Portal de Periódicos da CAPES

Hypertonic saline reverses acute intestinal edema and improves transit through changes in cytoskeletal composition

2006; Elsevier BV; Volume: 130; Issue: 2 Linguagem: Inglês

10.1016/j.jss.2005.11.497

1095-8673

Rangasudhagar Radhakrishnan, Hemachandar Radhakrishnan, Hui Xue, F.A. Moore, S.J. Allen, Charles S. Cox,

Pain Management and Placebo Effect

Introduction: We have shown that acute edema induced by resuscitation and mesenteric venous hypertension (MV-HTN) impairs intestinal transit and contractility and reduces the standardized engineering measures of intestinal stiffness[elastic modulus (EM)] and residual stress[opening angle (OA)]. In addition, we have shown that pretreatment with hypertonic saline (7.5% HS) preserves intestinal transit, stiffness, and residual stress. We proposed that acute intestinal edema decreases force transmission through the more elastic tissue, leading to decreased transit. Furthermore, recent bioengineering literature has demonstrated that intermediate filaments, such as Vimentin, determine tissue stiffness. We hypothesized that hypertonic saline given after acute intestinal edema will reverse these detrimental effects of acute edema. In addition, this change in intestinal properties is mediated by a change in intermediate filaments and the composition of the intestinal cytoskeleton. Methods: Rats were randomized to four groups: sham, MV-HTN with 80 cc/kg NS (NS 80), HS alone, and NS 80 with HS administration after 30 minutes. Intestinal edema was measured by wet to dry tissue weight ratio (W/D). A duodenal catheter was placed and, 30 minutes prior to sacrifice, FITC Dextran was injected. At sacrifice, dye concentrations were measured to determine intestinal transit. Segments of distal ileum were hung to a fixed point in a tissue bath and to a tensiometer and stretched in increments of 1 mm, recording the new length and the corresponding force from the tensiometer to determine EM. Next, two transverse cuts were made yielding a 1-2 mm thick ring shaped segment of tissue and then cut radially to open the ring. Then, the OA was measured. Finally, using deconvolution microscopy, frozen tissue samples of distal ileum were stained for the cytoskeletal components filamentous (F) actin and Vimentin (Vim). Relative concentrations and locations of each cytoskeletal component were determined through pixel counts from Corel Photo-Paint 10. NS 80 cause a significant increase in tissue edema and a significant decrease in intestinal transit, stiffness, and residual stress compared to sham. HS reverses these changes to sham levels. In addition, hypertonic saline caused significant alterations to the mucosal and submucosal intestinal cytoskeleton. Conclusion: HS prevents intestinal tissue edema formation and improves intestinal transit, possibly through more efficient transmission of muscle force through stiffer intestinal tissue. HS may increase tissue stiffness by increasing tissue levels of Vimentin. In addition, HS causes a significant increase in smooth muscle F actin that may allow for improved muscle function and increased transit.