When activated the sympathetic nervous system does which of the following?

Activation of the sympathetic nervous system

SNS activation strongly affects glucose metabolism [147]. For example, acute psychological stress increases plasma glucose in patients with T2DM [148]. Stressful stimuli of OSA, such as IH and arousals, also activate the SNS. IH exposure decreased insulin sensitivity in healthy volunteers, accompanied by increased SNS activity [146]. In another human study, acute hypoxia-induced IR was attenuated by sympathetic inhibition with clonidine [149]. During CPAP withdrawal, nocturnal glucose increased dynamically with elevations of the heart rate suggesting automatic influence [134]. A collection of hypoxia-sensitive cells in the carotid artery, called the carotid body, is responsible for SNS activation when blood oxygenation decreases. Shin et al. performed carotid sinus nerve denervation on mice before exposing them to chronic IH. Denervation prevented IH-stimulated hepatic glucose output and liver expression of phosphoenolpyruvate carboxykinase, a rate-limiting hepatic enzyme of gluconeogenesis. [150]. However, other rodent studies reported that IH decreased insulin sensitivity independently of sympathetic activation. For example, adrenal medullectomy improved glucose tolerance but did not prevent IR and fasting hyperglycemia stimulated by IH [151]; α-adrenergic blockade, β-adrenergic blockade, and adrenal medullectomy mitigated hyperglycemia and lipolysis during IH but did not prevent IR [152].

Location of Damage to the Sympathetic Pathway

After the diagnosis of Horner's syndrome is made, localizing whether the damage is along the preganglionic or postganglionic sympathetic pathway helps direct imaging, if indicated. Horner's syndrome sometimes manifests so characteristically that further efforts to localize the lesion are superfluous, as with patients with cluster headaches or patients with a history of surgery or trauma along the sympathetic pathway. Localization of a sympathetic lesion is a question of considerable clinical importance because many postganglionic defects are caused by vascular headache syndromes, cavernous sinus pathology, or carotid dissections, and preganglionic lesions sometimes result from malignant tumors or strokes to the central sympathetic location in the brain. These findings can assist the radiologist in interpretation of any diagnostic imaging. Pharmacological testing with hydroxyamphetamine drops can be helpful in localizing the lesion as well.

Hydroxyamphetamine releases norepinephrine from storage vesicles in the postganglionic sympathetic nerve endings at the iris dilator muscle. When the lesion is postganglionic, the third order nerve is dead, and no norepinephrine stores are available for release at the iris. When the lesion is complete, the pupil does not dilate at all. However, the dying neurons and their stores of norepinephrine may last for almost 1 week from the onset of damage. Therefore, a hydroxyamphetamine test administered within 1 week of a postganglionic lesion may give a false preganglionic localization if some of the norepinephrine stores remain. When Horner's syndrome is caused by preganglionic or central lesions, the pupils dilate normally because the postganglionic third order neuron and its stores of norepinephrine, although disconnected, are still intact.

To perform the hydroxyamphetamine test, the pupil diameters are measured before and 60 minutes after hydroxyamphetamine drops have been placed in both eyes. The change in anisocoria in room light is noted. If the affected pupil—the smaller one—dilates less compared with the normal pupil, an increase in anisocoria occurs, and the lesion is in the postganglionic neuron. If the smaller pupil now dilates so much that it becomes the larger pupil, the lesion is preganglionic and the postganglionic neuron is intact. The examiner must wait at least 48 hours after cocaine has been used before the administration of hydroxyamphetamine; cocaine inhibits the uptake of hydroxyamphetamine into the presynaptic sympathetic nerve terminal and seems to block its effectiveness. In general, if the anisocoria increases by at least 0.5 mm after hydroxyamphetamine administration, the lesion is most likely postganglionic. A decrease in anisocoria points toward a preganglionic location of the lesion. However, hydroxyamphetamine is no longer commercially available, and there are rare reports of false localization with hydroxyamphetamine. For these reasons, many clinicians forgo further localizing with hydroxyamphetamine and image the entire sympathetic pathway unless history or associated signs and symptoms clearly localize the lesion. For instance, acute Horner's syndrome with associated ipsilateral neck or facial pain requires urgent imaging of the neck for evaluation of a carotid dissection.

The Sympathetic Nervous System and Hypertension

The sympathetic nervous system comprises the vasomotor center that activates efferent pathways, which innervate sympathetic ganglia. Activated sympathetic nerves secrete catecholamines (norepinephrine, epinephrine), which induce effects on the heart, kidneys, and blood vessels through presynaptic and post-synaptic receptors. Increased activity of the sympathetic nervous system seems to play an important pathophysiological role in hypertension, particularly in the early stages.39,40 This is evidenced by elevated plasma norepinephrine levels, increased norepinephrine spillover rate, increased heart rate and blood pressure variability, increased α-adrenergic vasoconstriction and increased vascular reactivity to norepinephrine.41–43 Catecholamine-induced vasoconstriction of renal efferent arterioles influences renal sodium retention, which may further contribute to blood pressure elevation. Changes in other neurotransmitters, such as neuropeptide Y, a norepinephrine cotransmitter, adenosine, and dopamine in hypertension may also reflect sympathetic nervous system involvement.44 Pathophysiological processes characterized by increased sympathetic activity and impaired baroreflex control include obesity, obstructive sleep apnea, and polycystic ovary syndrome, often associated with resistant hypertension.45,46

Other contributory mechanisms of the sympathetic nervous system involve resetting of the mechanoreceptors, particularly the sinoaortic baroreceptors (high pressure), that are activated by increased arterial pressure, and the cardiopulmonary baroreceptors (low pressure), that are activated by increased central venous pressure.47 Baroreceptor activation leads to reduced heart rate and lower blood pressure by vagal stimulation and sympathetic inhibition.

Taken together, activation of the sympathetic nervous system and increased catecholamine secretion are major candidates underlying the cardiovascular pressor mechanisms that trigger blood pressure elevation and the trophic processes that maintain hypertension through effects on vascular structural changes, such as hypertrophy. Activation of the sympathetic nervous system also influences the RAS, a major player in established hypertension.48 Moreover, sympathetic overactivity has been implicated in the increased cardiovascular morbidity and mortality associated with early morning blood pressure surges. This has been attributed, in part, to increased α-sympathetic activation that occurs during prewakening.49 Targeting the sympathetic nervous system with anti-adrenergic drugs, anti-adrenergic devices (renal nerve denervation), and carotid baroreflex activation are increasingly being considered as effective antihypertensive therapies in patients with resistant hypertension.50

Adrenal Medullary Sympathetic Hormone Excess: Pheochromocytoma

Less than 0.1% of all cases of hypertension are caused by pheochromocytomas, or catecholamine-producing tumors derived from chromaffin tissue.54 Nevertheless, these tumors are clearly important to the anesthesiologist as previously 25% to 50% of hospital deaths in patients with pheochromocytoma occurred during induction of anesthesia or during operative procedures for other causes.55 This high mortality has been reduced with the improvements in anesthesia management during our current era.55a Although usually found in the adrenal medulla, these vascular tumors can occur anywhere (referred to as paragangliomas), with a proportion of up to 20%.55b Malignant spread, which occurs in less than 15% of pheochromocytomas, usually proceeds to venous and lymphatic channels with a predisposition for the liver. This tumor is occasionally familial or part of the multiglandular-neoplastic syndrome known as multiple endocrine adenoma type IIa or type IIb, and is manifested as an autosomal dominant trait. Type IIa consists of medullary carcinoma of the thyroid, parathyroid adenoma or hyperplasia, and pheochromocytoma. What used to be called type IIb is now often called pheochromocytoma in association with phakomatoses such as von Recklinghausen neurofibromatosis and von Hippel–Lindau disease with cerebellar hemangioblastoma. Frequently, bilateral tumors are found in the familial form. Localization of tumors can be achieved by MRI or CT, metaiodobenzylguanidine nuclear scanning, ultrasonography, or intravenous pyelography (in decreasing order of combined sensitivity and specificity).

Symptoms and signs that may be solicited before surgery or procedures and are suggestive of pheochromocytoma are as follows: excessive sweating; headache; hypertension; orthostatic hypotension; previous hypertensive or arrhythmic response to induction of anesthesia or to abdominal examination; paroxysmal attacks of sweating, headache, tachycardia, and hypertension; glucose intolerance; polycythemia; weight loss; and psychological abnormalities. In fact, the occurrence of combined symptoms of paroxysmal headache, sweating, and hypertension is probably a more sensitive and specific indicator than any one biochemical test for pheochromocytoma (Table 32.4).

The value of preoperative and preprocedure adrenergic receptor blocking drugs probably justifies their use as these drugs may reduce the perioperative complications of hypertensive crisis, the wide arterial blood pressure fluctuations during tumor manipulation (especially until venous drainage is obliterated), and the myocardial dysfunction. Mortality is decreased with resection of pheochromocytoma (from 40% to 60% to the current 0% to 6%) when adrenergic receptor blockade is introduced as preoperative and preprocedure preparatory therapy for such patients.56-60

Sympathectomy for Pain Control

The sympathetic nervous system clearly plays a role in a number of pain conditions. More modern nomenclature collectively refers to these pain conditions as sympathetically mediated pain. These conditions include causalgia and post-traumatic reflex sympathetic dystrophy. Any pain condition considered to belong to this category should initially be treated with local anesthetic blocks of the relevant portions of the sympathetic nervous system. Because a number of neurolytic medications are available as well as stereotactic placement of needles, it is often possible to execute a chemical interruption of the relevant sympathetic pathways. Open surgical sympathectomy therefore is called on less and less frequently. Unfortunately, there is a tendency to significant recurrence of pain after an initial successful period lasting a few months.

Sympathetic Nervous System

The sympathetic nervous system is implicated in the pathogenesis of hypertension in patients with ESRD. Total autonomic blockade, or selective inhibition of norepinephrine with debrisoquine, reduces total peripheral resistance and BP. However, plasma norepinephrine levels are variously reported as low, normal, or high, perhaps reflecting the complex nature of catecholamine release, reuptake, metabolism, and excretion in chronic renal failure. Converse and associates29 made direct recordings of postganglionic sympathetic nerve activity using implanted microelectrodes. They reported that the frequency of sympathetic nerve discharge was nearly three times greater in patients receiving hemodialysis than in normal subjects. Interestingly, after bilateral nephrectomy, BP and peripheral vascular resistance were lowered, and normal rates of sympathetic nerve discharge were seen. These investigators concluded that chronic renal failure activates the sympathetic nervous system via afferent nerve signals arising in the failing kidney.

These studies demonstrate the complexity of the underlying pathophysiology of hypertension in ESRD. They provide a rational basis for using therapies aimed at reducing ECF volume, for using calcium channel blockers (CCBs) and therapies that interrupt the renin-angiotensin-aldosterone system or the sympathetic nervous system.

When the sympathetic nervous system is activated quizlet?

What happens when the sympathetic nervous system is stimulated quizlet?