Publications
161 results found
Iodice V, Low DA, Vichayanrat E, et al., 2012, Cardiovascular Autonomic Dysfunction in Parkinson’s Disease and Parkinsonian Syndromes, Parkinson's disease, Editors: Ebadi, Pfeiffer, Publisher: Taylor and Francis, ISBN: 9780849315909
The cardiovascular system is influenced by a variety of factors that include the autonomic nervous system. Through the arterial baroreceptor reflex, the sympathetic and parasympathetic components of the autonomic nervous system exert beat-by-beat control over the maintenance of blood pressure, and both directly and indirectly influence the perfusion of various organs. In Parkinson’s disease and various parkinsonian syndromes, cardiovascular dysfunction may occur for a variety of reasons. Autonomic failure is an integral component of parkinsonian syndromes such as multiple system atrophy (MSA), where orthostatic (postural) hypotension is an important clue to underlying cardiovascular autonomic failure and in the recognition of this disorder. The majority of parkinsonian patients are over the age of 50, when the incidence of cardiovascular disorders increases regardless of associated disease. Many parkinsonian patients are on drugs (anti-parkinsonian or for coincidental medical disorders) that may have cardiovascular side effects. Furthermore, with advancing years there is impairment of autonomic function that may occur independently of the parkinsonian state. This chapter will describe aspects of cardiovascular dysfunction resulting from autonomic impairment in PD and parkinsonian syndromes.
Iodice V, Low DA, Vichayanrat E, et al., 2011, Cardiovascular autonomic dysfunction in MSA and Parkinson's disease: Similarities and differences, JOURNAL OF THE NEUROLOGICAL SCIENCES, Vol: 310, Pages: 133-138, ISSN: 0022-510X
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- Citations: 60
Berganzo K, Tijero B, Somme JH JH, et al., 2011, SCOPA-AUT scale in different parkinsonisms and its correlation with (123) I-MIBG cardiac scintigraphy, Parkinsonism and Related Disorders
INTRODUCTION: Our objective was to assess the usefulness of the Scales for Outcomes in Parkinson's disease - Autonomic (SCOPA-AUT) in the differential diagnosis of Parkinsonisms and clarify its relation with 123-I-MIBG cardiac scintigraphy.METHODS: A total of 112 patients with Parkinson's disease (PD), 12 with multiple system atrophy parkinsonian variant (MSA-P) and 20 with progressive supranuclear palsy (PSP) participated in the study. The following variables were collected: age, sex, age at onset, length of illness, type and dose of anti-Parkinson medication, and score on the Unified Parkinson's Disease Rating Scale. The Unified Multiple System Atrophy Rating Scale was administered to patients with MSA and the Progressive Supranuclear Palsy Rating Scale to those with PSP. Finally, the SCOPA-AUT was administered to all the patients. Cardiac 123I-MIBG SPECT scans were performed on a subset of patients (25 with PD and 5 with MSA-P).RESULTS: Statistically significant differences were observed (p < 0.01) in the SCOPA-AUT scores between patients with PD (14.75+/-8.09) and those with MSA (21.07+/-5.56), the latter having higher scores on the bowel function (20.07+/-13.40 vs 34.92+/-14.91) and urinary domains (30.21+/-21.55 vs 49.26+/-21.40) (p < 0.01). No correlation was found between the SCOPA-AUT score and anti-Parkinson's medication and heart:mediastinum (H/M) MIBG uptake ratio in the cardiac SPECT (at 4 h).DISCUSSION: Severity of dysautonomia as measured by the SCOPA-AUT was not correlated with clinical severity, time since onset or the H/M ratio. In the patients with PD, the only variable associated with the H/M ratio was age at onset of the disease.
Stoehr EJ, Gonzalez-Alonso J, Pearson J, et al., 2011, Dehydration reduces left ventricular filling at rest and during exercise independent of twist mechanics, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 111, Pages: 891-897, ISSN: 8750-7587
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- Citations: 47
Low DA, Keller DM, Wingo JE, et al., 2011, Sympathetic nerve activity and whole body heat stress in humans, Journal of Applied Physiology, Vol: 111, Pages: 1329-1334
We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA (n = 8) or SSNA (n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained (P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat
Low DA, Mathias CJ, 2011, Syncope: Physiology, Pathophysiology and Aeromedical Implications, The Neurosciences and the Practice of Aviation Medicine, Editors: Nicholson, Farnham, Surrey, Publisher: Ashgate, Pages: 275-290, ISBN: 9780754672920
Cui J, Shibasaki M, Low DA, et al., 2011, Muscle sympathetic responses during orthostasis in heat-stressed individuals., Clinical Autonomic Research, Vol: 21, Pages: 381-387
PURPOSE: Whole-body heat stress compromises the control of blood pressure during an orthostatic challenge, although the extent to which this occurs can vary greatly between individuals. The mechanism(s) responsible for these varying responses remain unclear. This study tested the hypothesis that the individuals who are best able to tolerate an orthostatic challenge while heat stressed are the ones with the largest increase in sympathetic activity during orthostasis, indexed from recordings of muscle sympathetic nerve activity (MSNA).METHODS: MSNA, arterial blood pressure, and heart rate were recorded from 11 healthy volunteers throughout passive whole-body heating and during 15 min of 60° head-up tilt (HUT) or until the onset of pre-syncopal symptoms.RESULTS: Whole-body heating significantly increased core temperature (~0.9°C), supine heart rate and MSNA. Eight of 11 subjects developed pre-syncopal symptoms resulting in early termination of HUT. The HUT tolerance time was positively correlated (R = 0.82, P = 0.01) with the increase in MSNA by HUT.CONCLUSION: These data suggest that the individuals with the largest increase in MSNA during upright tilt have the greatest capacity to withstand the orthostatic challenge while heat stressed.
Low DA, Hubing KA, Del Coso J, et al., 2011, Mechanisms of cutaneous vasodilation during the postmenopausal hot flash, Menopause: The Journal of the North American Menopause Society, Vol: 18(4), Pages: 359-365
OBJECTIVE: Menopausal hot flashes can seriously disrupt the lives of symptomatic women. The physiological mechanisms of the hot flash efferent responses, particularly in the cutaneous circulation, are not completely understood. The aim of this study was to examine the mechanisms of increases in skin blood flow during the postmenopausal hot flash in symptomatic women.METHODS: Healthy postmenopausal women rested in a temperature-controlled laboratory while responses before and during hot flashes were recorded for three unique protocols. In protocols 1 and 2, women were locally pretreated with an intradermal injection of botulinum toxin A (BTX; blocks the release of neurotransmitters from sympathetic cholinergic nerves) in the forearm (protocol 1) and in the glabellar region (protocol 2). In protocol 3, skin sympathetic nerve activity from the peroneal nerve was recorded, along with skin blood flow and sweating within the region innervated by that neural signal. Skin blood flow was indexed using laser-Doppler flowmetry at the BTX-treated and adjacent untreated control sites. The onset of a hot flash was objectively identified as a transient and pronounced increase in sternal sweat rate.RESULTS: The increases in forearm (protocol 1) and glabellar skin (protocol 2) blood flow during hot flashes were attenuated at the BTX sites relative to the adjacent untreated sites (P<0.05 for both protocols). In protocol 3, skin sympathetic nerve activity significantly increased during hot flashes and returned to pre-hot flash levels after the hot flashes.CONCLUSIONS: Increases in skin blood flow during postmenopausal hot flashes are neurally mediated primarily through BTX-sensitive nerves, presumably sympathetic cholinergic.
Keller DM, Low DA, Davis SL, et al., 2011, Skin surface cooling improves orthostatic tolerance following prolonged head-down bed rest, Journal of Applied Physiology, Vol: 110(6), Pages: 1592-1597
Prolonged exposure to microgravity, as well as its ground-based analog, head-down bed rest (HDBR), reduces orthostatic tolerance in humans. While skin surface cooling improves orthostatic tolerance, it remains unknown whether this could be an effective countermeasure to preserve orthostatic tolerance following HDBR. We therefore tested the hypothesis that skin surface cooling improves orthostatic tolerance after prolonged HDBR. Eight subjects (six men and two women) participated in the investigation. Orthostatic tolerance was determined using a progressive lower-body negative pressure (LBNP) tolerance test before HDBR during normothermic conditions and on day 16 or day 18 of 6° HDBR during normothermic and skin surface cooling conditions (randomized order post-HDBR). The thermal conditions were achieved by perfusing water (normothermia ∼34°C and skin surface cooling ∼12-15°C) through a tube-lined suit worn by each subject. Tolerance tests were performed after ∼30 min of the respective thermal stimulus. A cumulative stress index (CSI; mmHg LBNP·min) was determined for each LBNP protocol by summing the product of the applied negative pressure and the duration of LBNP at each stage. HDBR reduced normothermic orthostatic tolerance as indexed by a reduction in the CSI from 1,037 ± 96 mmHg·min to 574 ± 63 mmHg·min (P < 0.05). After HDBR, skin surface cooling increased orthostatic tolerance (797 ± 77 mmHg·min) compared with normothermia (P < 0.05). While the reduction in orthostatic tolerance following prolonged HDBR was not completely reversed by acute skin surface cooling, the identified improvements may serve as an important and effective countermeasure for individuals exposed to microgravity, as well as immobilized and bed-stricken individuals.
Pearson J, Low DA, Stoehr E, et al., 2011, Hemodynamic responses to heat stress in the resting and exercising human leg: insight into the effect of temperature on skeletal muscle blood flow, AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, Vol: 300, Pages: R663-R673, ISSN: 0363-6119
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- Citations: 89
Stoehr EJ, Gonzalez-Alonso J, Pearson J, et al., 2011, Effects of graded heat stress on global left ventricular function and twist mechanics at rest and during exercise in healthy humans, EXPERIMENTAL PHYSIOLOGY, Vol: 96, Pages: 114-124, ISSN: 0958-0670
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- Citations: 43
Iodice V, Low DA, Vichayanrat E, et al., 2011, Cardiovascular Autonomic Dysfunction in Parkinson’s Disease and Parkinsonian Syndromes., Florida, Publisher: CRC Press
Mathias CJ, Low DA, Iodice V, et al., 2011, Postural tachycardia syndrome—current experience and concepts, Nature Reviews Neurology, Vol: In press
Mathias CJ, Iodice V, Low DA, 2011, Autonomic Dysfunction—Recognition, Diagnosis, Investigation and Management – to include Autonomic Neurorehabilitation, Handbook of Clinical Neurology Series; Neurorehabilitation volume, Editors: Barnes, Good, Publisher: Elsevier
The autonomic nervous system, through its central connections and efferent pathways innervates every organ in the body, influences their function and is also involved in a number of integrative systems such as those concerned with maintenance of arterial blood pressure, organ perfusion and body temperature. Responsive functioning of the ANS is thus needed in a variaty of situations, it contribues to well being, and it is essential for survival. Autonomic dysfunction may occur in a number of neurological diseases and may complicate various medical disorders. This chapter will provide an outline of the scientific principles, followed by classification of autonomic disorders, an outline of the autonomic investigations, brief accounts of some of the key disorders and the pathophysiological mechanisms involved, and discussion of treatment emphasizing the importance of non-pharmacological methods, and, in particular the role of autonomic neuro-rehabilitation.
Shave R, Ross P, Low D, et al., 2010, Cardiac troponin I is released following high-intensity short-duration exercise in healthy humans, INTERNATIONAL JOURNAL OF CARDIOLOGY, Vol: 145, Pages: 337-339, ISSN: 0167-5273
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- Citations: 67
Cui J, Shibasaki M, Low DA, et al., 2010, Heat stress attenuates the increase in arterial blood pressure during the cold pressor test, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 109, Pages: 1354-1359, ISSN: 8750-7587
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- Citations: 24
Hubing KA, Wingo JE, Brothers RM, et al., 2010, Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal hot flash episodes, MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY, Vol: 17, Pages: 978-982, ISSN: 1072-3714
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- Citations: 17
Sanchez-Manso JC, Low D, Mathias CJ, 2010, Standard meal test in the evaluation of diabetic patients with suspected post-prandrial hypotension, 14th Congress of European-Federation-of-Neurological-Societies, Publisher: WILEY-BLACKWELL, Pages: 658-658, ISSN: 1351-5101
Wingo JE, Low DA, Keller DM, et al., 2010, Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans, Journal of Applied Physiology, Vol: 109, Pages: 1301-1306
Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34°C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ~1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.
Stoehr EJ, Gonzalez-Alonso J, Pearson J, et al., 2010, Challenging The Heart - Effects Of Exercise, Dehydration And Hyperthermia, 57th Annual Meeting of the American-College-Sports-Medicine/Inaugural World Congress on Exercise is Medicine, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: 6-6, ISSN: 0195-9131
Mathias CJ, Galizia G, 2010, Orthostatic hypotension and orthostatic intolerance., Endocrinology; adult and pediatric 6th edition, Editors: Jameson JL, De Groot LJ, Publisher: Elsevier
Mathias CJ, 2010, Diseases of the autonomic nervous system, Editors: Warrell DA, Cox TM, Firth JD, Oxford, Publisher: Oxford University Press
Shibasaki M, Davis SL, Cui J, et al., 2009, Botulinum toxin abolishes sweating via impaired sweat gland responsiveness to exogenous acetylcholine, British Journal of Dermatology, Vol: 161, Pages: 757-761
BACKGROUND: Botulinum toxin A (BTX) disrupts neurotransmitter release from cholinergic nerves. The effective duration of impaired sweat secretion with BTX is longer relative to that of impaired muscle contraction, suggesting different mechanisms in these tissues.OBJECTIVES: The aim of this study was to test the hypothesis that BTX is capable of altering sweating by reducing the responsiveness of the sweat gland to acetylcholine.METHODS: BTX was injected into the dorsal forearm skin of healthy subjects at least 3 days before subsequent assessment. On the day of the experiment, intradermal microdialysis probes were placed within the BTX-treated area and in an adjacent untreated area. Incremental doses of acetylcholine were administered through the microdialysis membranes while the sweat rate (protocol 1; n = 8) or a combination of sweat rate and skin blood flow (protocol 2; n = 8) were assessed.RESULTS: A relative absence of sweating was observed at the BTX site for both protocols (protocol 1: 0.05 +/- 0.09 mg cm(-2) min(-1); protocol 2: 0.03 +/- 0.04 mg cm(-2) min(-1), both at the highest dose of acetylcholine), while the sweat rate increased appropriately at the control sites (protocol 1: 0.90 +/- 0.46 mg cm(-2) min(-1); protocol 2: 1.07 +/- 0.67 mg cm(-2) min(-1)). Cutaneous vascular conductance increased to a similar level at both the BTX and control sites.CONCLUSIONS: These results demonstrate that BTX is capable of inhibiting sweat secretion by reducing the responsiveness of the sweat gland to acetylcholine, while not altering acetylcholine-mediated cutaneous vasodilatation.
Low DA, Wingo JE, Keller DM, et al., 2009, Dynamic cerebral autoregulation during passive heat stress in humans, AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, Vol: 296, Pages: R1598-R1605, ISSN: 0363-6119
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- Citations: 39
Wingo JE, Low DA, Keller DM, et al., 2009, Isolated effects of elevated local temperature on sweating in humans, Publisher: FEDERATION AMER SOC EXP BIOL, ISSN: 0892-6638
Cui J, Shibasaki M, Davis SL, et al., 2009, Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 106, Pages: 1125-1131, ISSN: 8750-7587
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- Citations: 14
Wingo JE, Low DA, Keller DM, et al., 2009, Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 106, Pages: 571-575, ISSN: 8750-7587
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- Citations: 23
Keller DM, Low DA, Wingo JE, et al., 2009, Acute volume expansion preserves orthostatic tolerance during whole-body heat stress in humans, Journal of Physiology-London, Vol: 587, Pages: 1131-1139
Whole-body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 +/- 10 years: mean +/- S.D.), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body heating, and whole-body heating + acute volume expansion. For the whole-body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-heat stress values. Whole-body heat stress alone reduced orthostatic tolerance by approximately 80% compared to normothermia (938 +/- 152 versus 182 +/- 57 CSI; mean +/- S.E.M., P < 0.001). Acute volume expansion during whole-body heating completely ameliorated the heat stress-induced reduction in orthostatic tolerance (1110 +/- 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat-stressed human.
Mathias CJ, 2009, Autonomic Dysfunction, Neurology. A Queen Square Textbook, Editors: Clarke C, Howard R, Rossor M, Shorvon S, Publisher: Wiley-Blackwell
Davis SL, Shibasaki M, Low DA, et al., 2009, Sustained impairments in cutaneous vasodilation and sweating in grafted skin following long-term recovery., J Burn Care Res, Vol: 30, Pages: 675-685, ISSN: 1559-047X
We previously identified impaired cutaneous vasodilation and sweating in grafted skin 5 to 9 months postsurgery. The aim of this investigation was to test the hypothesis that cutaneous vasodilation, but not sweating, is restored as the graft heals. Skin blood flow and sweat rate were assessed from grafted skin and adjacent noninjured skin in three groups of subjects: 5 to 9 months postsurgery (n=13), 2 to 3 years postsurgery (n=13), and 4 to 8 years postsurgery (n=13) during three separate protocols: 1) whole-body heating and cooling, 2) local administration of vasoactive drugs, and 3) local heating and cooling. Cutaneous vasodilation and sweating during whole-body heating were significantly lower (P<.001) in grafted skin when compared with noninjured skin across all groups and demonstrated no improvements with recovery time postsurgery. Maximal endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) cutaneous vasodilation remained attenuated (P<.001) in grafted skin up to 4 to 8 years postsurgery, indicating postsynaptic impairments. In grafted skin, cutaneous vasoconstriction during whole-body and local cooling was preserved, whereas vasodilation to local heating was impaired, regardless of the duration postsurgery. Split-thickness skin grafts have impaired cutaneous vasodilation and sweating up to 4 to 8 years postsurgery, thereby limiting the capability of this skin's contribution to thermoregulation during a heats stress. In contrast, grafted skin has preserved vasoconstrictor capacity.
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