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- Brown, Rachael, et al.
(författare)
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Assessing the integrity of sympathetic pathways in spinal cord injury.
- 2007
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Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1566-0702. ; 134:1-2, s. 61-8
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Tidskriftsartikel (refereegranskat)abstract
- STUDY DESIGN: Measurement of cutaneous sympathetic reflexes and hemodynamic responses to brief electrical stimuli applied above (forehead) and below (abdominal wall) a spinal lesion. OBJECTIVE: To assess the validity of using cutaneous vasoconstriction as a sensitive indicator of increases in sympathetic activity in spinal cord injury. SETTING: Prince of Wales Medical Research Institute, Australia. SUBJECTS: Twenty spinal cord injured subjects with injuries ranging from C3-T11 and nine able-bodied controls. METHOD: Cutaneous electrical stimulation was applied to the forehead and abdominal wall to subjects at unexpected times. Sudomotor and vasomotor responses, as well as continuous arterial pressure, heart rate and respiration were monitored. RESULTS: Sudomotor (electrodermal) responses to forehead stimulation were scarce in spinal cord injured subjects, whereas cutaneous vasoconstrictor responses (photoelectric pulse plethysmography) provided a sensitive indicator of any remaining central control of sympathetic function below the lesion. Electrical stimulation applied to the abdominal wall evoked vasoconstrictor reflexes below the lesion in the majority of spinal cord injured subjects, whereas only a limited number of electrodermal responses were observed. That these cutaneous vasoconstrictor responses could reflect parallel increases in muscle and splanchnic vasoconstrictor activity was indicated by the increases in blood pressure; patients lacking vasoconstrictor responses rarely showed stimulus-induced blood pressure increases. CONCLUSION: Our findings show that skin vasomotor responses to somatosensory stimulation provide a more sensitive tool than electrodermal responses for evaluation of sympathetic function below a spinal cord lesion. STATEMENT OF ETHICS: We certify that all applicable institutional and governmental regulations concerning the ethical use of human volunteers were followed during the course of this research, and all experiments were conducted with the understanding and consent of each subject.
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- Charkoudian, N., et al.
(författare)
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Relationship between muscle sympathetic nerve activity and systemic hemodynamics during nitric oxide synthase inhibition in humans
- 2006
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Ingår i: AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 291:3
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Tidskriftsartikel (refereegranskat)abstract
- Large interindividual differences exist in resting sympathetic nerve activity (SNA) among normotensive humans with similar arterial pressure (AP). We recently showed inverse relationships of resting SNA with cardiac output (CO) and vascular adrenergic responsiveness that appear to balance the influence of differences in SNA on blood pressure. In the present study, we tested whether nitric oxide (NO)-mediated vasodilation has a role in this balance by evaluating hemodynamic responses to systemic NO synthase (NOS) inhibition in individuals with low and high resting muscle SNA (MSNA). We measured MSNA via peroneal microneurography, CO via acetylene uptake and AP directly, at baseline and during increasing systemic doses of the NOS inhibitor NG-monomethyl-l-arginine (l-NMMA). Baseline MSNA ranged from 9 to 38 bursts/min (13 to 68 bursts/100 heartbeats). l-NMMA caused dose-dependent increases in AP and total peripheral resistance and reflex decreases in CO and MSNA. Increases in AP with l-NMMA were greater in individuals with high baseline MSNA ( PANOVA < 0.05). For example, after 8.5 mg/kg of l-NMMA, in the low MSNA subgroup ( n = 6, 28 ± 4 bursts/100 heartbeats), AP increased 9 ± 1 mmHg, whereas in the high-MSNA subgroup ( n = 6, 58 ± 3 bursts/100 heartbeats), AP increased 15 ± 2 mmHg ( P < 0.01). The high-MSNA subgroup had lower baseline CO and smaller decreases in CO with l-NMMA, but changes in total peripheral resistance were not different between groups. We conclude that differences in CO among individuals with varying sympathetic traffic have important hemodynamic implications during disruption of NO-mediated vasodilation.
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- Donadio, Vincenzo, et al.
(författare)
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Arousal elicits exaggerated inhibition of sympathetic nerve activity in phobic syncope patients.
- 2007
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Ingår i: Brain : a journal of neurology. - : Oxford University Press (OUP). - 1460-2156. ; 130:Pt 6, s. 1653-62
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Tidskriftsartikel (refereegranskat)abstract
- Alerting stimuli causing arousal have been shown to elicit a reproducible transient inhibition of muscle sympathetic nerve activity (MSNA) in healthy subjects. The aim of the present study was to test whether this inhibitory response to arousal is exaggerated in patients with a history of vasovagal syncope. We studied 24 untreated syncope patients, 12 of whom met the DSM-IV-TR diagnostic criteria for blood/injury phobia and 18 age-matched healthy subjects. MSNA was recorded from the peroneal nerve at the fibular head. Arousal was induced by randomly presented trains of five electrical pulses delivered to a finger. The pulses were triggered on five consecutive R waves of the ECG, with a delay of 200 ms. Patients also underwent cardiological and neurological examinations, tilt test and a structured interview to investigate diagnostic criteria for specific phobia. The syncope patients had significantly lower resting MSNA (29 +/- 2 bursts/min) and diastolic blood pressure (BP, 78 +/- 2 mmHg) compared to controls (36 +/- 2 bursts/min and 84 +/- 3 mmHg; P < 0.05), whereas no significant differences were found for resting heart rate and systolic BP. The phobic patient group exhibited prolonged sympathetic inhibitions to arousal stimuli compared to controls and non-phobic patients, whereas no difference was found between tilt-positive and tilt-negative patients or between controls and non-phobic patients. The findings suggest that the degree of inhibition in response to arousal stimuli is related to a subjective factor coupled to fear of blood/injury. The exaggerated inhibition in patients with phobia to blood/injury may be a factor predisposing to syncope in those patients.
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