Limits...
Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats.

Neri M, Cerretani D, Fiaschi AI, Laghi PF, Lazzerini PE, Maffione AB, Micheli L, Bruni G, Nencini C, Giorgi G, D'Errico S, Fiore C, Pomara C, Riezzo I, Turillazzi E, Fineschi V - J. Cell. Mol. Med. (2007 Jan-Feb)

Bottom Line: The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue.We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-alpha, MCP-1, and IL6, IL8, IL10 production.The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.

View Article: PubMed Central - PubMed

Affiliation: Department of Forensic Pathology, University of Foggia, Italy.

ABSTRACT

Background: To investigate the cardiotoxic role of reactive oxygen species (ROS) and of products derived from catecholamines auto-oxidation, we studied: (1) the response of antioxidant cardiac cellular defence systems to oxidative stress induced by norepinephrine (NE) administration, (2) the effect of NE administration on cardiac beta1-adrenergic receptors by means of receptor binding assay, (3) the cellular morphological alterations related to the biologically cross-talk between the NE administration and cytokines [tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), interleukins IL6, IL8, IL10].

Methods and results: A total of 195 male rats was used in the experiment. All animals underwent electrocardiogram (EKG) before being sacrificed. The results obtained show that NE administration influences the antioxidant cellular defence system significantly increasing glutathione peroxidase (GPx) activity, glutathione reductase (GR) and superoxide dismutase (SOD). The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue. We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-alpha, MCP-1, and IL6, IL8, IL10 production.

Conclusions: Our results support the hypothesis that catecholamines may induce oxidative damage through reactive intermediates resulting from their auto-oxidation, irrespective of their interaction with adrenergic receptors, thus representing an important factor in the pathogenesis of catecholamines-induced cardiotoxicity. The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.

Show MeSH

Related in: MedlinePlus

Effect of propranolol (2 mg/kg i.v.), prazosin (0.3 mg/kg i.v.) and norep-inephrine (3 mg/kg i.p.) exposure on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats. PP = treated with propranolol and prazosin, NE = treated with norepinephrine, NEPP = treated with norepinephrine, propranolol and prazosin.A= p < 0.05 compared with control group B= p < 0.01 compared with control group C= p < 0.001 compared with control group D= p < 0.05 compared with PP group E= p < 0.01 compared with PP group F= p < 0.001 compared with PP group G= p < 0.05 compared with NE group H= p < 0.01 compared with NE group
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4401229&req=5

fig02: Effect of propranolol (2 mg/kg i.v.), prazosin (0.3 mg/kg i.v.) and norep-inephrine (3 mg/kg i.p.) exposure on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats. PP = treated with propranolol and prazosin, NE = treated with norepinephrine, NEPP = treated with norepinephrine, propranolol and prazosin.A= p < 0.05 compared with control group B= p < 0.01 compared with control group C= p < 0.001 compared with control group D= p < 0.05 compared with PP group E= p < 0.01 compared with PP group F= p < 0.001 compared with PP group G= p < 0.05 compared with NE group H= p < 0.01 compared with NE group

Mentions: The results obtained 4 hrs after propranolol, prazosin and subsequent NE administration (NEPP group) (Fig. 2) show that also in this case the antioxidant cardiac cellular enzymatic defence system was influenced: in fact GPx (Fig. 2A) and GR (Fig. 2B) activities were increased compared to controls (p < 0.001 and p < 0.05, respectively), whereas SOD activity shows no statistically significant increase (Fig. 2C).


Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats.

Neri M, Cerretani D, Fiaschi AI, Laghi PF, Lazzerini PE, Maffione AB, Micheli L, Bruni G, Nencini C, Giorgi G, D'Errico S, Fiore C, Pomara C, Riezzo I, Turillazzi E, Fineschi V - J. Cell. Mol. Med. (2007 Jan-Feb)

Effect of propranolol (2 mg/kg i.v.), prazosin (0.3 mg/kg i.v.) and norep-inephrine (3 mg/kg i.p.) exposure on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats. PP = treated with propranolol and prazosin, NE = treated with norepinephrine, NEPP = treated with norepinephrine, propranolol and prazosin.A= p < 0.05 compared with control group B= p < 0.01 compared with control group C= p < 0.001 compared with control group D= p < 0.05 compared with PP group E= p < 0.01 compared with PP group F= p < 0.001 compared with PP group G= p < 0.05 compared with NE group H= p < 0.01 compared with NE group
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401229&req=5

fig02: Effect of propranolol (2 mg/kg i.v.), prazosin (0.3 mg/kg i.v.) and norep-inephrine (3 mg/kg i.p.) exposure on cardiac antioxidant cellular systems. Values are presented as the mean (S.D.) of nine rats. PP = treated with propranolol and prazosin, NE = treated with norepinephrine, NEPP = treated with norepinephrine, propranolol and prazosin.A= p < 0.05 compared with control group B= p < 0.01 compared with control group C= p < 0.001 compared with control group D= p < 0.05 compared with PP group E= p < 0.01 compared with PP group F= p < 0.001 compared with PP group G= p < 0.05 compared with NE group H= p < 0.01 compared with NE group
Mentions: The results obtained 4 hrs after propranolol, prazosin and subsequent NE administration (NEPP group) (Fig. 2) show that also in this case the antioxidant cardiac cellular enzymatic defence system was influenced: in fact GPx (Fig. 2A) and GR (Fig. 2B) activities were increased compared to controls (p < 0.001 and p < 0.05, respectively), whereas SOD activity shows no statistically significant increase (Fig. 2C).

Bottom Line: The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue.We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-alpha, MCP-1, and IL6, IL8, IL10 production.The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.

View Article: PubMed Central - PubMed

Affiliation: Department of Forensic Pathology, University of Foggia, Italy.

ABSTRACT

Background: To investigate the cardiotoxic role of reactive oxygen species (ROS) and of products derived from catecholamines auto-oxidation, we studied: (1) the response of antioxidant cardiac cellular defence systems to oxidative stress induced by norepinephrine (NE) administration, (2) the effect of NE administration on cardiac beta1-adrenergic receptors by means of receptor binding assay, (3) the cellular morphological alterations related to the biologically cross-talk between the NE administration and cytokines [tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), interleukins IL6, IL8, IL10].

Methods and results: A total of 195 male rats was used in the experiment. All animals underwent electrocardiogram (EKG) before being sacrificed. The results obtained show that NE administration influences the antioxidant cellular defence system significantly increasing glutathione peroxidase (GPx) activity, glutathione reductase (GR) and superoxide dismutase (SOD). The oxidized glutathione (GSH/GSSG) ratio significantly decreases and malondialdehyde (MDA) levels increase showing a state of lipoperoxidation of cardiac tissue. We describe a significant apoptotic process randomly sparse in the damaged myocardium and the effect of ROS on the NE-mediated TNF-alpha, MCP-1, and IL6, IL8, IL10 production.

Conclusions: Our results support the hypothesis that catecholamines may induce oxidative damage through reactive intermediates resulting from their auto-oxidation, irrespective of their interaction with adrenergic receptors, thus representing an important factor in the pathogenesis of catecholamines-induced cardiotoxicity. The rise of the cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium with respect to the cardiac dysfunction resulting from NE injection.

Show MeSH
Related in: MedlinePlus