Microvascular research
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Microvascular research · May 2009
Effect of T cells on vascular permeability in early ischemic acute kidney injury in mice.
Although previous studies have demonstrated that microvascular dysfunction and inflammation occur in ischemia-reperfusion injury (IRI), the underlying mechanisms are poorly understood. We hypothesized that T cells could mediate renal vascular permeability (RVP) during IRI. We evaluated renal vascular permeability by extravasation of Evans blue dye from the kidney in CD3, CD4 or CD8 T cell deficient mice as well as in TNF receptor knock out mice in our mouse model of kidney ischemia-reperfusion injury. ⋯ The rise in RVP after ischemia in wild type mice was attenuated in CD3, CD4 or CD8 T cell deficient mice as well as in TNF receptor knock out mice. The attenuation of RVP in CD3 T-cell deficient mice after ischemia was restored by adoptive transfer of T cells from WT mice. Our data demonstrate that T cells directly contribute to the increased RVP after kidney ischemia-reperfusion, potentially through T cell cytokine production.
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Microvascular research · Mar 2009
Noninvasive pulse wave analysis for the determination of central artery stiffness.
Central artery stiffness predicts cardiovascular structural damage and clinical outcome. It is controversial whether central artery stiffness can be determined by noninvasive measurements. We compared noninvasive determination of central artery stiffness obtained from applanation tonometry of the peripheral radial artery waveform with invasive measurements of the ratio of pulse-pressure-to-stroke-volume. ⋯ The association between invasive and noninvasive measurements was confirmed using Bland-Altman plots. Furthermore, a norepinephrine-induced increase of arterial stiffness was detected both invasively and noninvasively. Noninvasive determination of central artery stiffness obtained from peripheral radial artery waveform should be useful in clinical practice although it cannot be performed in every patient.
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Microvascular research · Jan 2009
ReviewAlteration of microvascular permeability in acute kidney injury.
Functional and structural abnormalities in the renal microvasculature are important processes contributing to the pathophysiology of ischemic acute kidney injury (AKI). Renewed interest in the complex interplay between tubular injury, inflammation and microvascular alterations has emerged in order to gain a better understanding of acute kidney injury syndromes. This review examines alterations of the renal microvasculature as they relate to ischemic and septic AKI with an emphasis on the mechanisms involved in altered microvascular permeability.
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Microvascular research · Jan 2009
ReviewRegulation of endothelial barrier function by reactive oxygen and nitrogen species.
Excessive generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), by activated neutrophils and endothelial cells, has been implicated in the pathophysiology of endothelial barrier dysfunction. Disruption of the integrity of this barrier markedly increases permeability to fluids, solutes and inflammatory cells and is the hallmark of many disorders such as acute lung injury (ALI) and sepsis. ⋯ However, no significant benefits have been observed, so far, in clinical trials of antioxidants for the treatment of endothelial barrier dysfunction. This article will review the available evidence implicating ROS and RNS in endothelial barrier dysfunction, explore potential underlying mechanisms, and identify areas of further research.