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Review
. 2000 Jun;46(6):861-8.
doi: 10.1136/gut.46.6.861.

Neuromyogenic properties of the internal anal sphincter: therapeutic rationale for anal fissures

R Bhardwaj  1 , C J Vaizey, P B Boulos, C H Hoyle
Affiliations
Review

Neuromyogenic properties of the internal anal sphincter: therapeutic rationale for anal fissures

R Bhardwaj et al. Gut. 2000 Jun.

Abstract

Lateral sphincterotomy diminishes internal anal sphincter hypertonia and thereby reduces anal canal pressure. This improves anal mucosal blood flow and promotes the healing of anal fissures. However, sphincterotomy can be associated with long term disturbances of sphincter function. The optimal treatment for an anal fissure is to induce a temporary reduction of anal canal resting pressure to allow healing of the fissure without permanently disrupting normal sphincter function. Broader understanding of the intrinsic mechanisms controlling smooth muscle contraction has allowed pharmacological manipulation of anal sphincter tone. We performed an initial Medline literature search to identify all articles concerning "internal anal sphincter" and "anal fissures". This review is based on these articles and on additional publications obtained by manual cross referencing. Internal anal smooth muscle relaxation can be inhibited by stimulation of non-adrenergic non-cholinergic enteric neurones, parasympathetic muscarinic receptors, or sympathetic beta adrenoceptors, and by inhibition of calcium entry into the cell. Sphincter contraction depends on an increase in cytoplasmic calcium and is enhanced by sympathetic adrenergic stimulation. Currently, the most commonly used pharmacological agent in the treatment of anal fissures is topical glyceryl trinitrate, a nitric oxide donor. Alternative agents that exhibit a similar effect via membrane Ca2+ channels, muscarinic receptors, and alpha or beta adrenoceptors are also likely to have a therapeutic potential in treating anal fissures.

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Figures

Figure 1
Figure 1
Internal anal sphincter (IAS) smooth muscle cell contraction is dependent on an increase in cellular calcium (Ca2+). This can be produced by direct influx of calcium through membrane Ca2+ channels or by stimulation of α1 adrenoceptors. The latter pathway results in release of Ca2+ from the sarcoplasmic reticulum mediated via inositol-1'4'5'- triphosphate (IP3). Relaxation is induced by antagonising membrane Ca2+ channels or α1 adrenoceptors. Stimulation of β2 adrenoceptors results in a return of Ca2+ to the sarcoplasmic reticulum, mediated through cyclic adenine-3'5'-monophosphate (cAMP). Stimulation of nitric oxide (NO) containing non-adrenergic non-cholinergic (NANC) enteric neurones induces a cyclic guanosine-3'5'-monophosphate (cGMP) mediated decrease in cellular Ca2+. Muscarinic nerve stimulation, through release of acetylcholine (Ach), promotes the synthesis of NO.
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References

    1. Br J Surg. 1990 Dec;77(12):1342-4 - PubMed
    1. Br J Surg. 1991 Dec;78(12):1429-30 - PubMed
    1. Br J Surg. 1989 May;76(5):431-4 - PubMed
    1. J Int Med Res. 1997 Sep-Oct;25(5):225-46 - PubMed
    1. Br J Surg. 1999 Jan;86(1):70-5 - PubMed

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