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Histochemical characteristic of perivascular space in the brain with an advanced edema.
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Amorphorous and colorless spaces, Virchow-Robin spaces (VRS), were often found by HE stain around blood vessels in the edematous brain. Histochemical characteristic of the enlarged VRS caused by an advanced edema and detected by lectin stain using Griffonia simplicifolia I agglutinin in the brain
Neutrophil elastase inhibitor prevents ischemic brain damage via reduction of vasogenic edema.
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Release of neutrophil elastase is one of the harmful inflammatory reactions in acute cerebral ischemia. Therefore, inhibition of elastase released from neutrophils could be a useful strategy for the treatment of acute stroke. To evaluate this hypothesis, the effect of sivelestat, a selective
The cysteinyl leukotriene 2 receptor mediates retinal edema and pathological neovascularization in a murine model of oxygen-induced retinopathy.
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Leukotrienes have been implicated in the pathogenesis of degenerative diabetic retinopathy, with research focusing primarily on leukotriene B(4), with little attention devoted to the cysteinyl leukotrienes (cysLTs), which act through cysLT receptors (CysLT(1)R and CysLT(2)R). We demonstrate here the
Cellular mechanisms of blood-retinal barrier dysfunction in macular edema.
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OBJECTIVE
To determine the mechanism of blood-retinal barrier (BRB) dysfunction in human and experimental specimens using immunocytochemistry.
METHODS
Extravascular albumin was localized in clinical specimens and retinas from transgenic mice that overexpress vascular endothelial growth factor (VEGF)
A novel quantification of blood-brain barrier damage and histochemical typing after embolic stroke in rats.
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Treatment strategies in acute ischemic stroke are still limited. Considering numerous translation failures, research is tending to a preferred use of human-like animal models, and a more-complex perspective of tissue salvaging involving endothelial, glial and neuronal components according to the
Sensitivity of different vascular beds in the eye to neovascularization and blood-retinal barrier breakdown in VEGF transgenic mice.
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Neovascularization (NV) causes visual deficits in ocular disorders such as diabetic retinopathy, age-related macular degeneration, and retinopathy of prematurity. An understanding of the angiogenic factors promoting this abnormal vascular growth is necessary to devise a therapeutic approach to
Method for the Culture of Mouse Pulmonary Microvascular Endothelial Cells.
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Pulmonary microvascular endothelial cells (ECs) are integral to the alveoli-capillary barrier of the lung. The EC barrier integrity is known to be disrupted in severe lung diseases such as acute respiratory distress syndrome (ARDS), pneumonia and pulmonary edema. Mice are commonly used to model
Thrombin enhances the barrier function of rat microvascular endothelium in a PAR-1-dependent manner.
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Thrombin is a multifunctional coagulation protease with pro- and anti-inflammatory vascular effects. We questioned whether thrombin may have segmentally differentiated effects on pulmonary endothelium. In cultured rat endothelial cells, rat thrombin (10 U/ml) recapitulated the previously reported
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