title: Activation of monocytes and endothelial cells depends on the severity of surgical stress.
abstract: Surgical injury not only induces a systemic endocrine-metabolic response but also influences the function of the leukocytes and endothelial cells leading to various systemic responses. These responses appear to depend on the severity of surgical stress, which differs according to the surgical procedures. In this study, we investigated the response of monocytes and endothelial cells, and the development of systemic inflammatory response syndrome (SIRS) in relation to the severity of surgical stress. The postoperative clinical course was evaluated between patients undergoing an esophagectomy (ER group) and a distal gastrectomy (DG group). The tumor necrosis factor alpha (TNF-alpha) production of monocytes, the serum interleukin 6 (IL-6) levels, the CD11b expression on either monocytes or granulocytes, and the intercellular adhesion molecule-1 (ICAM-1) expression on human umbilical vein endothelial cells (HUVECs) stimulated with culture supernatants of monocytes were compared between the 2 groups. The development of SIRS was observed in all patients in the ER group, whereas no patients demonstrated SIRS in the DG group. The serum IL-6 levels, TNF-alpha production of monocytes, and CD11b intensity on monocytes or granulocytes in the ER group were higher than those in the DG group. In the ER group, the ICAM-1 intensity on HUVECs with monocytes immediately after operation significantly increased compared with before the operation. In conclusion, both the CD11b expression on monocytes and the TNF-alpha production of monocytes are considered to reflect the degree of surgical stress, and the activation of endothelial cells stimulated with these activated leukocytes may therefore lead to both tissue and organ injury.
authors.affiliation: Department of Surgery I, National Defense Medical College, Namiki 3-2, Tokorozawa, Saitama 359-8513, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Aosasa
authors.forename: S
authors.initials: S
authors.lastname: Ono
authors.forename: H
authors.initials: H
authors.lastname: Mochizuki
authors.forename: H
authors.initials: H
authors.lastname: Tsujimoto
authors.forename: S
authors.initials: S
authors.lastname: Osada
authors.forename: E
authors.initials: E
authors.lastname: Takayama
authors.forename: S
authors.initials: S
authors.lastname: Seki
authors.forename: H
authors.initials: H
authors.lastname: Hiraide
mesh_terms: D000230:Adenocarcinoma / Q000150:complications / Q000276:immunology / Q000601:surgery; D000368:Aged; D000954:Antigens, Surface / Q000276:immunology; D002294:Carcinoma, Squamous Cell / Q000150:complications / Q000276:immunology / Q000601:surgery; D004730:Endothelium, Vascular / Q000276:immunology*; D004938:Esophageal Neoplasms / Q000150:complications / Q000276:immunology / Q000601:surgery; D016629:Esophagectomy; D005260:Female; D005743:Gastrectomy; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D013274:Stomach Neoplasms / Q000150:complications / Q000276:immunology / Q000601:surgery; D013312:Stress, Physiological / Q000209:etiology / Q000276:immunology*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000954:Antigens, Surface; D014409:Tumor Necrosis Factor-alpha