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Active vasodilation during fainting: a hypothesis revisited
J R Halliwill1, N M Dietz, M J Joyner
1Department of Anesthesiology and Physiology, Mayo Clinic, Rochester, MN 55905, USA.
Summary
Fainting (vasovagal syncope) may involve active vasodilation, not just passive, challenging current concepts. Evidence suggests sympathetic nervous system involvement and nitric oxide release contribute to this active vasodilation.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
Background:
- Current understanding attributes vasovagal syncope to passive vasodilation via withdrawal of sympathetic vasoconstrictor tone.
- This passive vasodilation concept has largely replaced theories of active, sympathetically mediated vasodilation in humans.
Observation:
- Evidence suggests the existence of sympathetically mediated active vasodilation in humans.
- Experimental data show neurally mediated nitric oxide release during sympathoexcitatory maneuvers.
- Forearm vasodilation was observed during vasovagal response following alpha-adrenergic blockade.
Findings:
- Active vasodilation may play a role in vasovagal syncope.
- Nitric oxide release is a potential mechanism for neurally mediated active vasodilation.
- Sympathetic nervous system activity can actively induce vasodilation.
Implications:
- Revisiting the role of active vasodilation in fainting is warranted.
- Findings may lead to new therapeutic targets for vasovagal syncope.
- Understanding active vasodilation mechanisms can advance cardiovascular and autonomic nervous system research.