Lipopolysaccharide-induced chorioamnionitis is confined to one amniotic compartment in twin pregnant sheep.

BACKGROUND: Chorioamnionitis is a major risk factor for preterm birth in multifetal pregnancies. However, there is little clinical data whether chorioamnionitis is restricted to one amniotic compartment in multifetal pregnancies. OBJECTIVE: To explore whether chorioamnionitis is confined to the exposed compartment and does not cross to the unaffected fetus in twin pregnancy. METHODS: In twin pregnant sheep, one of the twins was exposed to either 2 or 14 days of intra-amniotic lipopolysaccharide (LPS) while the co-twin was exposed to either 2 or 14 days of intra-amniotic saline (n = 3 for each exposure). Singletons were included in this study to compare the grade of inflammation with twins. All fetuses were delivered at 125 days of gestation (term = 150 days). Chorioamnionitis was confirmed by histological examination. Lung inflammation was assessed by cell count in bronchoalveolar lavage. Lung compliance was assessed at 40 cm H(2)O. Results were compared using analysis of variance (ANOVA) with a post-hoc Tukey analysis. RESULTS: Inflammation in placenta, membranes and lung of LPS-exposed twins was significantly higher after 2 and 14 days of exposure when compared to the saline-exposed co-twins. Lung compliance in LPS-exposed twins was significantly increased after 14 days when compared to saline-exposed co-twins. Intrauterine LPS exposure increased lung compliance and inflammation in the membranes, placenta and lung to the same extent in twins as in singletons. CONCLUSION: In twin pregnant sheep, inflammation of the membranes, placenta and fetal lung was strictly limited to the exposed fetus in the amniotic compartment in which the LPS was injected.

Nitrate patch prevents steroid-related bone necrosis.

Avascular necrosis of the femoral head is a common complication with disabling effect for young patients after high-dose corticosteroid treatment. We could show that steroids have a vasoconstrictive effect on lateral epiphyseal arteries of the femoral head which could lead to ischemia and subsequent necrosis. In this study we investigated the preventive effect of a nitrate patch on steroid-related bone necrosis in a rabbit model. New Zealand White rabbits (male; 3-4.5 kg bodyweight) were injected with 20 mg/kg bodyweight methylprednisolone (GC group; n = 6). Control animals (n = 6) were treated with phosphate-buffered saline. A third group (GC + N; n = 6) additionally received a nitrate patch (0.675 mg/day). Four weeks after i.m. methylprednisolone injection the animals were sacrificed. For histology and immunohistochemistry, tissue samples were fixed in 3% paraformaldehyde, embedded in paraffin, sectioned, dewaxed, and stained with Ladewig. For quantification of empty lacunae, a histologic sign of FHN, histomorphometry was performed. Histomorphometry revealed a significant increase of empty lacunae in glucocorticoid-treated animals compared to controls and GC + N-treated animals. No significant difference in empty lacunae count was detected between the GC + N group and controls. HE staining revealed the different osteocyte amount in the GC versus GC and nitrate patch-treated groups. This study demonstrates an increased number of empty osteocyte lacunae representing a pathologic feature of osteonecrosis, in the GC group. Less empty lacunae were counted in the GC animals after additional treatment with a nitrate patch. This finding suggests that nitrate co-treatment has the potential to prevent steroid-associated FHN.