Plasma catecholamines during paroxysmal neurogenic hypertension in quadriplegic man.

Mathias, C. J.; Christensen, N. J.; Corbett, J. L.; Frankel, H L; Spalding, J. M. K.

doi:10.1161/01.res.39.2.204

Cited by 167 publications

(61 citation statements)

References 19 publications

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“…Peripheral noradrenaline supersensitivity has been documented in chronic human SCI (Mathias et al, 1976;Arnold et al, 1995), and there is additional evidence for more noradrenaline release per impulse (Gao et al, 2002) as well as an increased number of peripheral receptors post SCI (Velasco et al, 1997). In rats, approximately 50% of the AD pressor response can be attributed to vascular hyper-responsiveness (Collins and DiCarlo, 2002).…”

Section: Discussionmentioning

confidence: 99%

Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury

Garrison

Schmit

2008

Clinical Neurophysiology

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Objective-To determine if sympathetically mediated vasoconstriction in the lower extremities is injury-level dependent. Although sympathetic responses have been measured in the limbs of people with high and low level SCI using blood flow measurements, including Doppler ultrasound and venous plethysmography, a direct comparison between injury levels has not been made.Methods-Volunteers with chronic SCI were grouped according to injury level. Above T6: high level (HL, n=7), and T6 and below: low level (LL, n=6). All subjects had complete motor and sensory loss. Leg arterial flows were recorded by venous occlusion plethysmography, and continuous heart rate and mean arterial pressure (MAP) were measured. The conditioning stimulus consisted of transcutaneous stimulation to the arch of the contralateral foot.Results-HL and LL subjects demonstrated a significant decrease in arterial conductance during stimulation with no significant difference found between groups. As expected, only group HL demonstrated a significant increase in MAP.Conclusions-These results support our hypothesis that local (leg) sympathetic responses are similar for both high and low level SCI.Significance-While low level SCI does not typically present with autonomic dysreflexia, bouts of increased reflex sympathetic activity could have ramifications for metabolism as well as renal and motor system function.

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Section: Discussionmentioning

confidence: 99%

Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury

Garrison

Schmit

2008

Clinical Neurophysiology

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“…27 Since CA has been implicated in the acute-exercise in duced elevations in T then one might expect an exaggerated T response in SCI athletes using boosting since T levels at rest are normal in this population. [18][19][20][21][22][23][24][25] In addition AD is associated with elevated cortisol (C) levels27 which have been suggested as a direct inhibitor of testosterone produc tion.28,29 The SCI athlete thus provides a model to examine the effects of CA and C on the exercise induced increment in testo sterone levels.…”

Section: Wheeler 1mentioning

confidence: 99%

Testosterone, cortisol and catecholamine responses to exercise stress and autonomic dysreflexia in elite quadriplegic athletes

et al. 1994

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Episodes of short high intensity exercise are associated with an increase in circulating total testosterone (T) in men. Mechanisms may include hemoconcen tration, decreased metabolic clearance and/or increased synthesis. Beta-blockade abolishes the T response suggesting a direct beta-adrenergic effect on the testes. Some spinal cord injured (SCI) athletes deliberately induce autonomic dysre flexia (boosting) to enhance performance. Associated with this practice are elevated catecholamine (CA) levels and exaggerated responses to serum cate cholamine levels. Since basal T levels are reported to be normal in the SCI male, the T response to acute high intensity exercise might be expected to be exaggerated by boosting and associated elevated CA levels. The acute exercise T response has not been examined in SCI men to date. To determine whether the increased CA values associated with boosting enhanced the exercise-induced T elevation we measured circulating levels of T, cortisol (C), norepinephrine (NE) and epinephrine (E) before and after maximal exertion and a simulated 7.S km race with and without boosting in eight elite quadriplegic athletes. Maximal incremental exercise and a simulated 7.S km race resulted in a rise in T similar to able bodied men under normal exercise conditions. Under boosted conditions the rise in T was eliminated while NE levels were significantly elevated above unboosted levels. The data may suggest an inhibitory role for CA on T production or release under conditions of extreme stress. Other possible mechanisms include C induced suppression, impaired gonadotropin stimulation of the Leydig cell and CA mediated alterations in gonadal blood supply.

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“…Sensitive techniques for catecholamine measurement indicated that the hypertension during bladder contraction and muscle spasm is accompanied by a rise in levels of plasma noradrenaline but not plasma adrenaline (Fig. 2) (Mathias et al, 1976a). Noradrenaline is the neurotransmitter at sympathetic adrenergic nerve terminals, while adrenaline is the principal secretion from the adrenal medulla (Von-Euler, 1954).…”

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Cardiovascular aspects of autonomic dysreflexia since Guttmann and Whitteridge (1947)

Frankel

Mathias

1979

Spinal Cord

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word: Dysreflexia.'AUTONOMIC DYSREFLEXIA ' in patients with high spinal cord lesions has been used in reference to the changes induced by a variety of stimuli which occur in target organs supplied by the sympathetic and parasympathetic nervous systems. The earliest description of the symptoms of autonomic dysreflexia which we have been able to find is by Hilton (1860) who described a 21-year-old man with a tetraplegia complete below C5 segment whose 'bowels (did) not open without medicine (senna). On some days he has peculiar sensations of chilliness, becoming pale, then feels hot and flushed both at defaecation and micturition. The more constipated the bowel, the more these peculiar sensations are experienced.' Hilton described these phenomena but drew no conclusion.It was during World War I that Head and Riddoch made detailed observations of autonomic dysreflexia in patients with spinal cord injuries. They accurately described the responses of sweat glands, genitalia, urinary bladder and rectum which were evoked by cutaneous stimulation below the level of the lesion and by injection of fluid into the bladder and the bowel (Head & Riddoch, 1917;Riddoch, 1917). Riddoch (1917) also described the initial stage of spinal shock during which tendon reflexes could not be elicited and retention of urine and faeces occurred. This stage was followed by the second stage of reflex activity when stimulation of the skin produced sweating around and above the segmental level of the lesion, evacuation of the bladder and rectum and erection of the penis and seminal emission important components of the 'mass reflex'.In recently injured patients with high spinal cord injuries who are in spinal shock there is minimal cardiovascular reflex activity presumably because both the parasympathetic and sympathetic pathways in the isolated spinal cord are depressed (Mathias et al., , 1979a. Pronounced cardiovascular changes, however, occur when spinal cord reflex activity returns. These were classically described by Guttmann and Whitteridge (1947) in patients with lesions at or above the level of T 5 during distension of the urinary bladder. They reported marked hypertension, a decrease in pulse rate, change of rhythm on the electrocardiograph (in particular extrasystoles), vasodilatation of the face, neck and nasal mucosa and vasoconstric tion of fingers and toes. The patients complained of flushing and sweating of the face and neck, blockage of nasal air passages and headache. The authors thought these were important alarm symptoms of visceral activity in parts of the paralysed body. Since then there have been numerous reports which have confirmed Gutt mann and Whitteridge's pioneering observations on the cardiovascular changes occurring during autonomic dysreflexia in patients with high thoracic and cervical spinal cord lesions. Similar changes also occur during cutaneous stimulation 46

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Plasma catecholamines during paroxysmal neurogenic hypertension in quadriplegic man.

Cited by 167 publications

References 19 publications

Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury

Leg sympathetic response to noxious skin stimuli is similar in high and low level human spinal cord injury

Testosterone, cortisol and catecholamine responses to exercise stress and autonomic dysreflexia in elite quadriplegic athletes

Cardiovascular aspects of autonomic dysreflexia since Guttmann and Whitteridge (1947)

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