Abstract
The purpose of this study was to experimentally investigate the cellular composition of post-surgical peritoneal fluid and peritoneal tissue and determine the patterns of14C-proline and14C-glucosamine incorporation by the peritoneal exudative cells and peritoneal tissue repair cells (PEC and PTRC). One group of rabbits underwent resection (2.0 cm) and reanastomosis of their ileum, and another group underwent peritoneal wall abrasion. Postoperatively (1–28 days), the PEC and PTRC were collected and incubated for 5 days with 0.5 μCi14C-glucosamine or14C-proline, and the specific activity thereafter determined by beta counting. On the 1st postoperative day, the total cell number (TCN) had increased (7.7×107 cells/rabbit) to 770 per cent of the control values primarily as a result of the PMN influx (89.9 per cent). On day 3, the TCN was 6.1×107, 58.5 per cent of which comprised macrophages, which had become the principle cell type by day 5. The incorporation of proline and glucosamine into the PEC increased significantly peaking on day 7 then decreasing to the control value by day 21. Proline incorporation into the PTRC increased significantly, reaching a peak value on day 5, which decreased by day 10. Glucosamine incorporation reached a peak value on day 7 then decreased by day 10. In conclusion, the increase in glucosamine and proline incorporation into the PTRC paralles the increase in PEC, comprised principally of macrophages. These findings suggest that analysis of the metabolic activities in peritoneal activated macrophages may provide a useful tool to dissect the central mediation of postsurgical peritoneal re-epithelialization.
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References
Ellis H. The cause and prevention of post-operative adhesions. Surg Gynecol Obstet 1971; 133: 497–511.
Ryan GB, Grobety J, Majro G. Mesothelial injury and recovery. Am J Pathol 1973; 71: 93–112.
Buckman RF, Woods M, Sargent L, Gervin AS. A unifying pathogenetic mechanism in the etiology of intraperitoneal adhesion. J Surg Res 1976; 20: 1–7.
diZerega GS, Holz GD. Cause of prevention of postsurgical pelvic adhesions. In: Osojsky K, ed. Advanced in clinical obstetrics and gynecology. Baltimore: Williams and Wilkins 1982; 277–289.
Hunt TK, Kinghton DR, Thakral KK, Andrews W, Michaeli D. Cellular control of repair. In: Hunt TK, Heppenstall RB, Pines E, Rovee D, eds. Soft and hard tissue repair. New York: Praeger publishers 1984; 2–19.
Montz FJ, diZerega GS. Postsurgical peritoneal re-epithelialization. In: DeCherney A, Polan ML, eds. Reproductive surgery. New York: C.K. Year Book Medical Publisher 1987; 31–47.
Adams DO, Hamilton TA. The cell biology of macrophage activation. Rev Immunol 1984; 2: 283.
Tsukamoto Y, Helsen WE, Wahl SM. Macrophage production of fibronectin. A chemoatractant for fibroblast. J Immunol 1981; 127: 673–678.
Leibovich SJ, Ross R. A macrophage-dependent factor that stimulates the proliferation of fibroblastin vitro. Am J Pathol 1976; 84: 501–513.
Drapier JC, Petit JF. Involvement of prostaglandins in LPS-mediated regulation of plasminogen activator synthesis by inflammatory macrophages. Int J Immunopharmac 1984; 6: 345–350.
Shimanuki T, Montz FJ, Nishimura K, Nakamura RM, diZerega GS. Localized prevention of post-surgical adhesion formation and reformation with oxidized regenerated cellulose. J Biomed Mater Res 1987; 21: 173–185.
Shimanuki T, Nakamura RM, diZerega GS. A kinetic analysis of peritoneal fluid cytology and arachidonic acid metabolism after abrasion and reabrasion of rabbit peritoneum. J Surg Res 1986; 41: 245–251.
Nishimura K, Nakamura RM, diZerega GS. Biochemical evaluation of postsurgical wound repair: Prevention of intraperitoneal adhesion formation with ibuprofen. J Surg Res 1983; 34: 219–226.
Nishimura K, diZerega GS. Ibuprofen inhibition of post-surgical adhesion formation: A time- and dose-response biochemical evaluation. J Surg Res 1984; 36: 115–124.
Lowry OH, Rusebrough NJ, Farr AL, Randall RJ. Protein measurement with the folin phenol reagent. J Biol Chem 1951; 193: 265–275.
Raferty AT. Regeneration of parietal and visceral peritoneum. Br J Surg 1973; 60: 293–299.
Raferty AT. Regeneration of parietal and visceral peritoneum in the immature animal. Br J Surg 1973; 60: 969–975.
Cohen IK, Moore CD, Diegelman RF. Onset and localization of collagen synthesis during wound healing in open rat skin wounds. Proc Suc Exp Biol Med 1979; 160: 458–462.
Dolynchuk KN, Bowness JM. The early metabolism of noncollagenous glycoproteins during wound healing. J Surg Res 1981; 31: 218–224.
Bertolami CN. Glycosaminoglycan interactions in early wound repair. In: Hunt TK, Heppenstall RB, Pines E, Rovee D, eds. Soft and hard tissue repair. New York: Praeger Publishers 1984; 67–97.
Green H, Hamerman D. Production of hyaluronate and collagen by fibroblast clones in culture. Nature 1964; 201: 710.
Green H, Goldberg G. Kinetics of collagen synthesis by established mammalian cell lines. Nature 1963; 200: 1097.
Graham MF, Diegelmann RF, Lindblad WJ, Gay S, Gay R, Cohen IK. Effects of inflammation on wound healing:In vitro studies andin vivo studies. In: Hunt TK, Heppenstall RB, Pines E, Rovee D, eds. Soft and hard tissue repair. New York: Praeger Publishers 1984; 361–379.
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Orita, H., Fukasawa, M., Washio, M. et al. Kinetic analysis of experimental post-operative peritoneal healing: The incorporation of proline and glucosamine by exudative and tissue repair cells. The Japanese Journal of Surgery 21, 322–328 (1991). https://doi.org/10.1007/BF02470954
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DOI: https://doi.org/10.1007/BF02470954