Abstract
ABSTRACTObjectives: Redox regulation plays a crucial role in balancing the cardiovascular system. In this prospective study we aimed to identify currently unknown correlations valuable to cardiovascular research and patient management.Methods: Blood samples from 500 patients were collected directly before cardiosurgical interventions (Ethics Committee reference number 85/11). Four central redox parameters were determined together with about 30 clinical, anthropometric, and metabolic parameters.Results: Creatinine levels and pulmonary hypertension were significant predictors of the total antioxidant status (TAOS) in the patients; total glutathione levels were linked to C-peptide, and creatinine, gender, and ventricular arrhythmia influenced nitrate/nitrite levels. Notably, significant interactions were found between medication and redox parameters. Calcium channel blockers (CCBs) were positive predictors of total glutathione levels, whereas angiotensin-converting enzyme inhibitors and CCBs were negative predictors of NOx levels. Age showed the highest correlation with the duration of the intensive care stay, followed by NOx levels, creatinine, TAOS, and C-reactive protein.Discussion: In this prospective study we determined multiple correlations between redox markers and parameters linked to cardiovascular diseases. The data point towards so far unknown interdependencies, particularly between antihypertensive drugs and redox metabolism. A thorough follow-up to these data has the potential to improve patient management.Abbreviations: A: absorption; ΔA: absorption difference; ABTS: 2,2′-azino-di(3-ethylbenzothiazoline sulfonate); ACE: angiotensin-converting enzyme; AO: antioxidant; ARB: angiotensin receptor blocker; BMI: body mass index; CAD: coronary artery disease; CCB: calcium channel blocker; CDC: coronary heart diseases; COPD: chronic obstructive pulmonary disease; CRP: C-reactive protein; CVD: cardiovascular diseases; Cu-OOH: cumene hydroperoxide; D: dilution factor; DAN: 2,3-diaminonaphtalene; DMSO: dimethylsulfoxide; DNA: deoxyribonucleic acid; DTNB: 5,5-dithiobis(2-nitrobenzoate); ε: extinction coefficient; EDRF: endothelium-derived relaxing factor; fc: final concentration; GPx: glutathione peroxidases; (h)GR: (human) glutathione reductase; GSH: (reduced) glutathione; GSSG: glutathione disulfide; GST: glutathione-S-transferase; Hb: hemoglobin; HDL: high-density lipoprotein; Hk: hematocrit; H2O2: hydrogen peroxide; ICS: intensive care stay; LDH: lactate dehydrogenase; LDL: low-density lipoprotein; MI: myocardial infarction; NED: N-(1-naphthyl)-ethylendiamine-dihydrochloride; NOS: nitric oxide synthase; NOx: nitrate/nitrite; NR: nitrate reductase; PBS: phosphate buffered saline; PCA: principle component analysis; PH: pulmonary hypertension; ROS: reactive oxygen species; RNS: reactive nitrogen species; RT: room temperature (25°C); SA: sulfanilamide; SOD: superoxide dismutase; SSA: sulfosalicylic acid; TAC: total antioxidant capacity; TAOS: total antioxidant status; TEAC: trolox equivalent antioxidative capacity; TG: triglycerides; tGSH: total glutathione; TNB-: 2-nitro-5-thiobenzoate; U: unit; UV: ultraviolet; VA: volume activity; Wc: working concentration; WHR: waist-hip ratio.
Highlights
A thoroughly tuned balance between oxidative challenge and antioxidant defense is essential for maintaining functionality and integrity of the cardiovascular system, including cardiac myocytes and endothelial cells [1,2]
Peripheral blood from 500 patients was taken at one time point in the morning directly before a cardiosurgical intervention
Redox regulation and oxidative stress are essentially involved in the pathophysiology of cardiovascular diseases (CVDs), the metabolic state of patients before surgery, the surgical intervention itself, and the ensuing recovery phase
Summary
A thoroughly tuned balance between oxidative challenge and antioxidant defense is essential for maintaining functionality and integrity of the cardiovascular system, including cardiac myocytes and endothelial cells [1,2]. Major sources of oxidative stress in the cardiovascular system are NAD(P)H oxidase (in membrane complexes), mitochondrial cytochromes, xanthine oxidoreductase, reactive nitrogen species (NOx), and hemoglobin [3]. Redox stress has been shown to be a part of the pathophysiology of cardiovascular diseases (CVDs) such as atherosclerosis, ischemia/reperfusion injury, cardiomyopathies, cardiac hypertrophy, hypertension, ventricular remodeling, and congestive heart failure [2,4,5]. Close links between oxidative stress, vascular inflammation, endothelial dysfunction, and cardiovascular risk factors have been revealed [6,7]. Altered redox parameters are proposed to serve as risk factors for CVDs [10]; they might be valuable predictors for complications and the outcome of cardiosurgical interventions
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