Although the pathogenesis of fissure is not fully understood, we do know that surgical and/or pharmacological sphincterotomy promotes the healing of chronic anal fissures. A number of studies support the hypothesis that local ischemia is the reason for failure to heal in anal fissure. Therefore, sphincterotomy may work because it decreases anal canal resting pressure and enhances microcirculation at the fissure site. The vasomotor tone of arterioles controlled by metabolic and endothelial factors determines perfusion of tissue and fissure healing. In a novel approach, this paper proposes mechanisms for nitric oxide synthesis, regulation and action in the internal anal sphincter. The design demonstrates the direct interdependence between the activity mechanisms of botulinum toxin and nitric oxide. Endothelial lining can modulate not only vascular tone but also internal anal sphincter (IAS) tone. The application of botulinum toxin likely releases the blockage in glyceryl trinitrate bioactivation in smooth muscle cells and suppresses basal continuous sympathetic activity, causing IAS relaxation. Sufficient distension of the IAS during defecation also reduces the risk of trauma during defecation and complication after the trauma. Both eruption of tissue in the fissure region and release of contraction vessel mediators tend to arrest fissure healing.

Keywords: Anal Canal - blood supply, Anal Canal - metabolism, Fissure in Ano - metabolism, Fissure in Ano - pathology, Anal Canal - pathology, Botulinum Toxins, Type A - therapeutic use, Calcium Channel Blockers - pharmacology, Chronic Disease - drug therapy, Fissure in Ano - pathology, Nitric Oxide - metabolism, Nitric Oxide Donors - therapeutic use, Wound Healing - drug effects