced the réponse to subsequent slow stretches of muscle spindles. Sensitization was different with primary and secondary muscle spindle afferents whereas Golgi tendon organ afferents never displayed stretch sensitization. One-to-one driving with small-amplitude sinusoidal stretches superimposed on ramp-and- hold stretches was almost exclusively seen with primary muscle spindle afferents, whereas secondaries seldom and tendon organ afferents never displayed driving. The afferent responses during slowly increasing isometric contractions and rapid relaxations were analysed. An increased discharge rate on relaxation was common among spindle afferents whereas it was never seen in tendon organs afferents. Two separate groups of spindles afferents were found with regard to fusimotor recruitment. The largest group was recruited at rather low and variable contractile forces whereas the smaller group was not recruited at all. The proportions of the three unit types, spindle primary, spindle secondary, and Golgi tendon organ afferents were estimated from a preliminary classification and the distribution of the eight response features were analyzed for each class of afferents. On the basis of these estimates and the response pattern of the individual unit Bayes’ theorem was used to calculate the probabilities that the unit was a spindle primary, a spindle secondary, or a tendon organ afferent. Estimates indicate that about 19 out of 20 muscle afferents are correctly classified when all eight features are analyzed. / <p>Diss. (sammanfattning) Umeå : Umeå universitet, 1988, härtill 6 uppsatser.</p> / digitalisering@umu

INTRODUÇÃO: Frente às evidências de que a depressão associa-se a eventos cardíacos, morte súbita, desenvolvimento de coronariopatia, e maior mortalidade por causas cardiovasculares, torna-se muito importante estudar as possíveis causas das alterações cardiovasculares na depressão. Alterações de sistema nervoso autonômico (SNA) vêm sendo descritas em pacientes deprimidos. Os estudos sobre funcionamento do SNA têm utilizado a dosagem de catecolaminas séricas e urinárias e análise de VFC, que são avaliações indiretas do funcionamento do SNA. Avaliações diretas, como a microneurografia, aparentemente ainda não foram utilizadas no estudo do funcionamento do SNA em pacientes com depressão maior. MÉTODOS: Neste estudo o comportamento do sistema nervoso simpático em indivíduos deprimidos, em período basal e após teste de estresse mental, foi comparado com controles. Realizaram as avaliações: 19 pacientes com depressão maior e 15 controles, com 18 a 45 anos de idade. Indivíduos que apresentassem condições médicas e/ou uso de medicamentos que pudessem interferir com o comportamento do sistema nervoso autonômico não foram incluídos. A avaliação psiquiátrica incluiu a administração da Escala de avaliação para depressão de Montgomery e Asberg (MADRS) e Entrevista Clínica Estruturada para o DSM-IV - Transtornos do Eixo I - Versão 2.0 (SCID-I /P). Atividade nervosa simpática muscular (ANMS) foi medida pela microneurografia. Fluxo sangüíneo muscular (FSM) no antebraço foi medido pela técnica de peltismografia de oclusão venosa. A pressão arterial (PA) foi monitorizada de forma não invasiva por um manguito inflado automaticamente, e a freqüência cardíaca (FC) foi medida por eletrocardiograma. O registro basal foi realizado por 3 minutos, seguido de teste de cores, que foi realizado por 4 minutos. RESULTADOS: Os grupos de pacientes deprimidos e controles não diferiram significativamente em relação a idade, peso e índice de massa corpórea. Os grupos de pacientes deprimidos e controles não apresentaram diferenças significativas nos valores de ANSM, PA sistólica, PA diastólica, PA média, FC, FSM e condutância vascular no antebraço no período basal. Não houve diferença significativa na reatividade ao estresse mental entre os grupos. Houve correlação positiva e significativa (0,84; p=0,0001) entre os valores de MADRS e de ANSM média no período basal dos pacientes com depressão. Houve correlação positiva e significativa (0,70; p=0,01) entre os valores do item tensão da MADRS e de ANSM média no período basal dos pacientes com depressão. CONCLUSÕES: Não foram encontradas diferenças nas medidas basais de atividade simpática entre indivíduos deprimidos e controles. Também não foram encontradas diferenças na reatividade cardiovascular a teste de estresse mental entre os grupos. Houve uma correlação positiva e significativa entre sintomas depressivos e atividade nervosa simpática muscular (ANSM), medida por microneurografia. Houve também uma correlação positiva e significativa entre sintomas ansiosos e ANSM. / INTRODUCTION: It is well established that depression is associated with cardiac events, sudden death, higher cardiovascular mortality and higher incidence of coronary artery disease (CAD). A number of biological mechanisms linking depression and CAD have been identified, including dysregulation of autonomic nervous system (ANS). Studies with heart rate variability and catecholamines measures have been perfomed in depressed patients. Microneurography is a direct and efficient method to measure sympathetic nerve traffic in humans. To our knowledge, there is no previous study with microneurography in depressed patients. METHODS: ANS functioning, during rest and mental stress, in depressed patients was compared to controls. Nineteen depressed patients and 15 controls (18 to 45 years old) were involved in the study. Subjects with medical conditions and/or use of medications that could interfere on ANS were not included. Psychiatric evaluation included the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I/P, Version 2.0) and the Montgomery and Asberg Depression Rating Scale (MADRS). Muscle sympathetic nervous activity (MSNA) was directly measured from the peroneal nerve using microneurography. Forearm blood flow (FBF) was measured by venous occlusion pletysmography. Blood pressure (BP) was monitored noninvasively by an automatic BP cuff, and heart rate (HR) was measured by electrocardiogram. Baseline register was performed by 3 minutes and Stroop color word test was performed for 4 minutes. RESULTS: There was no difference in age, weight and body mass index between the two groups studied. No significant difference was found between groups in regard to systolic BP (SBP), diastolic BP (DBP), mean BP (MBP), HR, MSNA, FBF and forearm vascular conductance at baseline. All parameters significantly increased during mental stress in the two groups. The reactivity to mental stress showed no difference between groups. There was a significant positive correlation between MADRS total scores and mean baseline MSNA (0,84; p=0,0001) among depressed patients. There was also a significant positive correlation between MADRS tension scores and mean baseline MSNA (0,70; p=0,01) among depressed patients. CONCLUSIONS: There were no differences in baseline measures of sympathetic activity between depressed patients and controls. The reactivity to mental stress between the groups did not differ as well. There was a positive significant correlation between depressive symptoms and mean baseline MSNA. There was a positive significant correlation between anxiety symptoms and mean baseline MSNA.

INTRODUÇÃO: A respiração lenta é indicada como tratamento não medicamentoso da hipertensão arterial. Porém, os mecanismos fisiológicos envolvidos na redução da pressão arterial (PA) ainda são desconhecidos. A redução na atividade nervosa simpática (ANS) pode ser um dos mecanismos envolvidos na redução da PA. OBJETIVOS: Avaliar o efeito crônico da respiração lenta na PA e na ANS em hipertensos. MÉTODOS: Foram randomizados hipertensos, com e sem uso de anti-hipertensivos, em grupo controle (GC), orientados a ouvir músicas serenas com uso de aparelho de MP3, ou grupo respiração lenta (GRL), treinados a reduzir a frequência respiratória com auxílio de um dispositivo eletrônico, tendo como alvo terapêutico uma frequência respiratória menor que 10 respirações por minuto, por um período de 15 minutos diários, durante 8 semanas. Antes e após o período de intervenção, foi realizada monitorização ambulatorial da pressão arterial (MAPA), dosagem de catecolaminas plasmáticas e medida da atividade nervosa simpática periférica (ANSP) pela técnica da microneurografia. RESULTADOS: Completaram o estudo 17 voluntários no GRL e 15 no GC. Não houve mudança na PA de consultório antes e após a intervenção nos dois grupos. Observou-se redução na pressão arterial sistólica (PAS) e diastólica (PAD) na vigília entre os períodos pré e pós-intervenção apenas no GC (131±10 / 92±9 vs 128±10 / 88±8 mmHg, p < 0,05). Não foi observada diferença na concentração de catecolaminas plasmáticas (pg/ml) em ambos os grupos entre os períodos pré e pós-intervenção: GRL 302 (220-256) vs 234 (156-318), p=0,35; e GC 201 (144-230) vs 221 (179-274), p=0,97. Nos voluntários que realizaram microneurografia, GRL (n=10) e GC (n=10), observou-se redução significativa da PAD de sono entre os períodos pré e pós- intervenção apenas no GC (83±6 vs 79±4 mmHg, p < 0,05) A ANSP (impulsos/minuto) medida pela microneurografia apresentou elevação no período pós-intervenção em comparação ao período pré-intervenção nos dois grupos: GRL (16±6 vs 22±8, p < 0,05) e GC (20±5 vs 23±5, p < 0,05). CONCLUSÕES: A respiração lenta, realizada por 15 minutos diários durante 8 semanas, não reduziu a pressão arterial, os níveis de catecolaminas plasmáticas e a atividade nervosa simpática periférica de hipertensos / INTRODUCTION: Slow breathing is indicated as nonpharmacological treatment of hypertension. However, the physiological mechanisms involved in blood pressure (BP) reduction are still unknown. The decrease in sympathetic nerve activity (SNA) may be one of the mechanisms involved in BP reduction. OBJECTIVES: To evaluate the chronic effect of slow breathing on BP and SNS in hypertensive patients. METHODS: Hypertensive patients, with or without use of antihypertensive drugs, were randomized to listen serene songs using an MP3 player (Control Group - CG) or device-guided slow breathing group (DGB), who were trained to reduce respiratory rate with assistance of an electronic device, targeting a respiratory rate of less than 10 breaths per minute, for a period of 15 minutes per day for 8 weeks. Before and after the intervention period, ambulatory blood pressure monitoring (ABPM), plasma catecholamines concentration and muscle sympathetic nerve activity (MSNA) using the microneurography technique were performed. RESULTS: 17 volunteers in the DGB and 15 in the CG completed the study. There was no change in office BP before and after intervention in both groups. There was a reduction in daytime systolic (SBP) and diastolic (DBP) before and after intervention only in the CG (131±10 / 92±9 vs 128±10 / 88±8 mmHg, p < 0,05). No difference in plasma catecholamines concentration (pg/ml) was observed in both groups before and after intervention: DGB 302 (220-256) vs 234 (156-318), p = 0.35; CG 201 (144-230) vs 221 (179-274), p=0.97. In the volunteers who underwent microneurography, DGB (n=10) and CG (n=10), there was a significant reduction in sleep DBP only in the CG: 83±6 vs 79±4 mmHg, p < 0,05. The MSNA (bursts/minute) measured by the microneurography showed a rise after the intervention in both groups: DGB (16±6 vs 22±8, p < 0.05) and CG (20±5 vs 23±5, p < 0.05). CONCLUSIONS: Slow breathing, performed for 15 minutes daily for 8 weeks, did not reduce blood pressure, plasma catecholamine concentration and muscle sympathetic nerve activity in hypertensive patients