ABSTRACT
Abnormal electromechanical properties occur in histologically normal colonic smooth muscle associated with the overlying mucosal inflammation. Isotonic quick-release of the muscle at the time of steady state contraction determined the maximum velocity of shortening by varying the afterload and extrapolating the curve, with the help of the Hill equation, to zero load. Mucosal inflammation inhibits underlying smooth muscle contraction in most parts of the gastrointestinal tract. The lack of improvement in the colitis muscle reduces the probability that abnormal phosphatase activity contributes to decreased force development in colitis muscle. The factors decreasing the function of smooth muscle associated with mucosal inflammation are undetermined. The factors decreasing the function of smooth muscle associated with mucosal inflammation are undetermined. The calcium dependence for contraction was determined by measuring calcium tension curve. An increased concentration of intracellular Ca2+ is pivotal for initiating actin myosin cross-bridge formation.
