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ischemia/triacylglycerol
Врската е зачувана во таблата со исечоци
Страница 1 од 76 резултати
Differential lipid deacylation during brain ischemia in a homeotherm and a poikilotherm. Content and composition of free fatty acids and triacylglycerols.
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The free fatty acid (FFA) and triacylglycerol content and composition are compared in the mouse and toad brain during ischemia. Mouse brain FFA are rapidly increased after decapitation, the maximal production rates being attained within the first minutes. Free arachidonic and stearic acids undergo
Accumulation of arachidonate in triacylglycerols and unesterified fatty acids during ischemia and reflow in the isolated rat heart. Correlation with the loss of contractile function and the development of calcium overload.
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Alterations in triacylglycerol and phospholipid metabolism are known to occur during the evolution of myocardial ischemic injury. The purpose of this study was to explore potential relationships between the accumulation of arachidonic acid and other fatty acids, the accumulation of triacylglycerol,
Myocardial triacylglycerol metabolism in ischemia.
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The utilization of transmural myocardial triacylglycerols, phospholipids and tissue free fatty acids was studied in dogs with and without left circumflex coronary artery occlusion for time intervals up to 4 hours. Results from 14C-labeling experiments reflected a continuous and dynamic turnover of
Changes in cerebral free fatty acids and triacylglycerols in focal cerebral ischemia.
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1. Focal cerebral ischemia was induced in anesthetized rats by occluding the stem of the proximal middle cerebral artery. 2. The levels of free fatty acids, such as stearic and arachidonic acids, in the ischemic cerebral cortex increased progressively until 60 min after occlusion, but thereafter
Cerebral phosphoinositide, triacylglycerol, and energy metabolism in reversible ischemia: origin and fate of free fatty acids.
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Levels of phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol (PI), phosphatidic acid, diacylglycerol (DAG), triacylglycerol (TAG), and free fatty acids (FFAs), as well as their fatty acid composition, were determined in rat forebrain during
Fructose-fed rat hearts are protected against ischemia-reperfusion injury.
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High fructose-fed (HFF) rat model is known to develop the insulin-resistant syndrome with a very similar metabolic profile to the human X syndrome. Such metabolic modifications have been associated with a high incidence of cardiovascular disease. The role of free radical attack in diabetes mellitus
Activation of Akt kinase accompanies increased cardiac resistance to ischemia/reperfusion in rats after short-term feeding with lard-based high-fat diet and increased sucrose intake.
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High-fat or high-carbohydrate food consumption contributes to changes in myocardial tolerance to ischemia. However, with respect to experimental models, most studies used diets with very high doses of cholesterol, saturated fatty acids, or fructose. In our study, we fed rats a high-fat diet based on
Distribution of carbon flux within fatty acid utilization during myocardial ischemia and reperfusion.
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Twenty-nine intact, working pig hearts were extracorporeally perfused and divided into two study groups (16 Aerobic and 13 Ischemic/Reflow hearts). Step function, equilibrium labeling with [14C]palmitate was used to develop uptake and washout curves of radioactive fatty acid products contained in
Trilinolein preserves mitochondria ultrastructure in isolated rat heart subjected to global ischemia through antioxidant activity as measured by chemiluminescence.
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Oxygen-derived free radicals (OFR) have been proposed as the cause of myocardial damage through lipid peroxidation during ischemia and reperfusion. Antioxidants can effectively ameliorate the damage induced by lipid peroxidation. Trilinolein is a triacylglycerol recently purified from the well known
Membrane lipids in the pathogenesis of brain edema: phospholipids and arachidonic acid, the earliest membrane components changed at the onset of ischemia.
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This chapter reviews studies concerning cellular membranes in the pathogenesis of cerebral edema. The main topics discussed are membrane lipids and the observation that the concentration of endogenous free fatty acids increases rapidly and reversibly in the brain after a single electroconvulsive
Comparison of the effect of cilostazol with aspirin on circulating endothelial progenitor cells and small-dense LDL cholesterol in diabetic patients with cerebral ischemia: a randomized controlled pilot trial.
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OBJECTIVE
A recent clinical trial showed the preventive effect of cilostazol on cerebrovascular diseases. We compared the effects of cilostazol with aspirin on circulating endothelial progenitor cells (EPCs), a surrogate marker for cardiovascular disease, and lipid metabolism in a randomized
Effects of nicotinic acid and mepacrine on fatty acid accumulation and myocardial damage during ischemia and reperfusion.
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To assess the nature of ischemia- and reperfusion-induced lipid changes and their consequences for myocardial function and integrity, Krebs-Henseleit perfused, isolated, working rat hearts were treated with nicotinic acid or mepacrine, putative inhibitors of triacylglycerol and phospholipid
Semen cassiae attenuates myocardial ischemia and reperfusion injury in high-fat diet streptozotocin-induced type 2 diabetic rats.
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Obese patients with type 2 diabetes mellitus (T2DM), which is characterized by hyperglycemia, are liable to more severe myocardial infarction. Semen Cassiae is proven to reduce serum lipid levels. This study investigated whether the Semen Cassiae extract (SCE) reduces myocardial ischemia and
Free fatty acids, neutral glycerides, and phosphoglycerides in transient focal cerebral ischemia.
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Cerebral ischemia is known to cause an increase in levels of free fatty acids (FFAs) and diacylglycerols (DGs), although the mechanism(s) leading to these changes is not well understood. In this study, we examined FFA and DG levels along with those of other lipids in rats during and after transient
Effect of intracellular lipid droplets on cytosolic Ca2+ and cell death during ischaemia-reperfusion injury in cardiomyocytes.
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Lipid droplets (LD) consist of accumulations of triacylglycerols and have been proposed to be markers of ischaemic but viable tissue. Previous studies have described the presence of LD in myocardium surviving an acute coronary occlusion. We investigated whether LD may be protective against cell
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