Manual of Equine Anesthesia and Analgesia. Группа авторов

       Efferent autonomic signals are transmitted to the body through two major subdivisions of the ANS, the SNS, and PNS. (see later discussion.)

      II Physiology of the autonomic nervous system

      A Neurotransmitters

       Acetylcholine (ACh) and norepinephrine (NE) are the main neurotransmitters.

       All preganglionic neurons are cholinergic in both the SNS and PNS nervous systems and secrete ACh.

       Postganglionic neurons of the PNS are cholinergic, while most postganglionic SNS neurons are adrenergic and secrete NE.The adrenal gland functions like a modified sympathetic ganglion and when stimulated by presynaptic SNS fibers, releases NE and epinephrine (EPI) into the circulation to act on sites distant from the gland; therefore, there is no postganglionic neuron.Sweat glands in horses are mostly apocrine and open into hair follicles. These glands and the piloerector muscles are stimulated by circulating EPI that acts on adrenergic (β2) receptors.Eccrine sweat glands are common in humans, but are less common in horses. In humans, they constitute 90% of sweat glands and they are stimulated by a postganglionic SNS neuron that secretes ACh.

      B Synthesis, duration of action, and degradation of ACh

       ACh is synthesized within the axoplasm in the terminal endings of cholinergic nerves.

       The ACh is transported to the interior of the vesicles where it is stored in a highly concentrated form until it is released along with ATP.

       After release, ACh persists in the tissue for a few seconds, then most of it is split into an acetate ion and choline by the enzyme acetylcholinesterase, which is present in the terminal neuron and the surface of the receptor organ.

C Synthesis, duration of action, and removal of NE

       Synthesis of norepinephrine from phenylalanine begins in the axoplasm of the terminal nerve endings of adrenergic nerve fibers and is completed inside the vesicles.

       In the adrenal medulla, this reaction goes one step further and transforms about 85% of the norepinephrine into epinephrine.

       After secretion, NE is rapidly (within a few seconds) removed from the secretory site and taken back to the vesicles, either unchanged or metabolized by monoamine oxidase (MAO). If it reaches the circulation, NE, and also EPI, are metabolized by MAO and catechol‐O‐methyltransferase (CMT) in the liver and kidney.

      D Receptors on the effector organs

      Cholinergic receptors are subdivided into muscarinic and nicotinic.

       Muscarinic receptors are present in all effector cells stimulated by the postganglionic PNS neurons, as well as in those stimulated by the postganglionic SNS cholinergic neurons. Subtypes of muscarinic receptors are described in Table 7.1.

       Nicotinic receptors are found in the synapses between the preganglionic and postganglionic neurons of the SNS and PNS, and at the neuromuscular junction.

       ACh is the neurotransmitter at all cholinergic receptors.

      Adrenergic receptors are subdivided into alpha (α₁ and α₂), beta (β₁ and β₂), and dopaminergic (DA).

       Norepinephrine (NE) excites α receptors more than β receptors.

       Epinephrine (EPI) excites α and β receptors approximately equally.

       Dopaminergic receptors

       There are five subtypes of dopaminergic receptors, D1 to D5. Dopaminergic receptors are primarily present in the CNS but are also present in the periphery.

       Dopamine can act by three mechanisms:It modulates the release of norepinephrine from adrenergic neurons.It activates α and β receptors.It activates dopaminergic receptors.

Table 7.1 Muscarinic receptor subtypes.

	M1	M2	M3	M4	M5
Location	CNSStomach	HeartCNS	CNSSalivary glands; airway smooth muscle	CNSHeart?	CNS
Clinical effects	H+ secretion	Bradycardia	Salivation	?	?

      III Function of the adrenal medulla

      A SNS innervation of the adrenals

       Stimulation of the SNS nerves to the adrenal medulla causes large quantities of EPI and NE to be released into the bloodstream.

       Approximately 80% of the secretion is EPI and 20% is NE.

      B Effect of NE release from adrenals

       The circulating NE causes constriction of most blood vessels, increased activity of the heart, inhibition of the GI tract, and dilation of the pupils.

      C Effect of EPI release from adrenals

       EPI, because it has greater affinity for β receptors, has a more profound effect on cardiac stimulation than does NE. However, NE is a more potent vasoconstrictor.

       NE and EPI increase systemic vascular resistance, mean arterial pressure and cardiac output through their α‐ and β‐receptor activity. Heart rate is more likely to increase with EPI due to a stronger chronotropic effect, whereas it decreases with NE, as a result of a baroreflex in response to the increase in systemic vascular resistance.

      IV Autonomic effects on the cardiovascular system

      A The heart

       SNS stimulation increases heart rate and contractility.

       PNS stimulation decreases heart rate and can result in asystole.

       Postsynaptic α2 receptors exert a positive inotropic effect and contribute to development of cardiac arrhythmias.

       Postsynaptic β1 receptors and presynaptic β2 receptors play similar roles in increasing heart rate and myocardial contractility.

      B Systemic blood vessels

       SNS stimulation constricts most systemic blood vessels, especially those of the abdominal viscera and the skin of the limbs.

       PNS stimulation has almost no effect on most blood vessels.

       Presynaptic α2 vascular receptors mediate vasodilation, whereas postsynaptic α1 and α2 vascular receptors mediate vasoconstriction.

       Postsynaptic