Microvascular research
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Microvascular research · Jul 2013
Epigallocatechin 3-gallate inhibits 7-ketocholesterol-induced monocyte-endothelial cell adhesion.
7-Ketocholesterol (7KC) induces monocytic adhesion to endothelial cells, and induces arteriosclerosis while high-density lipoprotein (HDL) inhibits monocytic adhesion to the endothelium. Epigallocatechin 3-gallate (EGCG) was found to have a protective effect against arteriosclerosis. Therefore, the purpose of this study was to examine the possible HDL-like mechanisms of EGCG in endothelial cells by investigating whether EGCG inhibits 7KC-induced monocyte-endothelial cell adhesion by activating HDL-dependent signal transduction pathways. 7KC and/or EGCG were added to human endothelial cells (ISO-HAS), and the adhesion of pro-monocytic U937 cells was examined. ⋯ Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII. These results suggest that inhibition of monocyte-endothelial cell adhesion by EGCG is associated with CaMKKII pathway activation by ROS. Inhibition of 7KC-induced monocyte-endothelial cell adhesion induced by EGCG may function similarly to HDL.
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Microvascular research · May 2013
Comparative StudyLaser speckle contrast imaging for assessment of liver microcirculation.
Laser speckle contrast imaging (LSCI) is a novel technique for microcirculation imaging not previously used in the liver. The aim of the present experimental study was to evaluate the use of LSCI for assessing liver microcirculation. ⋯ Alterations in LSCI signal during sequential inflow occlusions were in accordance with previously published results on hepatic hemodynamics in the rat and correlated well with our SDF imaging-derived sinusoidal blood flow velocity measurements. We found that LSCI was able to produce reproducible real-time blood perfusion measurements of hepatic microcirculation. Compared to established techniques for liver blood perfusion measurements LSCI holds the advantages of non-contact measurements over large surfaces with a high speed of data acquisition.
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Microvascular research · Jan 2013
Estradiol receptors agonists induced effects in rat intestinal microcirculation during sepsis.
The steroid hormone estradiol is suggested to play a protective role in intestinal injury during systemic inflammation (sepsis). Our aim was to determine the effects of specific estradiol receptor (ER-α and ER-ß) agonists on the intestinal microcirculation during experimental sepsis. Male and sham ovariectomized female rats were subjected to sham colon ascendens stent peritonitis (CASP), and they were compared to male and ovariectomized female rats underwent CASP and either estradiol receptor α (ER-α) agonist propyl pyrazole triol (PPT), estradiol receptor ß (ER-ß) agonist diarylpropiolnitrile (DPN), or vehicle treatment. ⋯ Male; Leukocyte adhesion (n/mm(2)) V(1) 154.8±19.2 vs 70±10.5, V(3) 115.5±23.1 vs 52.8±9.6]. Those results suggest that the observed effects of estradiol receptors on different phases of leukocytes recruitment with the improvement of the functional capillary density could partially explain the previous demonstrated salutary effects of estradiol on the intestinal microcirculation during sepsis. The observed activity of this class of compounds could open up a new avenue of research into the potential treatment of sepsis.
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Microvascular research · Jan 2013
In vivo evaluation of venular glycocalyx during hemorrhagic shock in rats using intravital microscopy.
Hemorrhage is responsible for a large percentage of trauma-related deaths but the mechanisms underlying tissue ischemia are complex and not well understood. Despite the evidence linking glycocalyx degradation and hemorrhagic shock, there is no direct data obtained in vivo showing glycocalyx thickness reduction in skeletal muscle venules after hemorrhage. We hypothesize that damage to the endothelial glycocalyx is a key element in hemorrhage pathophysiology and tested the hypothesis that hemorrhage causes glycocalyx degradation in cremaster muscle microvessels. ⋯ Venular glycocalyx thickness and local blood flow changes were correlated: venules with the greatest flow reductions showed the largest decreases in glycocalyx. These changes may have a significant impact in shock pathophysiology. Intravital microscopy and integrated systems such as the one described here may be important tools to identify mechanisms by which resuscitation fluids may improve tissue recovery and outcome following hemorrhage.
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Microvascular research · Nov 2012
β-carotene reverses the IL-1β-mediated reduction in paraoxonase-1 expression via induction of the CaMKKII pathway in human endothelial cells.
Interleukin-1 beta (IL-1β) induces endothelial dysfunction and reduces nitric oxide (NO) production. IL-1β also enhances adhesion molecule expression and induces arteriosclerosis. Conversely, high-density lipoprotein (HDL) induces endothelial NO synthase (eNOS), paraoxonase-1 (PON-1) activity, and maintains vascular health. ⋯ Importantly, β-carotene upregulated the IL-1β-mediated decrease of CaMKKII, PZK1, LKB1, eNOS and PON-1. β-carotene inhibited IL-1β-mediated cell adhesion of U937 to endothelial cells. The effect of β-carotene was reversed by a CaMKK inhibitor, STO-609. These findings indicate that β-carotene regulates the expression of PON-1, eNOS and adhesion molecules via CaMKK pathway activation. β-carotene may contribute to the functional maintenance of vascular endothelial cells in a manner similar to HDL, protecting them against stimuli such as IL-1β.