Related Experiment Videos
Neurally mediated syncope: pathogenesis, diagnosis, and treatment
1Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.
Neurology
|April 1, 1995
Summary
Neurally mediated syncope, a common cause of fainting, involves a reflex leading to low blood pressure. Increased nitric oxide may cause vasodilation, contributing to fainting episodes.
Area of Science:
- Cardiology
- Neuroscience
- Autonomic Nervous System
Background:
- Neurally mediated syncope is the most common cause of fainting in individuals without structural heart disease.
- It is triggered by a reflex involving afferent signals from mechanoreceptors, leading to parasympathetic overactivity.
- This results in bradycardia and sympathoinhibition, causing hypotension and vasodilation.
Purpose of the Study:
- To investigate the underlying pathophysiology of neurally mediated syncope.
- To explore the role of nitric oxide in the vasodilation observed during these episodes.
- To highlight the diagnostic utility of the upright tilt test.
Main Methods:
- Analysis of autonomic nervous system activity and neurochemical changes during syncope.
- Measurement of plasma concentrations of various hormones and vasoactive substances.
- Utilizing the upright tilt test for diagnosis and characterization.
Main Results:
- Sympathetic nerve activity and norepinephrine levels decrease inappropriately during episodes.
- Plasma levels of epinephrine, angiotensin II, vasopressin, and endothelin-1 increase appropriately.
- Evidence suggests increased nitric oxide synthesis contributes to arterial vasodilation and hypotension.
Conclusions:
- Neurally mediated syncope involves complex autonomic dysregulation.
- Nitric oxide-mediated vasodilation may be a key factor in the hypotension experienced.
- Understanding these mechanisms can pave the way for targeted therapeutic interventions.