Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to characterize the cellular responses in the peritoneal cavity and draining lymph in a sterile peritonitis model in conscious sheep. Lymph was collected from lymphatics that drained the peritoneal space (caudal mediastinal and thoracic ducts) as well as from lymph vessels that drained peripheral tissues (prescapular). Casein was used as the inflammatory agent. Dialysis solution (Dianeal 4.25%) containing 1g% casein and 25 microCi 125I-human serum albumin was infused into the peritoneal cavity in 50 ml/kg volumes. Peritoneal volumes increased from a mean infused volume of 1572 +/- 51 ml to a maximum of 2119 +/- 77 ml at 3 hours. Over 6 hours, the number of macrophages and lymphocytes in the peritoneal cavity remained relatively constant but the number of neutrophils increased from 9.9 +/- 4.2 x 10(7) to 9.2 +/- 1.9 x 10(9) total cells. Caudal lymph which drains directly from the peritoneal cavity through diaphragmatic stomata, demonstrated a 5 fold increase in flow rate over 6 hours following the Dianeal-casein infusion. Thoracic duct and prescapular flows declined approximately 70% and 50% respectively in the same time period. the concentration of lymphocytes and the lymphocyte outputs (product of volume and concentration) declined in all lymph compartments. No elevations in neutrophil numbers in the thoracic and prescapular lymph compartments were observed but neutrophil output in the caudal lymph increased steadily from 3.1 +/- 1.5 x 10(6) to 4.6 +/- 1.3 x 10(7)/hr at the 6 hour mark. We conclude that the major route of removal of inflammatory cells and fluid from the peritoneal cavity is through diaphragmatic lymphatics.
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PMID:Lymph flow and lymphatic drainage of inflammatory cells from the peritoneal cavity in a casein-peritonitis model in sheep. 780 84

Maternal protein restriction in rats leads to endothelial dysfunction and decreased NO bioavailability in the offspring. Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) are recognized to have pleiotropic actions including increasing NO bioavailability and reducing inflammation and oxidative damage. This study assessed statin treatment on vascular function in a model of endothelial dysfunction, which is independent of dyslipidemia. Wistar rats were fed a control (18% casein) or protein-restricted (9% casein) diet throughout pregnancy. At weaning, a subset of the protein-restricted group was given atorvastatin (10 mg/kg per day) in the drinking water. At 145 days of age, offspring were euthanized by CO(2) inhalation. Plasma samples were collected for markers of inflammation, vascular reactivity of the thoracic aorta, and small mesenteric arteries were assessed on the wire myograph, and tissues were snap frozen for molecular biology analysis. Thoracic aorta endothelial-dependent vasodilatation was attenuated in the male offspring from both protein-restricted groups compared with controls (P<0.05) but was similar in females (P value not significant). Endothelial-dependent dilatation of mesenteric arteries was attenuated in male and female protein-restricted offspring (P<0.05) and was corrected by atorvastatin. Maternal protein restriction increased plasma inflammatory markers granulocyte chemotactic protein, lipocalin-2, and beta(2)-microglobulin in male and C-reactive protein in female offspring (P<0.05). Atorvastatin had no effect on inflammatory markers in the males but restored C-reactive protein to control levels in the females (P<0.05). Aortic and mesenteric artery mRNA levels of endothelial NO synthase, superoxide dismutase 1, and tumor necrosis factor-alpha were unchanged. These data suggest that atorvastatin can restore endothelial function in this model, but its effects are gender specific and dependent on the vascular bed.
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PMID:Atorvastatin restores endothelial function in offspring of protein-restricted rats in a cholesterol-independent manner. 1922 Dec 11