hyperglycemia/hypoxia

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Stress hyperglycemia and the adrenergic regulation of pancreatic hormones in hypoxia.

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Stress hyperglycemia occurs in normal and chronically hypoxemic dogs when PaO2's are acutely lowered below 30 torr. Several factors are thought to contribute to the rise in blood glucose. The initial fall in PaO2 activates the sympathetic nervous system, stimulating alpha and beta adrenergic

Identification and validation of reference genes for quantitative RT-PCR analysis of retinal pigment epithelium cells under hypoxia and/or hyperglycemia.

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Retinal pigment epithelium (RPE) cell-based gene expression studies performed under hypoxia and/or hyperglycemia show huge potential for modeling cell responses in diabetic retinopathy, retinopathy of prematurity and other retinal diseases. However, normalization of gene expression on RPE cells

Proliferation, Migration, and Production of Nitric Oxide by Bone Marrow Multipotent Mesenchymal Stromal Cells from Wistar Rats in Hypoxia and Hyperglycemia.

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We studied proliferation, migration, and secretion of NO by bone marrow multipotent mesenchymal stromal cells from Wistar rats during conditioning under hypoxic and hyperglycemic conditions and the effect of erythropoietin on these parameters. A stimulating effect of erythropoietin on cell

[Hypoxia and hyperglycemia promote the proliferation and migration of human marrow mesenchymal stem cells in vitro].

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OBJECTIVE To investigate the cell proliferation, apoptosis and migration of human marrow mesenchymal stem cells (hMSCs) under hypoxia and hyperglycemia. METHODS The hMSCs from healthy adults were isolated and harvested by density gradient centrifugation followed by adherent cultures. The cells was

Hypoxia and high glucose activate tetrodotoxin-resistant Na(+) currents through PKA and PKC.

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Voltage-gated sodium channels are critical for the initiation and propagation of action potentials and for the regulation of neuronal excitability. Hyperglycemia and hypoxia are two main changes in diabetes frequently associated with several complications. Although many studies on

Modulating peripheral nerve damage from hyperglycemia/anoxia.

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Combined hyperglycemia and anoxia have a marked negative effect on peripheral nerve not seen with either alone. We studied whether nerve injury is related to the presence of hyperglycemia in the oxygenated state, anoxic state, or both. We performed recordings of the nerve action potential (NAP) from

Hypoxia and high glucose upregulate AT1 receptor expression and potentiate ANG II-induced proliferation in VSM cells.

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We examined the effect of hypoxia and high glucose (HG) on ANG II type 1 (AT(1)) receptor expression and proliferation in cultured vascular smooth muscle (VSM) cells. Exposure of quiescent cells to hypoxia in a serum-free DME-Ham's F-12 medium for 6-24 h induced a progressive increase in AT(1) mRNA

Effect of hypoxemia and hyperglycemia on pH in the intact cat retina.

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OBJECTIVE To examine the effects of acute hypoxemia and hyperglycemia on retinal pH to understand hyperglycemia-induced changes in the normal intact cat retina. METHODS Spatial profiles of extracellular hydrogen ion (H+) concentration were obtained from the cat retina, in vivo, using pH-sensitive

Cardioprotective effect of chronic hyperglycemia: effect on hypoxia-induced apoptosis and necrosis.

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It is generally accepted that mild forms of diabetes render the heart resistant to an ischemic insult. Because myocytes incubated chronically in medium containing high concentrations of glucose (25 mM) develop into a diabetes-like phenotype, we tested the hypothesis that high-glucose treatment

The effect of hyperglycemia on cerebral metabolism during hypoxia-ischemia in the immature rat.

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Unlike adults, hyperglycemia with circulating glucose concentrations of 25-35 mM/L protects the immature brain from hypoxic-ischemic damage. To ascertain the effect of hyperglycemia on cerebral oxidative metabolism during the course of hypoxia-ischemia, 7-day postnatal rats underwent unilateral

Effects of acarbose on the acceleration of postprandial hyperglycemia-induced pathological changes induced by intermittent hypoxia in lean mice.

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Postprandial hyperglycemia (PPH) and intermittent hypoxia related to the sleep apnea syndrome are important predictors of cardiovascular disease. We investigated the effects of intermittent hypoxia on pathological changes in the left ventricular (LV) myocardium caused by PPH in lean mice and

Human cortical fibroblast responses to high glucose and hypoxia.

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OBJECTIVE Approximately 30% of individuals with diabetes mellitus are susceptible to diabetic nephropathy, whereas ischemic injury uniformly induces renal impairment. As matrix accumulation correlates with progressive renal disease we assessed parameters associated with matrix turnover in response

Hypoxia-induced sympathetic inhibition of the fetal plasma insulin response to hyperglycemia.

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Large-for-delivery date babies, considered characteristic of diabetic pregnancy, are believed to result from fetal hyperinsulinemia. Paradoxically, infant birth weights tend to be low-for-delivery date in mothers with more severe diabetes. We tested the hypothesis that hypoxemia in such fetuses

Reference genes for expression studies in hypoxia and hyperglycemia models in human umbilical vein endothelial cells.

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Human umbilical vein endothelial cell (HUVEC)-based gene expression studies performed under hypoxia and/or hyperglycemia show huge potential for modeling endothelial cell response in cardiovascular disease and diabetes. However, such studies require reference genes that are stable across the whole

Scutellarin inhibits high glucose-induced and hypoxia-mimetic agent-induced angiogenic effects in human retinal endothelial cells through reactive oxygen species/hypoxia-inducible factor-1α/vascular endothelial growth factor pathway.

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Scutellarin inhibits hypoxia-induced and moderately high glucose-induced proliferation and vascular endothelial growth factor (VEGF) expression in human retinal endothelial cells (HRECs); thus, it could be a potential therapy for diabetic retinopathy. However, how scutellarin inhibits VEGF is

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