Biochemical changes involved in the mechanism of vasovagal syncope

Theopistou, Artemisia; Gatzoulis, K.; Economou, Emmanuel; Sideris, Skevos; Hantzos, Kostas; Stefanadis, Christodoulos; Toutouzas, Pavlos

doi:10.1016/s0002-9149(01)01682-4

Cited by 22 publications

(12 citation statements)

References 24 publications

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“…Neurocardiogenic syncope is attended by several other neuroendocrine changes, including elevated levels of beta-endorphin (160), atrial natriuretic peptide, corticotropin, and vasopressin (163, 299). The vasodilator effect of EPI may be mediated partly by increased production of nitric oxide (166).…”

Section: Applications Of Concepts Of Scientific Integrative Medicine mentioning

confidence: 99%

“…Since EPI is taken up avidly into non-neuronal cells via the Uptake-2 process (86), which involves a plasma membrane monoamine transporter and organic cation transporter 3 (74) but not the cell membrane NE transporter expressed by sympathetic nerves, it is also possible that the increase in nitric oxide production occurs independently of EPI binding to beta-2 adrenoceptors. Fainting reactions are associated with large increases in AVP levels (163, 299). AVP augments baroreflex restraint of SNS outflows in laboratory animals (154, 237) and might contribute to sympathoinhibition; however, whether AVP does so in humans in this setting is unclear (80).…”

Section: Applications Of Concepts Of Scientific Integrative Medicine mentioning

confidence: 99%

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Concepts of Scientific Integrative Medicine Applied to the Physiology and Pathophysiology of Catecholamine Systems

Goldstein

2013

Comprehensive Physiology

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This review presents concepts of scientific integrative medicine and relates them to the physiology of catecholamine systems and to the pathophysiology of catecholamine-related disorders. The applications to catecholamine systems exemplify how scientific integrative medicine links systems biology with integrative physiology. Concepts of scientific integrative medicine include (i) negative feedback regulation, maintaining stability of the body’s monitored variables; (ii) homeostats, which compare information about monitored variables with algorithms for responding; (iii) multiple effectors, enabling compensatory activation of alternative effectors and primitive specificity of stress response patterns; (iv) effector sharing, accounting for interactions among homeostats and phenomena such as hyperglycemia attending gastrointestinal bleeding and hyponatremia attending congestive heart failure; (v) stress, applying a definition as a state rather than as an environmental stimulus or stereotyped response; (vi) distress, using a noncircular definition that does not presume pathology; (vii) allostasis, corresponding to adaptive plasticity of feedback-regulated systems; and (viii) allostatic load, explaining chronic degenerative diseases in terms of effects of cumulative wear and tear. From computer models one can predict mathematically the effects of stress and allostatic load on the transition from wellness to symptomatic disease. The review describes acute and chronic clinical disorders involving catecholamine systems—especially Parkinson disease—and how these concepts relate to pathophysiology, early detection, and treatment and prevention strategies in the post-genome era.

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Section: Applications Of Concepts Of Scientific Integrative Medicine mentioning

confidence: 99%

Section: Applications Of Concepts Of Scientific Integrative Medicine mentioning

confidence: 99%

Concepts of Scientific Integrative Medicine Applied to the Physiology and Pathophysiology of Catecholamine Systems

Goldstein

2013

Comprehensive Physiology

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“…Vasopressin has been shown to increase up to 20-fold at the time of syncope when compared with baseline levels in tilt positive patients. 73 Recent studies suggest that the profound hypotension experienced before vasovagal syncope may be due to an increased synthesis of nitric oxide. The role of this powerful vasodilator in vasovagal syncope can be evaluated using urinary cyclic guanosine monophosphate as a biologic marker for nitric oxide activity.…”

Section: Reflex Syncope (Including Vasovagal Syncope)mentioning

confidence: 99%

Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope

Medow¹,

Stewart²,

Sanyal³

et al. 2008

Cardiology in Review

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Orthostatic hypotension (OH) occurs in 0.5% of individuals and as many as 7-17% of patients in acute care settings. Moreover, OH may be more prevalent in the elderly due to the increased use of vasoactive medications and the concomitant decrease in physiologic function, such as baroreceptor sensitivity. OH may result in the genesis of a presyncopal state or result in syncope. OH is defined as a reduction of systolic blood pressure (SBP) of at least 20 mm Hg or diastolic blood pressure (DBP) of at least 10 mm Hg within 3 minutes of standing. A review of symptoms, and measurement of supine and standing BP with appropriate clinical tests should narrow the differential diagnosis and the cause of OH. The fall in BP seen in OH results from the inability of the autonomic nervous system (ANS) to achieve adequate venous return and appropriate vasoconstriction sufficient to maintain BP. An evaluation of patients with OH should consider hypovolemia, removal of offending medications, primary autonomic disorders, secondary autonomic disorders, and vasovagal syncope, the most common cause of syncope. Although further research is necessary to rectify the disease process responsible for OH, patients suffering from this disorder can effectively be treated with a combination of nonpharmacologic treatment, pharmacologic treatment, and patient education. Agents such as fludrocortisone, midodrine, and selective serotonin reuptake inhibitors have shown promising results. Treatment for recurrent vasovagal syncope includes increased salt and water intake and various drug treatments, most of which are still under investigation.

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“…14 Furthermore, the occurrence of vasovagal reaction in subjects after orthotopic heart transplantation provides strong evidence that mechanisms other than the Bezold-Jarisch reflex are involved in the pathogenesis of vasovagal syncope. 15,16 Different humoral factors also seem to play a role, including epinephrine and a possible relative lack of norepinephrine, 17 a decrease of vasopressin and endothelin in plasma, 18,19 increased endorphin levels, 20,21 and possibly nitric oxide and serotonin. 22 However, the contributions of these neurohumoral factors are still controversial.…”

mentioning

confidence: 99%

Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

Béchir¹,

Binggeli²,

Corti³

et al. 2003

Circulation

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Background— The interplay of resting muscle sympathetic nerve activity (MSA) and the baroreceptor reflex in patients with vasovagal syncope remains elusive. Hence, the aim of the present study was to investigate MSA, baroreceptor sensitivity, heart rate, and blood pressure under resting conditions and during orthostatic stress in patients with a history of vasovagal syncope. Methods and Results— MSA was measured using microneurography at rest and during lower body negative pressure (LBNP) to mimic orthostatic stress in patients with a history of vasovagal syncope (n=10) and in age-matched healthy controls (n=8). Heart rate and blood pressure were simultaneously recorded. Cardiac baroreceptor sensitivity was calculated with the spectral technique (α coefficient). Resting MSA in the patients with syncope was significantly increased as compared with controls (42.4±2.3 versus 26.5±3.6 bursts/min, P =0.001), whereas activation of MSA during orthostatic stress in the patient group was significantly blunted (5.1±1.6 versus 15.2±2.1 bursts/min at LBNP −50 mm Hg, P =0.002). In the patients with syncope, cardiac baroreceptor sensitivity was significantly reduced under supine resting conditions (8.5±0.7 versus 13.0±1.1 ms/mm Hg, P =0.001), as well as under orthostatic stress (7.3±0.7 versus 13.4±1.5 ms/mm Hg, P =0.003). Conclusions— This study shows that in patients with vasovagal syncope, resting MSA is increased and baroreflex regulation during orthostatic stress is blunted, thus leading to impaired MSA adaptation. These results provide new insights into mechanisms of vasovagal syncope and suggest that pharmacological modulation of baroreceptor sensitivity may represent a promising treatment of neuromediated syncope.

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Biochemical changes involved in the mechanism of vasovagal syncope

Cited by 22 publications

References 24 publications

Concepts of Scientific Integrative Medicine Applied to the Physiology and Pathophysiology of Catecholamine Systems

Concepts of Scientific Integrative Medicine Applied to the Physiology and Pathophysiology of Catecholamine Systems

Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope

Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

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