Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure write by Neelam Khaper. This book was released on 2001. Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure available in PDF, EPUB and Kindle.
Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure
Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure write by . This book was released on 2001. Modulation of Oxidative Stress and Antioxidants by Losartan in Heart Failure available in PDF, EPUB and Kindle. In patients surviving a myocardial infarction M), the heart undergoes a remodefing process characterized by hypertrophy which can also lead to heart failure. Although hypertrophy is an early response that may temporarily preserve cardiac function, numerous studies have suggested that this long term process of remodefing is also associated with an increase in oxidative stress and cardiac decompensation. The objectives of the present research on rat hearts subsequent to MI therefore, were to: (i) characterize changes in the oxidative stress and enzymatic antioxidants, (superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase) in relation to their rnRNA abundance and protein content; (ii) study changes in nonenzymatic antioxidants at different stages of heart failure in relation to cardiac function in order to have a more comprehensive information about the antioxidant reserve, and (iii) study the effects of RAS inhibition at the AT1 receptor site by losartan on the myocardial enzymatic and non-enzymatic antioxidants (SOD, GSHPx, catalase, vitamins A and E) and oxidative stress (Lipid hydroperoxides, reduced and oxidized glutathione and the redox ratio) in relation to the changes in hemodynamic function during the sequelae of congestive heart failure. It is concluded that inhibition of the RAS at the AT1 receptor site with losartan, in addition to reducing cardiac remodeling and improving hemodynamic function, reduces oxidative stress and improves myocardial endogenous antioxidants subsequent to myocardial infarction. The study suggests a newer role for losartan in the treatment of heart failure. Although changes in the SOD and catalase activities during heart failure correlated with changes in mRNA for these enzymes, the precise mechanism/s for decrease in oxidative, stress and improvement in antioxidant reserve after losartan treatment is/are unclear at this time. (Abstract shortened by UMI.).
Modulation of Oxidative Stress in Heart Disease
Modulation of Oxidative Stress in Heart Disease - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Modulation of Oxidative Stress in Heart Disease write by Sajal Chakraborti. This book was released on 2019-11-10. Modulation of Oxidative Stress in Heart Disease available in PDF, EPUB and Kindle. This book highlights the multifaceted roles of Reactive Oxygen Species (ROS) in modulating normal cellular and molecular mechanisms during the development of different types of heart disease. Each chapter in the book deals with the role that altered redox homeostasis plays in the pathophysiology of heart disease. In addition, the book explains how reactive oxidant species interact with their targets and provides novel strategies for attenuating oxidative stress-induced types of heart disease. The book not only covers ROS-induced response in heart disease at the cellular level, but also demonstrates that an imbalance of redox states has its roots in our genes, and explains the ways gene expression is regulated. In turn, it reviews potential sources of ROS, their pathological effects on the heart, and potential sites for therapeutic interventions.
Oxidative Stress in Heart Diseases
Oxidative Stress in Heart Diseases - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Oxidative Stress in Heart Diseases write by Sajal Chakraborti. This book was released on 2019-11-06. Oxidative Stress in Heart Diseases available in PDF, EPUB and Kindle. This book bridges the gap between fundamental and translational research in the area of heart disease. It describes a multidisciplinary approach, and demonstrates biochemical mechanisms associated with dysregulation of redox signaling, which leads heart disease. Presenting recent studies on improved forms of ROS scavenging enzymes; specific inhibitors for different ROS generating enzymes; and oxidant induced signaling pathways and their antagonists that allow subtle modulation of redox signaling, it also discusses the spatial and temporal aspects of oxidative stress in the cardiovascular system, which are of vital importance in developing better strategies for treating heart disease. Each chapter offers researchers valuable insights into identifying targets for drug development for different types of heart disease.
Oxidative Stress and Vascular Disease
Oxidative Stress and Vascular Disease - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Oxidative Stress and Vascular Disease write by John F. Keaney Jr.. This book was released on 1999-12-31. Oxidative Stress and Vascular Disease available in PDF, EPUB and Kindle. One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.
