title: Oxidant stress mechanisms in heart failure.
abstract: Evidences clearly indicate that HF is accompanied by excessive generation of OFRs and depletion of endogenous antioxidant system. The resultant oxidant stress depresses myocardial contractility and function by decreasing Ca++ uptake in sarcoplasmic reticulum and by impaired Ca(++)-ATPase in cardiac tissue. The various sources of OFRs production in HF include increased production of nitric oxide, cytokines, prostaglandins, auto-oxidation of catecholamines, activation of polymorph leucocytes and ischemia induced xanthine-xanthine oxidase. The prevention of oxidative stress by antioxidant translates into better metabolism and function of myocytes. It appears that antioxidant drugs may represent a novel adjunct to the existing therapeutic armamentarium in patients of HF irrespective of its etiology and severity.
authors.affiliation: Deptt. of Medicine, KGMC Lucknow, India.
authors.forename: M
authors.initials: M
authors.lastname: Chandra
authors.forename: K
authors.initials: K
authors.lastname: Surendra
authors.forename: R K
authors.initials: RK
authors.lastname: Kapoor
authors.forename: A
authors.initials: A
authors.lastname: Ghatak
authors.forename: G
authors.initials: G
authors.lastname: Kaur
authors.forename: N R
authors.initials: NR
authors.lastname: Pandey
authors.forename: M K
authors.initials: MK
authors.lastname: Misra
mesh_terms: D000818:Animals; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*