The effects of preganglionic and postganglionic denervation on the responses of the nictitating membrane to sympathomimetic substances

Innes, I. R.; Kosterlitz, H. W.

doi:10.1113/jphysiol.1954.sp005083

Cited by 30 publications

(10 citation statements)

References 8 publications

(20 reference statements)

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“…3). When cocaine was then given it had the usual effect on the chronotropic responses and, as was to be expected, the contractions of the acutely decentralized and chronically denervated membranes became nearly equal (Innes & Kosterlitz, 1954) The effect of veratramine Veratramine inhibits the cardioaccelerator action of adrenaline, noradrenaline and electrical stimulation of the accelerator nerve (Krayer, 1949;Krayer & van Maanen, 1949). These authors state that veratramine probably exerts its inhibitory effect by blocking the pacemaker against the sympathomimetic amines.…”

Section: Sympathomimetic Amines On Heart Ratementioning

confidence: 91%

“…Sometimes it was necessary to remove part of the first rib. In a few experiments the action of the sympathomimetic amines on the decentralized or denervated nictitating membrane was recorded simultaneously (Innes & Kosterlitz, 1954 The stock solutions were kept at -5°C. The final dilutions were made immediately before the experiment with Ringer-Locke solution containing ascorbic acid (0 2 mg/ml.).…”

Section: Methodsmentioning

confidence: 99%

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The action of sympathomimetic amines on the rate of the denervated heart of the cat

Innes¹,

Kosterlitz²

1954

The Journal of Physiology

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Section: Sympathomimetic Amines On Heart Ratementioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

The action of sympathomimetic amines on the rate of the denervated heart of the cat

Innes¹,

Kosterlitz²

1954

The Journal of Physiology

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“…In animal experiments, decentralization of postganglionic sympathetic neurons by cutting their preganglionic inputs results in hypersensitivity response to norepinephrine (148). In humans with quadriplegia and cervical SCI, enhanced pressor response to norepinephrine was observed (224).…”

Section: Peripheral α-Adrenoceptor Hyperresponsivenessmentioning

confidence: 98%

Autonomic Consequences of Spinal Cord Injury

Hou

Rabchevsky

2014

Comprehensive Physiology

171

112

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Spinal cord injury (SCI) results not only in motor and sensory deficits but also in autonomic dysfunctions. The disruption of connections between higher brain centers and the spinal cord, or the impaired autonomic nervous system itself, manifests a broad range of autonomic abnormalities. This includes compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. These disabilities evoke potentially life-threatening symptoms that severely interfere with the daily living of those with SCI. In particular, high thoracic or cervical SCI often causes disordered hemodynamics due to deregulated sympathetic outflow. Episodic hypertension associated with autonomic dysreflexia develops as a result of massive sympathetic discharge often triggered by unpleasant visceral or sensory stimuli below the injury level. In the pelvic floor, bladder and urethral dysfunctions are classified according to upper motor neuron versus lower motor neuron injuries; this is dependent on the level of lesion. Most impairments of the lower urinary tract manifest in two interrelated complications: bladder storage and emptying. Inadequate or excessive detrusor and sphincter functions as well as detrusor-sphincter dyssynergia are examples of micturition abnormalities stemming from SCI. Gastrointestinal motility disorders in spinal cord injured-individuals are comprised of gastric dilation, delayed gastric emptying, and diminished propulsive transit along the entire gastrointestinal tract. As a critical consequence of SCI, neurogenic bowel dysfunction exhibits constipation and/or incontinence. Thus, it is essential to recognize neural mechanisms and pathophysiology underlying various complications of autonomic dysfunctions after SCI. This overview provides both vital information for better understanding these disorders and guides to pursue novel therapeutic approaches to alleviate secondary complications.

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“…After sympathectomy the effect of noradrenaline was usually enhanced but the increase was not quite so great as that recorded with adrenaline. Differences in the responses of sympathectomized smooth muscle to different sympathomimetic amines have been noted in experimental animals (Lockett, 1950;Innes & Kosterlitz, 1954) but these have still to be fully elucidated (Wakim & Essex, 1952).…”

Section: Discussionmentioning

confidence: 99%

Effect of adrenaline and noradrenaline on blood vessels of the hand before and after sympathectomy

Duff¹

1955

The Journal of Physiology

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The effects of preganglionic and postganglionic denervation on the responses of the nictitating membrane to sympathomimetic substances

Cited by 30 publications

References 8 publications

The action of sympathomimetic amines on the rate of the denervated heart of the cat

The action of sympathomimetic amines on the rate of the denervated heart of the cat

Autonomic Consequences of Spinal Cord Injury

Effect of adrenaline and noradrenaline on blood vessels of the hand before and after sympathectomy

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