We studied the effects of continuous intravenous air embolization on lung fluid balance in unanesthetized sheep. Following a 2-h base line, we infused 300-micrometers-diam air bubbles into the pulmonary artery at a rate sufficient to increase pulmonary vascular resistance by 60-300% and for periods of 0.25-3 h. Air emboli produced a dose- and duration-dependent increase in lung lymph and protein flow due mainly to an increase in endothelial barrier permeability but also to elevated pressure in the over-perfused microcirculation. When we stopped the air infusion, the vascular resistance fell as the air emboli were reabsorbed. Lung lymph and protein flow increased further and then returned slowly to base line with a half-time proportional to the duration of embolization. Increasing left atrial pressure during air embolization caused an increase in lymph flow and protein clearance and an average decrease of 15 Torr in arterial O2 tension, all changes in excess of that caused by either increased pressure or air emboli alone.
Significance
Metformin is the most commonly prescribed drug for the treatment of type 2 diabetes mellitus, yet the mechanism by which it lowers plasma glucose concentrations has remained elusive. Most studies to date have attributed metformin’s glucose-lowering effects to inhibition of complex I activity. Contrary to this hypothesis, we show that inhibition of complex I activity in vitro and in vivo does not reduce plasma glucose concentrations or inhibit hepatic gluconeogenesis. We go on to show that metformin, and the related guanides/biguanides, phenformin and galegine, inhibit complex IV activity at clinically relevant concentrations, which, in turn, results in inhibition of glycerol-3-phosphate dehydrogenase activity, increased cytosolic redox, and selective inhibition of glycerol-derived hepatic gluconeogenesis both in vitro and in vivo.
Positron emission tomography (PET) is used for staging and response evaluation in primary gastric lymphoma (PGL). However, the implications of [(18)F]-2-fluoro-2-deoxy-D-glucose ((18)F-FDG) uptake in PGL at first diagnosis have not been reported. The relationship between (18)F-FDG uptake and the expression of facilitative glucose transporters (GLUTs), hexokinase II (HK II), and Ki67, as well as malignant potential in PGL, was assessed in this study. We analyzed 23 patients with PGL [nine with diffuse large B-cell lymphoma (DLBCL); seven with high-grade mucosa-associated lymphoid tissue (MALT) lymphoma; and seven with low-grade MALT lymphoma]. The expression levels of GLUT1, GLUT3, HK II, and Ki67 were evaluated according to the percentage of positive area determined by immunohistochemistry. Standardized uptake values correlated significantly with pathological malignant potentials (low-grade/high-grade MALT lymphoma and DLBCL: p = 0.001-0.002), Ki67 (p < 0.001), and GLUT1 expression (p = 0.02). We determined that (18)F-FDG uptake is related to GLUT1 expression and tumor histological grade as well as Ki67 in PGL.
Postprandial portal hyperemia is mainly due to mesenteric arterial vasodilation; reduced postprandial portal hyperemia in patients with cirrhosis is attributable to portocollateral runoff.
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