| Popis: |
There is little doubt that using the anal sphincter as a pharmacological target has contributed to our understanding of anorectal physiology. The ability to pharmacologically modulate anal sphincter function has led to significant changes in our approach to the management of certain benign anorectal diseases. In this chapter, we will describe current knowledge of the pharmacology and pharmacotherapy of the anal sphincter, as well as the physiological aspects of the sphincter complex, in particular, its innervation. The discussion includes the current state of knowledge of the neurotransmitters involved in the control of the anal sphincter and suggested mechanisms for their manipulation principally designed to manage patients with anal fissure disease and fecal incontinence. The anal sphincter consists of an inner ring of smooth muscle, the internal anal sphincter (IAS), surrounded by an outer ring of striated muscle, the external anal sphincter (EAS). The IAS is an involuntary muscle that is in a continuous state of contraction as a result of its intrinsic myogenic properties and extrinsic innervation by the autonomic nerves (1). The EAS, being a voluntary muscle, is innervated by the pudendal (somatic) nerve. Together they play a central role in the maintenance of continence.The IAS contributes up to 85% of the overall resting anal pressure, while the EAS is thought to contribute up to 50% of the anal pressure, particularly during periods of rectal distension (2). When required, the voluntary component can be called upon to momentarily raise the anal pressure in order to defer defecation. The functioning anal sphincter therefore relies on the autonomic and myogenic innervation of the IAS, as well as the somatic innervation of the EAS. |
