Microcirculation : the official journal of the Microcirculatory Society, Inc
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Endothelial glycocalyx injury causes microcirculatory perfusion disturbances in experimental studies, but the relevance in a clinical setting remains unknown. We investigated whether glycocalyx dimensions are reduced after onset of CPB and whether this is associated with alterations in microvascular perfusion. ⋯ This study shows that endothelial glycocalyx dimensions decrease after onset of CPB and are closely related to microvascular perfusion when assessed with a novel, noninvasive technique.
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Exogenously administered CO interferes with PMN recruitment to the inflamed organs. The mechanisms of CO-dependent modulation of vascular proadhesive phenotype, a key step in PMN recruitment, are unclear. ⋯ These findings indicate that CORM-3 pretreatment interferes with JNK/AP-1 signaling and suppresses LPS-induced upregulation of the proadhesive phenotype in hCMEC/D3.
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TBI causes localized cerebral ischemia that, in turn, is accompanied by both changes in BBB permeability and recruitment of CD34(+) cells to the injured tissue. However, it remains unknown whether CD34(+) cell recruitment is linked to BBB permeability. This study is a preliminary investigation into possible correlations between CD34(+) cell recruitment and BBB permeability following TBI in a rat model. ⋯ The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.
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Comparative Study Observational Study
Assessing skeletal muscle variations in microvascular pressure and unstressed blood volume at the bedside.
Quantitative NIRS measurements for MBV partitioning inside microvessels are of current physiologic and clinical interest. In this study, in healthy subjects, we sought new bedside NIRS variables for noninvasively measuring Vu and Pi changes. ⋯ The new NIRS variables we report could be a practical bench-to-bedside tool to assess venous driving pressure for systemic perfusion and measure changes in Vu within the microvascular bed.
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Microvascular hyperpermeability that occurs due to breakdown of the BBB is a major contributor of brain vasogenic edema, following IR injury. In microvascular endothelial cells, increased ROS formation leads to caspase-3 activation following IR injury. The specific mechanisms, by which ROS mediates microvascular hyperpermeability following IR, are not clearly known. We utilized an OGD-R in vitro model of IR injury to study this. ⋯ These results suggest that OGD-R-induced hyperpermeability is ROS and caspase-3 dependent and can be regulated by their inhibitors.