AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY
The autonomic nervous system (ANS) maintains homeostasis
by integrating signals from peripheral and central sensors to
modulate organ perfusion and function. Autonomic “tone”
maintains cardiac muscle, visceral organs, and vascular smooth
muscle in a state of intermediate function. From this state,
rapid increases or decreases in autonomic outflow can adjust
blood flow and organ activity in response to the environment.
The rapidity of the ANS response is impressive considering
that neurotransmitters must be released from terminals, cross
a synaptic cleft to an effector site, bind to a receptor, and initiate
an intracellular event. For example, in just a few seconds,
ANS activation can double heart rate (HR) and arterial blood
pressure (BP). In a nearly similar time frame it can cause
sweating, nausea, loss of bladder control, and fainting. The
sympathetic nervous system (SNS) has been called the “fightor-
flight” response system and is activated under stress. In
contrast, the parasympathetic nervous system is responsible
for “rest and digest.” The anatomy and physiology of the ANS
are discussed in Chapter 12.
In the perioperative and intensive care settings, multiple
factors disrupt the typically tight ANS control of organ and
vascular homeostasis. Thus pharmacologic activation or inhibition
of the ANS is commonplace in these settings. For
example, both general and regional anesthesia have powerful
influences on normal ANS function. When an inhaled anesthetic
acts to directly relax vascular smooth muscle and lower
BP, the ANS reacts to counteract hypotension via baroreflex
adjustments of ANS activity. However, a second effect of
volatile anesthetics is to impair baroreflex function. The net
effect of these influences requires treatment of unwanted
hypotension with sympathomimetic or vagolytic drugs.
Laryngoscopy and tracheal intubation or surgical incision
powerfully activate the SNS; adrenergic receptor blocking
drugs are used to dampen these responses.
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