Background: Immature motility of the ileum may contribute to life-threatening diseases. Little is known about the normal biomechanics of the neonatal ileum in relation to the protein composition of its contractile machinery. Methods: We analyzed the tissue architecture, the biomechanics in intact and β-escin-permeabilized preparations, and the protein composition in neonatal (P0) and adult murine ileum. results: Muscle thickness of the P0 ileum was −50% of the adult ileum and passive compliance was higher. Carbachol-and KCl-elicited contractions were tonic rather than phasic as in the adult. Ca 2+ sensitivity was higher and relaxation rate was slower in β-escin-permeabilized P0 compared with adult ileum. The expression level of β-actin relative to α-actin was higher, and those of total actin, myosin, myosin light chain kinase, the catalytic subunit of myosin phosphatase and telokin were lower compared with the adult. The expression level of MYPT1 was similar, but P0 ileum expressed only the M133; the adult ileum also expressed the M130 isoform. conclusion: The mechanical features and protein composition of the P0 ileum are similar to those of adult tonic smooth muscles. We propose that this is highly adaptive during fetal life allowing the small intestine to act predominantly as a container. d uring development from fetal to newborn and adult life, the gastrointestinal tract (GIT) gradually establishes its mature structure and function. Anatomic features of the digestive tract are present already in human fetal life by 8 wk gestational age (1). However, gastrointestinal motility of preterm individuals is reduced (2). Obviously, this poses severe problems regarding oral food intake which are aggravated by the fact that the immaturity of the GIT, singly or in concert with other perinatal risk factors, may contribute to complications such as spontaneous intestinal perforation, not uncommon in extremely low-birth-weight infants (3). The underlying cause of spontaneous intestinal perforation, one of the leading risk factors of death in neonatal medicine, is still poorly understood. Conceivably an immature intestinal motility is an important determinant leading to stasis of the intestinal contents and overgrowth of infectious enteritis pathogens (4). The ensuing inflammatory response leads to a viscous cycle by not only further impairing of propulsive gut movements but also derogating vascular smooth muscle (SM) function, leading to reduced blood supply and finally to necrosis.Intestinal motility is driven by the concerted action of enteric neurons, pacemaker, and SM cells (2). Although several studies addressed different aspects of the fetal and postnatal maturation of innervation, electrical activity, and global contractile activity of the GIT (5-7), only few studies addressed in some depth the properties of the downstream effector, the SM. Investigations from avian (8) and mammalian stomach (9-11), and guinea pig gallbladder (12) as well as from non-GIT organs like urinary bladder (13,14), revealed major difference...
