Damage to the heart is one of the most critical manifestations of transfusional iron overload. Because at present no experimental model is available to simulate iron-induced heart disease in the intact animal, we have employed rat myocardial cells in culture for studying the harmful effects of iron and the protective effects of iron chelation(1-4). Our previous studies have shown that iron toxicity in myocyte cultures is associated with profound, and reproducible changes in contractility and electophysiologic behaviour (5,6); that these abnormalities are associated with a marked increase in lipid peroxidation reflected in a change in composition of membrane lipids and an increased production of malondialdehyde (4,7); that these alterations may be prevented, or reversed by deferoxamine or the selective application of pharmacologic stimulants such as caffeine or calcium and; that iron toxicity may be significantly modified by the use of antioxidants such as α-tocopherol, by ascorbic acid, or by simultaneous hypoxia.
Hearts Of Iron IV For Mac
If the other three had been terrible to look on, this one was more terrible than the three together. She was clad in iron plate, and she had a wicked sword by her side and a knobby club in her hand She halted by the bodies of her sisters, and bitter tears streamed down into her beard.
BACKGROUND. Iron bioavailability has been identified as a factor that influences cellular hypoxia sensing, putatively via an action on the hypoxia-inducible factor (HIF) pathway. We therefore hypothesized that clinical iron deficiency would disturb integrated human responses to hypoxia.
METHODS. We performed a prospective, controlled, observational study of the effects of iron status on hypoxic pulmonary hypertension. Individuals with absolute iron deficiency (ID) and an iron-replete (IR) control group were exposed to two 6-hour periods of isocapnic hypoxia. The second hypoxic exposure was preceded by i.v. infusion of iron. Pulmonary artery systolic pressure (PASP) was serially assessed with Doppler echocardiography.
CONCLUSION. Clinical iron deficiency disturbs normal responses to hypoxia, as evidenced by exaggerated hypoxic pulmonary hypertension that is reversed by subsequent iron administration. Disturbed hypoxia sensing and signaling provides a mechanism through which iron deficiency may be detrimental to human health. 2ff7e9595c
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