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

Lateral sphincterotomy diminishes internal anal sphincter hypertonia and th ereby reduces anal canal pressure. This improves anal mucosal blood flow an d promotes the healing of anal fissures. However, sphincterotomy can be ass ociated with long term disturbances of sphincter function. The optimal trea tment for an anal fissure is to induce a temporary reduction of anal canal resting pressure to allow healing of the fissure without permanently disrup ting normal sphincter function. Broader understanding of the intrinsic mech anisms controlling smooth muscle contraction has allowed pharmacological ma nipulation of anal sphincter tone. We performed an initial Medline literatu re 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 mus cle relaxation can be inhibited by stimulation of nonadrenergic non-choline rgic enteric neurones, parasympathetic muscarinic receptors, or sympathetic beta adrenoceptors, and by inhibition of calcium entry into the cell. Sphi ncter contraction depends on an increase in cytoplasmic calcium and is enha nced by sympathetic alpha adrenergic stimulation. Currently, the most commo nly 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 alp ha or beta adrenoceptors are also likely to have a therapeutic potential in treating anal fissures.