Abnormalities in dendritic cell and macrophage accumulation in the pancreas of nonobese diabetic (NOD) mice during the early neonatal period.

Dendritic cell (DC), macrophage (Mphi) and lymphocyte infiltrations have been observed in normal human perinatal pancreata, but have never been investigated so early in control mice. In type 1 diabetes-prone NOD mice, these cells are thought to infiltrate first the periphery of the islets of Langerhans around weaning before further islet infiltration and beta-cell destruction. We quantified, during the first month of life, the numbers of DC (characterized by CD11c positivity and dendritic morphology), histiocyte-like Mphi (characterized by ER-MP23 positivity) and Mphi with scavenging potential (characterized by BM8 positivity) in C57BL/6, DBA/2 and BALB/c control, and NOD and lymphocyte-deficient NODscid mouse pancreata. First, CD11c+ DC were present at low densities from birth onwards in control pancreata, while densities were higher in NOD and NODscid. Second, high numbers of BM8+ and ER-MP23+ Mphi were observed at birth in all strains investigated. After birth, particularly BM8+ cells disappeared progressively in control strains, but not in NOD and NODscid. Third, NOD mice also had more ER-MP23+ Mphi at birth compared to controls. Finally, DC and Mphi localizations were similar in all strains, i.e., mostly as dispersed cells in perivascular, periductular, peri-islet areas and interlobular septa. The most remarkable finding was that particularly BM8+ Mphi, were seen at sites of islet neogenesis and predominantly at the duct-islet interface. Our data showed that different types of APC were present in the pancreas during postnatal development in various control mouse strains and some differences were observed in NOD and NODscid mice from birth onwards.

Inhaled NO reduces leukocyte-endothelial cell interactions and myocardial dysfunction in endotoxemic rats.

Inhaled nitric oxide (NO) has been shown to have some protective effect in the peripheral distal inflamed vasculature. The objective of the study was to determine whether inhaled NO would reduce endotoxin-induced leukocyte activation and myocardial contractile dysfunction. Rats were treated with either saline or endotoxin (10 mg/kg iv) and then allowed to breathe (4 h) either air or air plus NO (10 ppm). In endotoxemic rats, mesenteric venular endothelium leukocyte firm adhesion increased compared with control rats (1.15 +/- 0.32 vs. 4.08 +/- 0.96 leukocytes/100 microm; P < 0.05). Inhaled NO significantly attenuated endotoxin-induced venular endothelium leukocyte adhesion (4.08 +/- 0.96 vs. 1.86 +/- 0.76 leukocytes/100 microm; P < 0.05) and FITC-conjugated anti-intercellular adhesion molecule-1 fluorescence intensity. Endotoxin-induced myocardial dysfunction and leukocyte content increases were reduced in inhaled NO-treated rats. These observations suggest that inhaled NO reduces the degree of cardiovascular dysfunction and inflammation in endotoxemic rats.

[Post-partum suppurating thrombophlebitis of the ovarian vein presenting with pleuropulmonary manifestations]. / Thrombophlébite suppurée de la veine ovarienne du post-partum révélée par des manifestations pleuropulmonaires.

Following a normal delivery, a 22-year-old primigravida experienced fever resistant to antibiotic therapy. On the tenth post partum day, thoracic pain and chest X-ray were in favour of acute pneumonitis of left inferior lobe. Considering the extension to the right lung and a normal bronchic fibrescopy, a computed tomography (CT) was performed which showed a right ovarian vein thrombophlebitis, right minor subpleural opacities and left pneumopathy. The final diagnosis was post partum ovarian vein suppurated thrombophlebitis with pulmonary septic metastases from haematogenic diffusion. Post partum thrombophlebitis is a rare event with an incidence of 1 per 2,000 deliveries. Pulmonary inaugurating symptoms result rather from pulmonary embolism than from septic metastases. Post partum persisting and unexplained fever should be explored with abdominal CT-scan.

[Measurement of gastric mucosal pH by tonometry in major abdominal surgery]. / Mesure du pH intramuqueux gastrique par tonométrie au cours de la chirurgie abdominale majeure.

OBJECTIVE: To investigate whether changes in gastric intramucosal pH (pHim) occur during major abdominal surgery, and if so, to determine the relationship between classic global indices of tissue perfusion such as mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP), urine flow (UF) and arterial pH (pHa). STUDY DESIGN: Prospective descriptive study. PATIENTS: Seven ASA2 patients undergoing major abdominal surgery. METHODS: After induction of anaesthesia and endotracheal intubation, a tonometer nasogastric tube was positioned in the stomach. Measurements of tonometric PCO2 (PCO2ss), end-tidal PCO2 (PETCO2), PaCO2, bicarbonates [bicarb], pHa, MAP, HR, CVP and UF were collected at baseline (HO), and one, two, three, and 24 hours (H1, H2, H3, and H24) after the beginning of surgery. RESULTS: Haemodynamics did not significantly change during anaesthesia. During recovery HR increased and CVP decreased significantly. The pHim decreased significantly from 7.42 +/- 0.03 at H0 to 7.30 +/- 0.02 at H3. This was associated with a significant decrease in pHa (from 7.43 +/- 0.02 at H0 to 7.33 +/- 0.02 at H3) and in [bicarbo] from 22 +/- 1 mmol at H0 to 20 +/- 1 mmol at H3). The PaCO2 increased significantly from 33.5 +/- 1.5 mmHg at H0 to 39.5 +/- 2.8 at H3. On the other hand, pHimcorr (7.40- (pHa-pHim) and delta CO2 (PCO2ss-PETCO2) did not vary during anaesthesia. Postoperative organ failure did not occur in these patients. CONCLUSIONS: The pHim may decrease during anaesthesia without evidence of abnormal tissue perfusion. In order to avoid.

[Postoperative disorders of hemostasis caused by antifactor V circulating anticoagulant]. / Trouble postopératoire de l'hémostase par anticoagulant circulant anti-facteur V.

The case of a 34-year-old woman who experienced a biological haemostasis disorder, without clinical manifestations, is reported. The disorder was caused by a factor V inhibitor induced by a prolonged administration of antibiotics required by a postoperative biliary peritonitis. Therapeutic strategies in patients with an acquired factor V inhibitor are reviewed.