Regional cellular responses to intraperitoneal infection. (57/318)

Leucocytes in different body compartments were examined in a murine intra-abdominal abscess model: (i) peripheral blood; (ii) peritoneal exudate; (iii) abscess wall; and (iv) abscess pus, with respect to their phagocytic ability, CR3 expression and Ia antigen expression (murine MHC antigen). The ability of serum or supernatant in each compartment to opsonize Staphylococcus aureus was also determined. Mice responded to caecal ligation and puncture (CLP) with systemic monocytosis, an increased amount of opsonins in peritoneal fluid and an increased phagocytosis in pus leucocytes. This increased phagocytic ability and CR3 expression both subsequently decreased. Monocyte/macrophage Ia expression was reduced in all measured compartments over time. In contrast, sham-operated animals, without an intra-abdominal abscess, responded to operation with an even greater increase in peritoneal exudate phagocytic ability and in monocyte/macrophage Ia expression in all compartments which was sustained beyond 1 week. Decreased peritoneal exudate cell and peripheral blood Ia was still present after 28 days in CLP animals, compared with both sham and normal animals (P less than 0.05, P less than 0.02, respectively). For all parameters, changes observed in peripheral blood did not reflect those present near the site of infection. Proper understanding of local or regional infection must take into account and ultimately alter these generally unappreciated changes in and about the actual site of infection.  (+info)

Involvement of the spleen in preleukemic development of a murine retrovirus-induced promonocytic leukemia. (58/318)

An acute myeloid leukemia can result from the inoculation of Moloney murine leukemia virus into BALB/c mice undergoing a 2,6,10,14-tetramethylpentadecane-induced chronic inflammatory response in the peritoneal cavity. This leukemia is ultimately observed in the peritoneal cavity as an ascites with cells infiltrating the granulomatous tissue. It has been proposed, however, that hematopoietic organs such as the spleen and bone marrow are involved in preleukemic development of Moloney murine leukemia. Therefore, to determine if the spleen plays a role in this development, mice were splenectomized at various times relative to virus inoculation. When splenectomies were performed 3 days before and 2, 4, 6, and 8 weeks after virus inoculation there was, in all cases, a decreased death rate compared to sham-splenectomized controls. The greatest difference in death rate due to promonocytic leukemia was observed when mice were splenectomized at 4 weeks after virus inoculation. The decrease in disease incidence observed as a result of splenectomy was not caused by decreased virus spread in hematopoietic organs or an alteration in the profile of the cellular infiltrate in the granuloma. It was found, however, that the spleens of 2,6,10,14-tetramethylpentadecane-treated mice, relative to those of normal mice, have a significantly increased number of granulocyte-macrophage colony-forming cells and a slightly increased number of multipotential colony-forming cells. These observations suggest that a population of target cells for transformation, consisting of granulocyte-macrophage precursor cells, may reside in the spleen. Alternatively, partially transformed cells may reside temporarily in the spleen during the developmental stages of the disease process.  (+info)

The effect of intra-abdominal pressure on the generation of 8-iso prostaglandin F2alpha during laparoscopy in rabbits. (59/318)

BACKGROUND: Carbon dioxide pneumoperitoneum induces peritoneal oxidative stress. The aim of this study was to verify the effect of intra-abdominal pressure on oxidative stress in the peritoneum and on post-operative adhesion formation. METHODS: Forty-one rabbits underwent laparoscopic surgery: either gasless, or with CO(2)-pneumoperitoneum at pressures of 5, 10 or 15 mmHg. Serial parietal peritoneal biopsies were taken at various time-points: immediately after reaching the abdominal cavity, 30, 60, 90 and 120 min afterwards, and 15 min after abdominal desufflation. 8-iso prostaglandin F(2alpha) (8-iso PGF(2alpha)), a marker of oxidative stresss, was assayed by enzyme immunoassay and adhesion formation was scored by second-look laparoscopy on day 14. RESULTS: The gasless group showed no significant changes in 8-iso PGF(2alpha). Conversely, significant changes occurred in CO(2)-pneumoperitoneum in a time- and pressure-dependent manner. Adhesions developed only in the CO(2)-pneumoperitoneum groups, and total adhesion score was correlated with the amount of CO(2) insufflated and intra-abdominal pressure, but not with 8-iso PGF(2alpha), which was correlated with intra-abdominal pressure. CONCLUSION: Intra-abdominal pressure increased 8-iso PGF(2alpha) in the parietal peritoneum in a graded fashion, whilst gasless laparoscopy had no impact. It also influenced the frequency and severity of adhesion formation, but no causal link was found between 8-iso PGF(2alpha) and post-operative adhesion formation.  (+info)

Incidence and significance of peritoneal eosinophilia during peritoneal dialysis-related peritonitis. (60/318)

OBJECTIVE: To determine the incidence and significance of peritoneal eosinophilia (PEo) during peritoneal dialysis (PD)-related peritonitis. DESIGN: Retrospective observational study. SETTING: Tertiary-care public hospital. PATIENTS AND METHOD: We performed a cytological study of dialysate at the start of 465 cases of peritonitis diagnosed between January 1987 and May 2002. Cases associated with PEo (> 10% eosinophils) were classified according to their infectious or seemingly noninfectious origin. We compared the two groups, trying to disclose differentiating patterns of presentation. RESULTS: We found PEo in 42 cases. Infectious peritonitis was the final diagnosis in 22 of the 42 cases; a diagnosis of idiopathic eosinophilic peritonitis was finally established in 20 cases. The etiologic spectrum of infectious peritonitis with PEo did not differ markedly from the global spectrum of peritonitis in our unit. Infectious peritonitis with PEo tended to appear later in the course of PD therapy, presented with more severe clinical symptoms, displayed higher total peritoneal leukocyte and neutrophil counts, and showed lower degrees of PEo than idiopathic eosinophilic peritonitis, but overlap between the groups was significant. CONCLUSIONS: Peritoneal eosinophilia is infrequent but not rare during infectious PD-related peritonitis. Our findings agree with established concepts on idiopathic eosinophilic peritonitis, but overlap in presentation with infectious eosinophilic peritonitis is significant, which should be taken into consideration at the time of planning therapy for this condition.  (+info)

Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo. (61/318)

BACKGROUND: Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. METHODS: Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. RESULTS: The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P < 0.03) and caused profound mesothelial damage. The vessel density in the omentum and the mesentery was significantly correlated to both the number of tissue mast cells and the hyaluronan content in the peritoneal lavage, which might suggest a role for mast cells and hyaluronan in the induction of angiogenesis. CONCLUSIONS: Instillations of low pH lactate buffer, a high glucose concentration and glucose degradation products contribute differently and often cumulatively to peritoneal injury in vivo.  (+info)

Laparoscopic repair of a uteroperitoneal fistula. (62/318)

Repairs of pelvic fistulas using abdominal, vaginal, and laparoscopic approaches have been described. In the present case report, we describe our experience with the laparoscopic repair of a uteroperitoneal fistula.  (+info)

Diaphragmatic defect with peritoneopericardial communication. (63/318)

An 81-year-old man had a congenital defect of the central tendon of the diaphragm, including a peritoneopericardial communication with herniation of the omentum to the pericardial sac in front of the heart. In addition, he had a critically stenosed congenital bicuspid aortic valve and severe coronary artery disease. The patient underwent reduction of the herniated omentum into the abdominal cavity, coronary artery bypass grafting, aortic valve replacement, and closure of the peritoneopericardial communication with a synthetic patch. Three years later, the patient was doing well, with a normally functioning pericardial valve in the aortic position and no sign of omentum around the heart.  (+info)

Association rate between deep peritoneal endometriosis and other forms of the disease: pathogenetic implications. (64/318)

BACKGROUND: It has been suggested recently that deep endometriosis and the other forms of the disease do not share a common pathogenetic mechanism. In this study, we hypothesize that, if this is true, deep peritoneal endometriosis and the other forms should not be significantly associated. METHODS: Clinical and surgical records of all women who were referred to the Department of Obstetrics and Gynecology, Clinica 'L.Mangiagalli' between January 1995 and June 2002 and who were diagnosed with deep peritoneal pelvic endometriosis at the time of surgery were retrieved. The concomitant presence of superficial endometriotic implants, endometriomas and pelvic adhesions was evaluated. A binomial probability distribution model was used to calculate the 95% confidence interval (95% CI) of the association rates. RESULTS: Ninety-three women with deep peritoneal endometriosis were identified. The presence of superficial endometriotic implants, endometriomas and pelvic adhesions was documented in 61.3% (95% CI 51.4-71.2%), 50.5% (95% CI 40.3-60.7%) and 74.2% (95% CI 65.3-83.1%) of patients with deep endometriotic nodules, respectively. Overall, deep peritoneal endometriosis was the only form of the disease in only 6.5% (95% CI 2.8-12.3%) of cases. No relevant differences regarding these associations were observed according to the location and the size of the deep endometriotic nodules. CONCLUSIONS: Results from this study do not support the hypothesis that deep endometriosis should be considered as a distinct entity of the disease.  (+info)