PubMed · 10860420
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A Larsson, E K Tønnesen. 2000-05-15. [Sepsis--pathogenesis].. https://pubmed.ncbi.nlm.nih.gov/10860420/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Several observations imply that the early inflammatory response involving activated neutrophils, tissue macrophages, and cytokines plays an important role in the pathogenesis of neonatal respiratory distress syndrome (RDS) and progression to bronchopulmonary dysplasia (BPD). The aim of this study was to test the hypothesis that changes in circulating neutrophil number and function and plasma levels of cytokines, consistent with neutrophil activation and migration to the tissues, occur during the early stages of neonatal RDS. For this purpose we measured peripheral blood levels of certain immunological parameters that promote neutrophil activation and transendothelial migration. Twenty preterm neonates with severe RDS and 20 healthy infants matched for gestational age were the subjects. The absolute neutrophil count (ANC), and plasma levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF), and sL-selectin using an enzyme-linked immunosorbent assay (ELISA), neutrophil CD11b expression, and respiratory burst activity (RBA) using flow cytometry, were measured within 24 h after birth. The two groups were comparable regarding perinatal characteristics. None of the neonates studied had any clinical or laboratory evidence of infection by the time of blood sampling. The immunological investigation showed that the RDS neonates had significantly lower ANC (P = 0.032), higher expression of the CD11b on neutrophils (P = 0.0065), and higher G-CSF and IL-6 plasma levels (P = 0.0047 and P < 0.0001, respectively) in comparison to healthy preterm neonates. The neutrophil RBA and plasma sL-selectin levels did not differ significantly between the two groups. We conclude that in neonates with severe RDS, there is evidence of a systemic neutrophil activation early in the course of the disease, supporting the view of a contributing role of activated neutrophils in the pathogenesis of RDS.
Nitric oxide (NO) is involved in the regulation of SMC proliferation during intimal hyperplasia as has been shown by the inhibitory effect on intimal hyperplasia of adenovirus-mediated ceNOS overexpression in injured arteries in pig. Good assays to quantify the NO-producing enzymes, i.e., NO synthases (NOS), are essential to analyze the mechanism of action of NO in this process. We have developed novel flow cytometric assays for the simultaneous detection of NOS-3 protein, using NOS-3 specific antibodies, and NO production using 4,5-diaminofluorescein-diacetate (DAF-2/DA). The presence of NOS-3 protein and NO production is demonstrated on human A549 and HepG2 cells infected with a NOS-3 adenovirus (Ad.NOS-3). A comparative study showed that the flow cytometric assays are equally sensitive as Western blot analysis, the citrulline assay, or the Sievers assay. On human endothelial and SMC, NOS-3 protein and NO production were simultaneously detected with the assays, both under basal conditions and after Ad.NOS-3transduction. Simultaneous analysis of NOS-3 protein and NO production, made possible by the here-described novel flow cytometric assays, is of significant value to those investigating NOS-3 and NO.
BACKGROUND: Surgical preparation (distension) of the saphenous vein (SV) is applied routinely during harvesting in coronary artery bypass grafting (CABG). However, mechanical distension may impair the endothelium, which plays an important role in long-term patency. The present study investigated the effect of surgical preparation of the SV on nitric oxide (NO) release from the endothelium by direct measurement of NO. METHODS: Saphenous vein segments taken from CABG patients were cut open longitudinally and placed in an organ chamber. An NO-sensitive electrode and NO meter were used to directly measure NO release induced by acetylcholine (ACh) and bradykinin (BK) from the surgically prepared veins (PV) compared with the control (nondistended) veins. RESULTS: The basal release of NO in the PV group was significantly lower than that in the control group (3.4 +/- 1.4 nM, n = 9 versus 9.9 +/- 2.8 nM, n = 13, p = 0.002). The maximum concentrations of NO release induced by ACh and BK in the PV group were also significantly lower than those in the control veins (for ACh 10(-6) mol/L: 9.6 +/- 3.1 nM, n = 8 versus 41.9 +/- 11.2 nM, n = 12, p = 0.005; for BK 10(-8) mol/L: 8.3 +/- 3.7 nM, n = 7 versus 37.9 +/- 6.1 nM, n = 9, p = 0.003). Further, the duration of NO release in the PV group was significantly shorter than that in control veins (1.5 +/- 1.3 minutes, n = 8 versus 8.1 +/- 1.9 minutes, n = 8, p < 0.001). CONCLUSIONS: Surgical preparation almost abolishes NO release by the SV and this may significantly contribute to the low long-term patency rate of the vein graft.