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• W2517503705 abstract "A surgical trauma results within minutes in exudation, platelets, and fibrin deposition. Within hours, the denuded area is covered by tissue repair cells/macrophages, starting a cascade of events. Epithelial repair starts on day 1 and is terminated by day 3. If repair is delayed by decreased fibrinolysis, local inflammation, or factors in peritoneal fluid, fibroblast growth starting on day 3 and angiogenesis starting on day 5 results in adhesion formation. For adhesion formation, quantitatively more important are factors released into the peritoneal fluid after retraction of the fragile mesothelial cells and acute inflammation of the entire peritoneal cavity. This is caused by mechanical trauma, hypoxia (e.g., CO2 pneumoperitoneum), reactive oxygen species (ROS; e.g., open surgery), desiccation, or presence of blood, and this is more severe at higher temperatures. The inflammation at trauma sites is delayed by necrotic tissue, resorbable sutures, vascularization damage, and oxidative stress. Prevention of adhesion formation therefore consists of the prevention of acute inflammation in the peritoneal cavity by means of gentle tissue handling, the addition of more than 5% N2O to the CO2 pneumoperitoneum, cooling the abdomen to 30°C, prevention of desiccation, a short duration of surgery, and, at the end of surgery, meticulous hemostasis, thorough lavage, application of a barrier to injury sites, and administration of dexamethasone. With this combined therapy, nearly adhesion-free surgery can be performed today. Conditioning alone results in some 85% adhesion prevention, barriers alone in 40%–50%. A surgical trauma results within minutes in exudation, platelets, and fibrin deposition. Within hours, the denuded area is covered by tissue repair cells/macrophages, starting a cascade of events. Epithelial repair starts on day 1 and is terminated by day 3. If repair is delayed by decreased fibrinolysis, local inflammation, or factors in peritoneal fluid, fibroblast growth starting on day 3 and angiogenesis starting on day 5 results in adhesion formation. For adhesion formation, quantitatively more important are factors released into the peritoneal fluid after retraction of the fragile mesothelial cells and acute inflammation of the entire peritoneal cavity. This is caused by mechanical trauma, hypoxia (e.g., CO2 pneumoperitoneum), reactive oxygen species (ROS; e.g., open surgery), desiccation, or presence of blood, and this is more severe at higher temperatures. The inflammation at trauma sites is delayed by necrotic tissue, resorbable sutures, vascularization damage, and oxidative stress. Prevention of adhesion formation therefore consists of the prevention of acute inflammation in the peritoneal cavity by means of gentle tissue handling, the addition of more than 5% N2O to the CO2 pneumoperitoneum, cooling the abdomen to 30°C, prevention of desiccation, a short duration of surgery, and, at the end of surgery, meticulous hemostasis, thorough lavage, application of a barrier to injury sites, and administration of dexamethasone. With this combined therapy, nearly adhesion-free surgery can be performed today. Conditioning alone results in some 85% adhesion prevention, barriers alone in 40%–50%. Discuss: You can discuss this article with its authors and with other ASRM members at https://www.fertstertdialog.com/posts/11305-role-of-the-peritoneal-cavity-in-the-prevention-of-postoperative-adhesions-pain-and-fatigue Discuss: You can discuss this article with its authors and with other ASRM members at https://www.fertstertdialog.com/posts/11305-role-of-the-peritoneal-cavity-in-the-prevention-of-postoperative-adhesions-pain-and-fatigue Intraperitoneal adhesions after surgery occur in 80%–90% of women (1Weibel M.A. Majno G. Peritoneal adhesions and their relation to abdominal surgery. A postmortem study.Am J Surg. 1973; 126: 345-353Abstract Full Text PDF PubMed Scopus (295) Google Scholar). They are a major cause of postoperative pain, infertility (2Tulandi T. Collins J.A. Burrows E. Jarrell J.F. McInnes R.A. Wrixon W. et al.Treatment-dependent and treatment-independent pregnancy among women with periadnexal adhesions.Am J Obstet Gynecol. 1990; 162 (Erratum: Am J Obstet Gynecol 1990;163(1 Pt 1):271): 354-357Abstract Full Text PDF PubMed Scopus (88) Google Scholar), small bowel obstruction (3Menzies D. Ellis H. Intestinal obstruction from adhesions—how big is the problem?.Ann R Coll Surg Engl. 1990; 72: 60-63PubMed Google Scholar, 4Moran B.J. Adhesion-related small bowel obstruction.Colorectal Dis. 2007; 9 Suppl 2: 39-44Crossref PubMed Scopus (24) Google Scholar), and surgical reinterventions which cause a huge cost for the society (5Parker M.C. Ellis H. Moran B.J. Thompson J.N. Wilson M.S. Menzies D. et al.Postoperative adhesions: ten-year follow-up of 12,584 patients undergoing lower abdominal surgery.Dis Colon Rectum. 2001; 44: 822-829Crossref PubMed Google Scholar, 6Lower A.M. Hawthorn R.J. Ellis H. O'Brien F. Buchan S. Crowe A.M. The impact of adhesions on hospital readmissions over ten years after 8849 open gynaecological operations: an assessment from the Surgical and Clinical Adhesions Research Study.BJOG. 2000; 107: 855-862Crossref PubMed Google Scholar, 7Ellis H. Moran B.J. Thompson J.N. Parker M.C. Wilson M.S. Menzies D. et al.Adhesion-related hospital readmissions after abdominal and pelvic surgery: a retrospective cohort study.Lancet. 1999; 353: 1476-1480Abstract Full Text Full Text PDF PubMed Scopus (553) Google Scholar, 8Parker M.C. Wilson M.S. van Goor H. Moran B.J. Jeekel J. Duron J.J. et al.Adhesions and colorectal surgery—call for action.Colorectal Dis. 2007; 9 Suppl 2: 66-72Crossref PubMed Google Scholar, 9van Goor H. Consequences and complications of peritoneal adhesions.Colorectal Dis. 2007; 9 Suppl 2: 25-34Crossref PubMed Scopus (116) Google Scholar, 10Nappi C. di Spiezio S.A. Greco E. Guida M. Bettocchi S. Bifulco G. Prevention of adhesions in gynaecological endoscopy.Hum Reprod Update. 2007; 13: 379-394Crossref PubMed Scopus (57) Google Scholar), as recently confirmed (11Ten Broek R.P. Strik C. Issa Y. Bleichrodt R.P. Van G.H. Adhesiolysis-related morbidity in abdominal surgery.Ann Surg. 2013; 258: 98-106Crossref PubMed Scopus (30) Google Scholar, 12Okabayashi K. Ashrafian H. Zacharakis E. Hasegawa H. Kitagawa Y. Athanasiou T. et al.Adhesions after abdominal surgery: a systematic review of the incidence, distribution and severity.Surg Today. 2014; 44: 405-420Crossref PubMed Scopus (14) Google Scholar, 13Sikirica V. Bapat B. Candrilli S.D. Davis K.L. Wilson M. Johns A. The inpatient burden of abdominal and gynecological adhesiolysis in the US.BMC Surg. 2011; 11: 13Crossref PubMed Scopus (24) Google Scholar). The pathophysiology of adhesion formation has been considered to be a local healing process of opposing surgical lesions (14Mais V. Peritoneal adhesions after laparoscopic gastrointestinal surgery.World J Gastroenterol. 2014; 20: 4917-4925Crossref PubMed Scopus (7) Google Scholar, 15Bolnick A. Bolnick J. Diamond M.P. Postoperative adhesions as a consequence of pelvic surgery.J Minim Invasive Gynecol. 2014; 22: 549-563Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar, 16Braun K.M. Diamond M.P. The biology of adhesion formation in the peritoneal cavity.Semin Pediatr Surg. 2014; 23: 336-343Abstract Full Text Full Text PDF PubMed Google Scholar, 17De Wilde R.L. Bakkum E.A. Brolmann H. Crowe A. Koninckx P. Korell M. et al.Consensus recommendations on adhesions (version 2014) for the ESGE Adhesions Research Working Group (European Society for Gynecological Endoscopy): an expert opinion.Arch Gynecol Obstet. 2014; 290: 581-582Crossref PubMed Google Scholar), and prevention was based on barriers. Over the past decade the important role of the entire peritoneal cavity in this process became apparent, and the combined treatment of the peritoneal cavity during surgery together with application of a barrier after surgery resulted in nearly adhesion-free surgery, which provides the additional benefits of less postoperative pain and a faster recovery (18Koninckx P.R. Corona R. Timmerman D. Verguts J. Adamyan L. Peritoneal full-conditioning reduces postoperative adhesions and pain: a randomised controlled trial in deep endometriosis surgery.J Ovarian Res. 2013; 6: 90Crossref PubMed Scopus (14) Google Scholar). This prompted us to review the role of the peritoneal cavity in the pathophysiology and in the prevention of postoperative adhesion formation. The United States National Library of Medicine (www.pubmed.com) from 2000 to May 2016 was searched for “postoperative adhesions” OR “peritoneal adhesions” (n = 4,826) together with factors in peritoneal cavity by adding “peritoneal cavity” (n = 257 of which seven relevant), “cooling” (n = 5), “temperature” (n = 39), or “N2O” (n = 2). Because relevant articles could not be identified the 2,058 articles on adhesions since 2010 were hand searched. The peritoneum has a large surface of 1.7 m2 and is composed of a single layer of mesothelial cells, a basal membrane, and some loose connective tissue resting on the underlying tissues with blood vessels and lymphatics. The mesothelial cells facilitate gliding of bowels by means of microvilli, glycosaminoglycans, and surfactant. The intact peritoneal cavity is a virtual cavity similar to the inside of mouth and bowels. The peritoneum used to be considered a semipermeable membrane with fast diffusion of fluid and small molecules but limited diffusion of larger molecules. Indeed, the concentrations of smaller blood proteins, such as albumin, LH, and FSH, are 40% lower than in plasma, whereas larger molecules, such as factors V and VIII, are virtually absent, preventing thrombin activation. Locally secreted macromolecules as CA125 and glycodelins accumulate with concentrations much higher than in plasma (19Koninckx P.R. Heyns W. Verhoeven G. Van B.H. Lissens W.D. De M.P. et al.Biochemical characterization of peritoneal fluid in women during the menstrual cycle.J Clin Endocrinol Metab. 1980; 51: 1239-1244Crossref PubMed Google Scholar, 20Koninckx P.R. Brosens I.A. Heyns W.H. Peritoneal fluid in female fertility and sterility.Contracept Fertil Sex. 1980; 8: 145-152Google Scholar, 21Koninckx P.R. De M.P. Brosens I.A. Diagnosis of the luteinized unruptured follicle syndrome by steroid hormone assays on peritoneal fluid.Br J Obstet Gynaecol. 1980; 87: 929-934Crossref PubMed Google Scholar, 22Pattinson H.A. Koninckx P.R. Brosens I.A. Vermylen J. Clotting and fibrinolytic activities in peritoneal fluid.Br J Obstet Gynaecol. 1981; 88: 160-166Crossref PubMed Google Scholar, 23Cornillie F.J. Lauweryns J.M. Seppala M. Riittinen L. Koninckx P.R. Expression of endometrial protein PP14 in pelvic and ovarian endometriotic implants.Hum Reprod. 1991; 6: 1411-1415PubMed Google Scholar, 24Koninckx P.R. Muyldermans M. Meuleman C. Cornillie F.J. CA 125 in the management of endometriosis.Eur J Obstet Gynecol Reprod Biol. 1993; 49: 109-113Abstract Full Text PDF PubMed Google Scholar). Mesothelial cells also actively regulate the exchange with vessels and extracellular spaces by means of gap junctions and vesicular transport. Surprisingly, the intact mesothelial layer also actively inhibits the diffusion of gases such as CO2 (25Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Pathogenesis of CO2 pneumoperitoneum–induced metabolic hypoxemia in a rabbit model.J Am Assoc Gynecol Laparosc. 2002; 9: 306-314Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 26Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Reduction of CO2-pneumoperitoneum–induced metabolic hypoxaemia by the addition of small amounts of O2 to the CO2 in a rabbit ventilated model. A preliminary study.Hum Reprod. 2002; 17: 1623-1629Crossref PubMed Google Scholar) and N2O (unpublished observations). In women, the peritoneal fluid also contains transudation from growing ovarian follicles, increasing the volume and the concentrations of sex steroid hormones. The peritoneal cavity thus is a microenvironment with specific concentrations of hormones, cytokines, growth factors, cellular components such as macrophages, natural killer cells, and lymphocytes, and a specific immune system. Peritoneal fluid circulates clockwise, explaining a higher incidence of endometriosis on the left side. The peritoneum also has specific pain receptors (27Cervero F. Visceral versus somatic pain: similarities and differences.Dig Dis. 2009; 27 Suppl 1: 3-10Crossref PubMed Scopus (23) Google Scholar, 28Cervero F. Laird J.M. Visceral pain.Lancet. 1999; 353: 2145-2148Abstract Full Text Full Text PDF PubMed Scopus (301) Google Scholar). The peritoneal cavity therefore has to be considered as a separate active organ and not a passive container (29Koninckx P.R. Kennedy S.H. Barlow D.H. Endometriotic disease: the role of peritoneal fluid.Hum Reprod Update. 1998; 4: 741-751Crossref PubMed Scopus (151) Google Scholar, 30Koninckx P.R. Kennedy S.H. Barlow D.H. Pathogenesis of endometriosis: the role of peritoneal fluid.Gynecol Obstet Invest. 1999; 47 Suppl 1: 23-33Crossref PubMed Google Scholar). The large flat mesothelial cells react within seconds to minor trauma, such as exposure to air, by retraction resulting in bulging of cells and consequent direct exposure of the basal membrane (31Volz J. Koster S. Spacek Z. Paweletz N. Characteristic alterations of the peritoneum after carbon dioxide pneumoperitoneum.Surg Endosc. 1999; 13: 611-614Crossref PubMed Scopus (87) Google Scholar). This retraction is so rapid that in vivo fixation is necessary to study the intact mesothelial layer. This retraction increases over time (25Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Pathogenesis of CO2 pneumoperitoneum–induced metabolic hypoxemia in a rabbit model.J Am Assoc Gynecol Laparosc. 2002; 9: 306-314Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 26Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Reduction of CO2-pneumoperitoneum–induced metabolic hypoxaemia by the addition of small amounts of O2 to the CO2 in a rabbit ventilated model. A preliminary study.Hum Reprod. 2002; 17: 1623-1629Crossref PubMed Google Scholar). Identified traumas are mechanical trauma, exposure to a CO2 pneumoperitoneum (32Molinas C.R. Mynbaev O. Pauwels A. Novak P. Koninckx P.R. Peritoneal mesothelial hypoxia during pneumoperitoneum is a cofactor in adhesion formation in a laparoscopic mouse model.Fertil Steril. 2001; 76: 560-567Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar, 33Molinas C.R. Koninckx P.R. Hypoxaemia induced by CO2 or helium pneumoperitoneum is a co-factor in adhesion formation in rabbits.Hum Reprod. 2000; 15: 1758-1763Crossref PubMed Google Scholar), desiccation, infection, and chemical irritants. Normal saline solution detaches the mesothelial cells after 30 minutes with a loss of fibrinolytic activity (34Ryan G.B. Grobety J. Majno G. Mesothelial injury and recovery.Am J Pathol. 1973; 71: 93-112PubMed Google Scholar). This “toxicity” was confirmed recently in vitro (35Polubinska A. Breborowicz A. Staniszewski R. Oreopoulos D.G. Normal saline induces oxidative stress in peritoneal mesothelial cells.J Pediatr Surg. 2008; 43: 1821-1826Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 36Polubinska A. Winckiewicz M. Staniszewski R. Breborowicz A. Oreopoulos D.G. Time to reconsider saline as the ideal rinsing solution during abdominal surgery.Am J Surg. 2006; 192: 281-285Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar, 37Breborowicz A. Oreopoulos D.G. Is normal saline harmful to the peritoneum?.Perit Dial Int. 2005; 25 Suppl 4: S67-S70PubMed Google Scholar) and in vivo (38Cwalinski J. Staniszewski R. Baum E. Jasinski T. Mackowiak B. Breborowicz A. Normal saline may promote formation of peritoneal adhesions.Int J Clin Exp Med. 2015; 8: 8828-8834PubMed Google Scholar). Within hours transforming growth factor β increases and tissue plasminogen activator decreases. By retraction, the contiguous mesothelial cells are transformed into individual cells which causes passive diffusion through the exposed basal membrane (31Volz J. Koster S. Spacek Z. Paweletz N. Characteristic alterations of the peritoneum after carbon dioxide pneumoperitoneum.Surg Endosc. 1999; 13: 611-614Crossref PubMed Scopus (87) Google Scholar, 39Volz J. Koster S. Laparoscopy. To inflate or lift?.Cancer. 1999; 86 ([editorial]): 749-750Crossref PubMed Scopus (1) Google Scholar, 40Suematsu T. Hirabayashi Y. Shiraishi N. Adachi Y. Kitamura H. Kitano S. Morphology of the murine peritoneum after pneumoperitoneum vs. laparotomy.Surg Endosc. 2001; 15: 954-958Crossref PubMed Scopus (53) Google Scholar, 41Ordemann J. Jakob J. Braumann C. Kilian M. Bachmann S. Jacobi C.A. Morphology of the rat peritoneum after carbon dioxide and helium pneumoperitoneum: a scanning electron microscopic study.Surg Endosc. 2004; 18: 1389-1393Crossref PubMed Scopus (10) Google Scholar, 42Obradovic M.M. Stojimirovic B.B. Trpinac D.P. Milutinovic D.D. Obradovic D.I. Nesic V.B. Ultrastructural changes of peritoneal lining cells in uremia.Adv Perit Dial. 2000; 16: 26-30PubMed Google Scholar) and initiates acute inflammation (43Corona R. Verguts J. Schonman R. Binda M.M. Mailova K. Koninckx P.R. Postoperative inflammation in the abdominal cavity increases adhesion formation in a laparoscopic mouse model.Fertil Steril. 2011; 95: 1224-1228Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar). The peritoneal cavity thus becomes part of the body, which is an efficient defense mechanism against infection via recruiting immunoglobulins and macrophages. Similarly the decreased bowel motility helps to keep an infection localized. This retraction and the subsequent passive diffusion also explains the increasing resorption of CO2 (25Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Pathogenesis of CO2 pneumoperitoneum–induced metabolic hypoxemia in a rabbit model.J Am Assoc Gynecol Laparosc. 2002; 9: 306-314Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 26Mynbaev O.A. Molinas C.R. Adamyan L.V. Vanacker B. Koninckx P.R. Reduction of CO2-pneumoperitoneum–induced metabolic hypoxaemia by the addition of small amounts of O2 to the CO2 in a rabbit ventilated model. A preliminary study.Hum Reprod. 2002; 17: 1623-1629Crossref PubMed Google Scholar) requiring increasing ventilation during laparoscopic surgery. The repair of a peritoneal injury with damage of the basal membrane and the subendothelial connective tissue is a strictly timed process (Fig. 1) . Within minutes, with onset of acute inflammation and activation of the coagulation cascade, platelets attach and coalesce over the lesion. The increased blood flow, dilation of arterioles, increased permeability of the capillaries, and migration of neutrophils and macrophages onto the lesion forms a fibrin mesh. Within hours, the lesion is covered with macrophages and/or “tissue repair cells” which acquire enhanced fibrinolytic activity (34Ryan G.B. Grobety J. Majno G. Mesothelial injury and recovery.Am J Pathol. 1973; 71: 93-112PubMed Google Scholar). These cells start to remove cell debris while platelet-derived growth factors activate migration and proliferation of fibroblast/mesothelial cells. Visible mesothelial cell growth starts after 24 hours, followed by fibroblast proliferation on day 3 and angiogenesis on day 5. It is unclear whether these cells are fibroblasts, macrophages, or stem cells (44Kim Y.D. Jun Y.J. Kim J. Kim C.K. Effects of human adipose-derived stem cells on the regeneration of damaged visceral pleural mesothelial cells: a morphological study in a rabbit model.Interact Cardiovasc Thorac Surg. 2014; 19: 363-367Crossref PubMed Scopus (3) Google Scholar, 45Wang N. Shao Y. Mei Y. Zhang L. Li Q. Li D. et al.Novel mechanism for mesenchymal stem cells in attenuating peritoneal adhesion: accumulating in the lung and secreting tumor necrosis factor alpha-stimulating gene-6.Stem Cell Res Ther. 2012; 3: 51Crossref PubMed Scopus (0) Google Scholar, 46Han J.Y. Goh R.Y. Seo S.Y. Hwang T.H. Kwon H.C. Kim S.H. et al.Cotransplantation of cord blood hematopoietic stem cells and culture-expanded and GM-CSF–/SCF–transfected mesenchymal stem cells in SCID mice.J Korean Med Sci. 2007; 22: 242-247Crossref PubMed Google Scholar, 47Lucas P.A. Stem cells for mesothelial repair: an understudied modality.Int J Artif Organs. 2007; 30: 550-556PubMed Google Scholar) and whether they originate from the peritoneal fluid, the mesothelium, the submesothelial connective tissue, the vascular endothelium, or blood cells (47Lucas P.A. Stem cells for mesothelial repair: an understudied modality.Int J Artif Organs. 2007; 30: 550-556PubMed Google Scholar, 48Herrick S.E. Mutsaers S.E. The potential of mesothelial cells in tissue engineering and regenerative medicine applications.Int J Artif Organs. 2007; 30: 527-540PubMed Google Scholar, 49Mutsaers S.E. Prele C.M. Lansley S.M. Herrick S.E. The origin of regenerating mesothelium: a historical perspective.Int J Artif Organs. 2007; 30: 484-494PubMed Google Scholar, 50Mutsaers S.E. Wilkosz S. Structure and function of mesothelial cells.Cancer Treat Res. 2007; 134: 1-19PubMed Google Scholar, 51Mutsaers S.E. Mesothelial cells: their structure, function and role in serosal repair.Respirology. 2002; 7: 171-191Crossref PubMed Scopus (182) Google Scholar). Mesothelial cells and the endothelial and hematopoietic cells are derived from a common progenitor cell originating embryologically in the splanchnic mesothelium (52Munoz-Chapuli R. Perez-Pomares J.M. Macias D. Garcia-Garrido L. Carmona R. Gonzalez M. Differentiation of hemangioblasts from embryonic mesothelial cells? A model on the origin of the vertebrate cardiovascular system.Differentiation. 1999; 64: 133-141Crossref PubMed Scopus (51) Google Scholar). Opposing lesions attach with a fibrin mesh. In the absence of bowel movements, nonopposing lesions can attach as well, because the inflammatory process damages the fragile mesothelial cells of opposing organs. The time courses of repair and cell proliferation explain why the speed of fibrinolysis (53Holmdahl L.E. The role of fibrinolysis in adhesion formation.Eur J Surg Suppl. 1997; : 24-31PubMed Google Scholar) that breaks this fibrin attachment determines whether the healing results in repair (54DiZerega G.S. Campeau J.D. Peritoneal repair and post-surgical adhesion formation.Hum Reprod Update. 2001; 7: 547-555Crossref PubMed Scopus (172) Google Scholar) or adhesion formation. If fibrinolysis is fast, the mesothelial repair, starting on day 1 from numerous small islands (55Gomel V. Urman B. Gurgan T. Pathophysiology of adhesion formation and strategies for prevention.J Reprod Med. 1996; 41: 35-41PubMed Google Scholar), is completed within 3 days, i.e., before the fibroblast and angiogenetic proliferation processes become fully activated. This also explains why repair of small and large areas is equally rapid (56Ellis H. Harrison W. Hugh T.B. The healing of peritneum under normal and pathological conditions.Br J Surg. 1965; 52: 471-476Crossref PubMed Google Scholar). If this repair mechanism is not completed by day 3, the proliferating fibroblasts invade the fibrin scaffold, which together with angiogenesis starting on day 5 leads invariably to adhesion formation. Repair can be delayed by local factors such as a decreased fibrinolysis, presence of necrotic tissue, tissue ischemia, and oxidative stress secondary to vascular damage or sutures, and by infection (57Awonuga A.O. Belotte J. Abuanzeh S. Fletcher N.M. Diamond M.P. Saed G.M. Advances in the pathogenesis of adhesion development: the role of oxidative stress.Reprod Sci. 2014; 21: 823-836Crossref PubMed Scopus (7) Google Scholar). Furthermore, the injured area may be shielded from the blood stream through vascular damage, and from the peritoneal fluid by the fibrin plug. A drug therefore would have difficulty reaching the injured area. This explains why the effect of tissue plasminogen activator, administered intraperitoneally after a minor surgical trauma, varies from poor (58Hellebrekers B.W. Trimbos-Kemper T.C. Trimbos J.B. Emeis J.J. Kooistra T. Use of fibrinolytic agents in the prevention of postoperative adhesion formation.Fertil Steril. 2000; 74: 203-212Abstract Full Text Full Text PDF PubMed Scopus (139) Google Scholar) to 40% effective (59Binda M.M. Hellebrekers B.W. Declerck P.J. Koninckx P.R. Effect of Reteplase and PAI-1 antibodies on postoperative adhesion formation in a laparoscopic mouse model.Surg Endosc. 2009; 23: 1018-1025Crossref PubMed Scopus (4) Google Scholar). The mesothelial cell retraction (31Volz J. Koster S. Spacek Z. Paweletz N. Characteristic alterations of the peritoneum after carbon dioxide pneumoperitoneum.Surg Endosc. 1999; 13: 611-614Crossref PubMed Scopus (87) Google Scholar, 39Volz J. Koster S. Laparoscopy. To inflate or lift?.Cancer. 1999; 86 ([editorial]): 749-750Crossref PubMed Scopus (1) Google Scholar, 40Suematsu T. Hirabayashi Y. Shiraishi N. Adachi Y. Kitamura H. Kitano S. Morphology of the murine peritoneum after pneumoperitoneum vs. laparotomy.Surg Endosc. 2001; 15: 954-958Crossref PubMed Scopus (53) Google Scholar, 41Ordemann J. Jakob J. Braumann C. Kilian M. Bachmann S. Jacobi C.A. Morphology of the rat peritoneum after carbon dioxide and helium pneumoperitoneum: a scanning electron microscopic study.Surg Endosc. 2004; 18: 1389-1393Crossref PubMed Scopus (10) Google Scholar, 42Obradovic M.M. Stojimirovic B.B. Trpinac D.P. Milutinovic D.D. Obradovic D.I. Nesic V.B. Ultrastructural changes of peritoneal lining cells in uremia.Adv Perit Dial. 2000; 16: 26-30PubMed Google Scholar) and the acute inflammation (43Corona R. Verguts J. Schonman R. Binda M.M. Mailova K. Koninckx P.R. Postoperative inflammation in the abdominal cavity increases adhesion formation in a laparoscopic mouse model.Fertil Steril. 2011; 95: 1224-1228Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar) in the entire peritoneal cavity release substances into the peritoneal fluid that delay the local repair and enhance adhesion formation (Fig. 2) (60Koninckx P.R. Ussia A. Adamyan L. The role of the peritoneal cavity in adhesion formation.Fertil Steril. 2012; 97: 1297Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar). In a laparoscopic mouse model, adhesions between opposing lesions in the lower abdomen increase proportionally to the duration of bowel manipulation in the upper abdomen (61Schonman R. Corona R. Bastidas A. De Cicco C Koninckx P.R. Effect of upper abdomen tissue manipulation on adhesion formation between injured areas in a laparoscopic mouse model.J Minim Invasive Gynecol. 2009; 16: 307-312Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar, 62Schonman R. De Cicco C Corona R. Soriano D. Koninckx P.R. Accident analysis: factors contributing to a ureteric injury during deep endometriosis surgery.BJOG. 2008; 115: 1611-1615Crossref PubMed Scopus (10) Google Scholar). The severity of the acute inflammation in the entire peritoneal cavity and the associated enhanced adhesion formation is the sum of the duration and intensity of all the factors that damage the mesothelial cells. The mechanical trauma caused by manipulation explains the decrease in the rate of adhesions with increased surgical experience, as shown in learning curves in rabbits and in mice (63Ordonez J.L. Dominguez J. Evrard V. Koninckx P.R. The effect of training and duration of surgery on adhesion formation in the rabbit model.Hum Reprod. 1997; 12: 2654-2657Crossref PubMed Scopus (38) Google Scholar, 64Corona R. Verguts J. Binda M.M. Molinas C.R. Schonman R. Koninckx P.R. The impact of the learning curve on adhesion formation in a laparoscopic mouse model.Fertil Steril. 2011; 96: 193-197Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar). CO2 pneumoperitoneum causes superficial mesothelial hypoxia (32Molinas C.R. Mynbaev O. Pauwels A. Novak P. Koninckx P.R. Peritoneal mesothelial hypoxia during pneumoperitoneum is a cofactor in adhesion formation in a laparoscopic mouse model.Fertil Steril. 2001; 76: 560-567Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar, 33Molinas C.R. Koninckx P.R. Hypoxaemia induced by CO2 or helium pneumoperitoneum is a co-factor in adhesion formation in rabbits.Hum Reprod. 2000; 15: 1758-1763Crossref PubMed Google Scholar, 65Yesildaglar N. Ordonez J.L. Laermans I. Koninckx P.R. The mouse as a model to study adhesion formation following endoscopic surgery: a preliminary report.Hum Reprod. 1999; 14: 55-59Crossref PubMed Scopus (32) Google Scholar, 66Molinas C.R. Campo R. Elkelani O.A. Binda M.M. Carmeliet P. Koninckx P.R. Role of hypoxia inducible factors 1alpha and 2alpha in basal adhesion formation and in carbon dioxide pneumoperitoneum-enhanced adhesion formation after laparoscopic surgery in transgenic mice.Fertil Steril. 2003; 80 Suppl 2: 795-802Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar, 67Molinas C.R. Campo R. Dewerchin M. Eriksson U. Carmeliet P. Koninckx P.R. Role of vascular endothelial growth factor and placental growth factor in basal adhesion formation and in carbon dioxide pneumoperitoneum–enhanced adhesion formation after laparoscopic surgery in transgenic mice.Fertil Steril. 2003; 80 Suppl 2: 803-811Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar). Indeed, the CO2 pneumoperitoneum–enhanced adhesion formation is absent in mice deficient of one or both of the two hypoxemia-inducible factors, HIF-1α and HIF-2α. The severity of the effect increases exponentially when partial oxygen concentrations are below 7 mm Hg (or 1% of oxygen), which is consistent with the affinity of O2 for the HIF receptor. The effect increases with the intraperitoneal pressure (68Yesildagla" @default.
• W2517503705 created "2016-09-16" @default.
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• W2517503705 creator A5079348182 @default.
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• W2517503705 date "2016-10-01" @default.
• W2517503705 modified "2023-10-11" @default.
• W2517503705 title "Role of the peritoneal cavity in the prevention of postoperative adhesions, pain, and fatigue" @default.
• W2517503705 cites W138996667 @default.
• W2517503705 cites W1424176171 @default.
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