November 1, 2001Open Access
View Full PaperPhysiological Society Symposium ‐ Vagal Control: From Axolotl to Man
Key Result
Vagal/muscarinic stimulation prolongs ventricular refractoriness in humans and has a small but distinct negative inotropic effect on the left ventricle, accentuated by elevated sympathetic activity.
Structured PICO
Does vagal/muscarinic stimulation affect left ventricular function and refractoriness in humans?
P
Population
Humans
I
Intervention
Vagal/muscarinic stimulation
O
Outcome
Left ventricular function (inotropic state and refractoriness)surrogate
This review highlights the physiological role of parasympathetic innervation in regulating human ventricular function and refractoriness, challenging older beliefs that vagal effects were confined to supraventricular structures.
Abstract
Until about 40 years ago, it was thought that the parasympathetic innervation of the mammalian heart was confined to supraventricular structures. Hence, neither the vagus nor its primary neurotransmitter, acetylcholine (ACh), were believed to have significant effects on the inotropic state of the ventricles or on their excitability. However, it is now well-established that vagallmuscarinic stimulation prolongs ventricular refractoriness in humans and has a small but distinct negative inotropic effect on the left ventricle, which is accentuated in the presence of elevated sympathetic activity (Loffelholz & Pappano, 1985). This brief review will consider the evidence for a vagal/ muscarinic regulation of left ventricular (LV) function in humans and discuss the mechanisms that may be responsible for this effect.