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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
IHD is a leading cause of morbidity and mortality in the United States and other parts of the world. Despite therapeutic breakthroughs over the past decades such as coronary bypass, percutaneous coronary intervention, antiplatelet and antithrombotic therapies, and angioplasty, the prevalence of IHDs remains extremely high and constitutes a devastating factor for heart failure.610,611 This devastating prevalence is usually due to microvascular dysfunction. Among various therapeutic strategies of IHD, enormous efforts have been made to limit ischemia/reperfusion (I/R) injury, which occurs when the ischemic myocardium is reperfused with oxygen and substrate-rich blood, which paradoxically worsens heart function.611 This is often due to relief in vasospasm reinstitution of O2 extraction. Ischemic myocardium, with nutrient and oxygen deprivation and buildup of ROS, uses glycolysis as the primary source of metabolic energy. As a consequence, metabolic acidosis, hyperkalemia, and Ca2+ overload develop in cardiomyocytes after coronary artery occlusion or glucose mandated lack of O2 extraction, leading not only to cardiomyocyte apoptosis during the acute phase but also to delayed adverse myocardial remodeling, which further compromises cardiac function.611 Therefore, limiting I/R-induced myocardial ROS accumulations and apoptosis benefits both short- and long-term survival and quality of life. Although the mechanism responsible for I/R-induced cardiac abnormalities has been focused largely on necrosis and type I (apoptotic) programmed cell death,611 an intriguing and provocative paradigm has emerged recently that highlights a unique role for deregulated macroautophagy (hereafter referred to as autophagy) in the heart that may render cardiomyocytes more prone to I/R injury and long-term postinfarction cardiac remodeling.610,612It has been perceived that autophagy induced by ischemic preconditioning is essential for cardioprotection. To this end, new and innovative strategies to maintain or restore myocardial autophagy homeostasis and its attendant cardiomyocyte survival have been the subject of intensive investigation. This condition occurs to a milder degree in the periphery resulting in painful weakness and fatigue, which chemically sensitive patients frequently develop after a pollutant exposure. This pollutant-induced vascular spasm or small blood vessel leak usually results in the symptoms induced in the chemically sensitive.
Environmental benign RP-HPLC method for the simultaneous estimation of anti-hypertensive drugs using analytical quality by design
Published in Green Chemistry Letters and Reviews, 2023
Naveenarani Dharuman, Karunanidhi Santhana Lakshmi, Manikandan Krishnan
Benidipine is a long-acting, dihydropyridine calcium channel blocker used as an anti-anginal and anti-hypertensive agent [6]. It is chemically (benidipine, (±)-(R*)−3- [(R*)−1-benzyl-3-piperidyl] methyl-1,4-dihydro-2,6-dimethyl- 4-(m-nitrophenyl)−3,5-pyridine dicarboxylate hydrochloride (Figure 1a). It inhibits L, T, and N-type calcium channels and has a strong vascular selectivity. The drug has anti-oxidant properties and an increase in nitric oxide production. In addition, it shows cardioprotective benefits in patients with ischemic heart disease. It also shows renal protective effects [7]. Chlorthalidone (Figure 1b) is a thiazide type diuretic used exclusively as antihypertensive. It is effective in BP reduction and improving cardiovascular outcomes [8]. The IUPAC name of chlorthalidone is benzenesulfonamide, 2-chloro-5-(2,3-dihydro-1-hydroxy-3-oxo-1H-isoindol-1-yl) [9]. It blocks the sodium-chloride cotransporter in the ascending loop of Henle's distal convoluted tubule [10]. The literature study reveals that few HPLC (High-performance liquid chromatography) techniques were reported for chlorthalidone [11–14], while for benidipine HPLC/UPLC (Ultra performance liquid chromatography) [15] and with the combination of BEN and CHD stability indicating HPLC [16] and RP-HPLC [17] technique has been discussed.