| Internal anal sphincter | |
|---|---|
Coronal section through theanal canal. B. Cavity ofurinary bladder V.D.Vas deferens. S.V.Seminal vesicle. R. Second part ofrectum. A.C. Anal canal. L.A.Levator ani. I.S. Internal anal sphincter. E.S.External anal sphincter. | |
![]() Coronal section ofrectum andanal canal | |
| Details | |
| Nerve | Pelvic splanchnic nerves (S4), thoracicolumbar outflow of the spinal cord |
| Actions | Keeps theanal canal andorifice closed, aids in the expulsion of thefeces |
| Identifiers | |
| Latin | musculus sphincter ani internus |
| TA98 | A05.7.05.011 |
| TA2 | 3018 |
| FMA | 15710 |
| Anatomical terms of muscle | |
Theinternal anal sphincter,IAS, orsphincter ani internus is a ring ofsmooth muscle that surrounds about 2.5–4.0 cm of theanal canal. It is about 5 mm thick, and is formed by an aggregation of the smooth (involuntary) circular muscle fibers of the rectum.[citation needed]
The internal anal sphincter aids the sphincter ani externus to occlude the anal aperture and aids in the expulsion of thefeces. Its action is entirelyinvoluntary. It is normally in a state of continuous maximal contraction to prevent leakage of faeces or gases.Sympathetic stimulation stimulates and maintains the sphincter's contraction, andparasympathetic stimulation inhibits it. It becomes relaxed in response to distention of the rectal ampulla, requiring voluntary contraction of the puborectalis and external anal sphincter to maintain continence,[1] and also contracts during thebulbospongiosus reflex.[2][3][4][5]
The internal anal sphincter is the specialised thickened terminal portion of the inner circular layer of smooth muscle of the large intestine. It extends from thepectinate line (anorectal junction) proximally to just proximal to theanal orifice distally (the distal termination is palpable). Its muscle fibres are arranged in a spiral (rather than a circular) manner.[6]
At its distal extremity, it is in contact with but separate from theexternal anal sphincter.[citation needed]
The sphincter receives extrinsic autonomic innervation via theinferior hypogastric plexus, with sympathetic innervation derived from spinal levels L1-L2, and parasympathetic innervation derived from S2-S4.[6]
The internal anal sphincter isnot innervated by thepudendal nerve (which provides motor and sensory innervation to the external anal sphincter).[7]
The sphincter is contracted in its resting state, butreflexively relaxes in certain contexts (most notably duringdefecation).[6]
Transient relaxation of its proximal portion occurs with rectal distension and post-prandial rectal contraction (therecto-anal inhibitory reflex and sampling reflex, respectively) while the distal portion of the sphincter remains contracted and theexternal anal sphincter becomes contracted to maintain continence; this transient relaxation allows passage of stool into the proximal anal canal - this filling is sensed.[6]
The IAS contributes 55% of the resting pressure of the anal canal. It is very important for bowel continence, especially for liquid and gas. When the rectum fills beyond a certain capacity, the rectal walls are distended, triggering the defecation cycle. This begins with therectoanal inhibitory reflex (RAIR), where the IAS relaxes. This is thought to allow a small amount of rectal contents to descend into the anal canal where specialized mucosa samples whether it is gas, liquid or solid. Problems with the IAS often present as degrees offecal incontinence (especially partial incontinence to liquid) or mucousrectal discharge.[8]
Sympathetic stimulation is mediated byalpha-2 adrenergic receptors and results in contraction of the sphincter.[6]
Parasympathetic stimulation is mediated bymuscarinic acetylcholine receptors and results in relaxation of the sphincter.[6]
Nitrergic stimulation also produces relaxation which has pharmacological significance.[6]
Nitrergic pharmaceutical agents produce relaxation of the muscular tone of the sphincter and are applicable in pathological contexts where this tone is abnormally increased.[6]
In 2011, it was announced by theWake Forest School of Medicine that the firstbioengineered, functional anal sphincters had been constructed in a laboratory made from muscle and nerve cells, providing a proposed solution for anal incontinence.[9][10]
This article incorporates text in thepublic domain frompage 426 of the 20th edition ofGray's Anatomy(1918)
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