Motor and sensory deficits are well-known consequences of spinal cord injury (SCI). During the last decade, a significant number of experimental and clinical studies have focused on the investigation of autonomic dysfunction and cardiovascular control following SCI. Numerous clinical reports have suggested that unstable blood pressure control in individuals with SCI could be responsible for their increased cardiovascular mortality. The aim of this review is to outline the incidence and pathophysiological mechanisms underlying the orthostatic hypotension that commonly occurs following SCI. We describe the clinical abnormalities of blood pressure control following SCI, with particular emphasis upon orthostatic hypotension. Possible mechanisms underlying orthostatic hypotension in SCI, such as changes in sympathetic activity, altered baroreflex function, the lack of skeletal muscle pumping activity, cardiovascular deconditioning and altered salt and water balance will be discussed. Possible alterations in cerebral autoregulation following SCI, and the impact of these changes upon cerebral perfusion are also examined. Finally, the management of orthostatic hypotension will be considered.

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Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

Orthostatic intolerance is common when astronauts return to Earth: after brief spaceflight, up to two-thirds are unable to remain standing for 10 min. Previous research suggests that susceptible individuals are unable to increase their systemic vascular resistance and plasma noradrenaline concentrations above pre-flight upright levels. In this study, we tested the hypothesis that adaptation to the microgravity of space impairs sympathetic neural responses to upright posture on Earth. We studied six astronauts approximately 72 and 23 days before and on landing day after the 16 day Neurolab space shuttle mission. We measured heart rate, arterial pressure and cardiac output, and calculated stroke volume and total peripheral resistance, during supine rest and 10 min of 60 deg upright tilt. Muscle sympathetic nerve activity was recorded in five subjects, as a direct measure of sympathetic nervous system responses. As in previous studies, mean (+/- S.E.M.) stroke volume was lower (46 +/- 5 vs. 76 +/- 3 ml, P = 0.017) and heart rate was higher (93 +/- 1 vs. 74 +/- 4 beats min(-1), P = 0.002) during tilt after spaceflight than before spaceflight. Total peripheral resistance during tilt post flight was higher in some, but not all astronauts (1674 +/- 256 vs. 1372 +/- 62 dynes s cm(-5), P = 0.32). No crew member exhibited orthostatic hypotension or presyncopal symptoms during the 10 min of postflight tilting. Muscle sympathetic nerve activity was higher post flight in all subjects, in supine (27 +/- 4 vs. 17 +/- 2 bursts min(-1), P = 0.04) and tilted (46 +/- 4 vs. 38 +/- 3 bursts min(-1), P = 0.01) positions. A strong (r(2) = 0.91-1.00) linear correlation between left ventricular stroke volume and muscle sympathetic nerve activity suggested that sympathetic responses were appropriate for the haemodynamic challenge of upright tilt and were unaffected by spaceflight. We conclude that after 16 days of spaceflight, muscle sympathetic nerve responses to upright tilt are normal.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2001.012575

Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight.

Background— Orthostatic intolerance is characterized by postural tachycardia syndrome (POTS) with exaggerated tachycardia, orthostatic symptoms, and “pooling” (which comprises acrocyanosis and dependent edema when upright). My colleagues and I tested the hypothesis that pooling results from increased venous compliance in POTS patients. Methods and Results— Fifteen patients aged 13 to 19 years were compared with 11 healthy, age-matched controls. The POTS group was divided into patients with high venous pressure (Pv>20 mm Hg) and normal Pv on the basis of resting supine Pv obtained in previous work. Subjects were studied using strain gauge plethysmography to measure blood flow, Pv, and the venous compliance volume-pressure relation while supine and during incremental head-up tilt testing at −10°, 0°, 20°, and 35°. Volume-pressure relations of controls and POTS patients with normal Pv and high Pv were not different and were unchanged by orthostasis. Supine leg peripheral resistance was greater than control r...

Pooling in Chronic Orthostatic Intolerance Arterial Vasoconstrictive but not Venous Compliance Defects

Syncope or near-syncope is a not uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value. It is not necessarily abnormal, and individuals who are usually asymptomatic show the same reaction if a stress is sufficiently great to result in hypotension. Blood pressure is regulated mainly by baroreceptor reflexes by their control of vascular resistance and heart rate. The ability to vasoconstrict powerfully is important in resisting syncope; heart rate responses are of much less physiological significance. The intriguing unanswered question is what suddenly changes vasoconstriction and tachycardia to vasodilatation and bradycardia. It is now known not to be due to stimulation of cardiac receptors and some cerebral signal is more probable. People are more likely to faint when upright, motionless, warm, following meals, dehydrated or emotionally stressed, and these factors may be involved in some reflex syncopes including micturition and defaecation syncopes. Plasma volume is of considerable importance and increasing this by interventions such as salt loading, exercise training, and even sleeping with the bed head raised can often be of clinical benefit.

Pathophysiology of syncope.

Background— We tested the hypothesis that individual variability in orthostatic tolerance is dependent on the degree of neural and vasomotor reserve available for vasoconstriction. Methods and Results— Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in 12 healthy young volunteers during 60° head-up tilt (HUT), followed by a cold pressor test (CPT) in HUT. Orthostatic tolerance was determined by progressive lower-body negative pressure (LBNP) to presyncope. The same protocols were performed randomly in normovolemic and hypovolemic conditions. We found that mean arterial pressure increased and stroke volume decreased, whereas heart rate (HR), MSNA, and total peripheral resistance (TPR) increased during HUT (all P<0.01). Application of the CPT in HUT did not increase HR or decrease stroke volume further but elevated mean arterial pressure (P<0.01) and increased MSNA and TPR in some subjects. There was a positive correlation between the time to presyncope from −50 mm Hg LBNP (equivalen...

Vasoconstrictor reserve and sympathetic neural control of orthostasis

Violin concerto in D major (1805)

Perspectives on Beethoven

Des Heilands letzte Stunden

In quest of the distinctive language of Classical and Romantic performance

Es una traduccion de: Brown, Clive: “Tempo”, en Classical and Romantic Performance Practice (1750-1900),
Oxford, © Oxford University Press, Inc., cap. 8, pp. 282-312.

Clive Brown

Papers

Violin concerto in D major (1805)

Perspectives on Beethoven

Des Heilands letzte Stunden

In quest of the distinctive language of Classical and Romantic performance

El tempo en la música clásica y romántica (1750-1900)